Background: Ventilator associated pneumonia (VAP) is one of the most important form of hospital acquired infections which is associated with increased mortality and morbidity. VAP occurs in about 9 to 27% of all intubated patients. Intubation is associated with 3 to 10 fold increase in the incidence of VAP among all patients receiving mechanical ventilation. In contrast to other nosocomial infections, the crude mortality rate occurring due to VAP ranges from 24% to 76%. ICU patients with VAP have a 2 to 10-fold higher risk of death when compared with patients without pneumonia. Aim: The present study is undertaken to find out the frequency of occurrence of VAP in clinically suspected patients who are mechanically ventilated for more than 48 hours and the major pathogens causing VAP and their antibiotic sensitivity pattern. Methods: A total of 392 patients who are mechanically ventilated for more than 48 hours with clinical suspicion of VAP were included in the study. Endotracheal aspirate was collected and subjected to Grams stain and culture. Culture was performed by quantitative culture technique. Growth on the culture plate was identified by standard microbiological techniques and subjected to antibiotic sensitivity testing by Kirby Bauer disc diffusion method and CLSI guidelines. Results: Among the 392 clinically suspected VAP patients enrolled in the study 52.8% patients were diagnosed with VAP as per the CPIS score. The most common age group affected was 28- 40 years with male preponderance. 18% of the infections were categorized as early onset VAP while 72% as late onset VAP. Pseudomonas aeruginosa, Staphylococcus aureus and Acinetobacter baumannii were the most common isolates.78.5% of Gram negative bacteria were β lactamase producers.89.6% of the Pseudomonas aeruginosa and 96.2 % of Acinetobacter baumannii were meropenem and 84.6% of Staphylococcus aureus strains were methicillin resistant. Conclusion: Staphylococcus aureus was the most common organism causing early onset and Pseudomonas aeruginosa in late onset VAP.
1. Cristina M, Riccardo P, Nitin P et al Ventilator Associated Pneumonia: Evolving Definitions and Preventive Strategies. Respir Care 2013;58;6.
2. Apostolopoulou E, Bakakos P, Katostaras T, Gregorakos L. Incidence and risk factors for ventilator-associated pneumonia in multidisciplinary intensive care units in Athens, Greece. Respir Care 2003;48:681-88.
3. Steven M. K and Jonathon D. T. Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention. Clin Microbiol Rev 2006:19(4):637-9.
4. Niederman MS, Craven DE, Bonten MJ. American Thoracic Society and Infectious Diseases Society of America (ATS/IDSA). Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J RespirCrit Care Med 2005;171(4):388–416.
5. Zolfaghari PS and Wyncoll DL. The tracheal tube: gate way to ventilator-associated pneumonia. Crit Care 2011;15:310-12.
6. Rakshit P, Nagar VS, Deshpande AK. Incidence, clinical outcome, and risk stratification of ventilator associated pneumonia-a prospective cohort study. Indian J Crit Care Med 2005;9:211-16.
7. Fujitani S and Yuginton VL: Quantitative cultures for diagnosing ventilator- associated pneumonia: a critique. Clin Infect Dis 2006;43(2):106-113.
8. Bauer, Kirby, Sherri, Turek. Antibiotic susceptibility testing methods, Am.J.Clin Path 1966;45:493 -498.
9. Clinical and Laboratory Standards Institute (2006). Performance Standards for Antimicrobial Disk Susceptibility Tests, Approved Standard, 9th edn. Clinical and Laboratory Standards document M2-A9 [ISBN1-56238-586-0] Clinical and Laboratory Standards Institute: Wayne, PA, USA.
10. Coudron PE, Moland ES, Sanders CC. Occurrence and Detection of Extended-Spectrum ß-lactamases in members of the family Enterobacteriaceae at a Veterans Medical Center: Seek and You May Find. J ClinMicrobiol 1997; 35:2593-7.
11. Brun-Buisson C, Legrand P, Philippon A, Montravers F, Ansquer M, Duval J et al. Transferable enzymatic resistance to third-generation cephalosporins during a nosocomial outbreak of multi resistant Klebsiella pneumoniae. Lancet 1987;8:302-6.
12. French, G.L., Ling, J., Hui, Y.W. Determination of methicillin-resistance in Staphylococcus aureus by agar dilution and disc diffusion methods. Journal of Antimicrobial Chemotherapy 1987: 20; 599-608.
13. Gadani H, Vyas A, Kar AK. A study of ventilator-associated pneumonia:Incidence, outcome, risk factors and measures to be taken for prevention.Indian J Anaesth. 2010;54:535-40.
14. Ferrer R, Artigas A. Clinical review: Non- antibiotic strategies for preventing ventilator- associated pneumonia. Crit Care 2001;6(1): 45-51.
15. Porzecanski I and Bowton DL. Diagnosis and treatment of ventilator-associated pneumonia. Chest 2006;130:597-604.
16. Dey A, Bairy I. Incidence of multidrug-resistant organisms causing Ventilator associated pneumonia in a tertiary care hospital: A nine months’ prospective study. Ann Thorac Med. 2007;2:52–7.
17. Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J RespirCrit CareMed. 2002;165:867-903.
18. Rello J, Quintana E, Ausina V et al.Incidence, etiology, and outcome ofnosocomial pneumonia in mechanicallyventilated patients. Chest 1991;100(2):439–444
19. Fagon JY, Chastre J, Vuagnat A,Trouillet JL, Novara A, GibertC.Nosocomial pneumonia and mortalityamong patients in intensive care units.JAMA 1996;275(11):866–869.
20. Rahbar M, Monnavar KM, Vatan KK, Fadaei-haq A, Shakerian F. Carbapenemresistance in gram-negative bacilli isolates in an Iranian 1000-bed TertiaryHospital. Pak J Med Sci. 2008; 24(4):537-40.
21. Jakbrittu R.P, Boloor R. Characterisation of aerobic bacteria isolated fromendotracheal aspirate in adult patients suspected ventilator associatedpneumonia in a tertiary care center in Mangalore. Saudi J Anaesth. 2012;6(2):115–19.
22. Gupta A, Agrawal A, Mehrotra S, Singh A, Malik S, Khanna A. Incidence, risk stratification, antibiogram of pathogens isolated and clinical outcome of ventilator associated pneumonia. Indian J Crit Care Med. 2011;15:96-101.
Occult carcinoma of breast presenting as axillary nodal metastasis – a case report
We report the case of a 50-year-old woman with occult breast cancer who presented with a hard metastatic nodule in the left axilla. Histology identified a metastatic ductal carcinoma deposits in the lymph nodes, but mammography of left breast showed only diffuse thickening of skin and subcutaneous tissue.Left modified radical mastectomy was performed and histopathology revealed invasive ductal carcinoma 1mm x 1mm size with multiple axillary node metastasis.
1. Halsted WS. The result of radical operations for the cure of carcinoma of the breast. Ann Surg 1907;46:1–19.
2. Owen HW, Dockerty MB, Gray HK. Occult carcinoma of the breast. Surg Gynecol Obstet 1954;98:302–8.
3. Baron PL, Moore MP, Kinne DW, Candela FC, Osborne MP, Petrek JA. Occult breast cancer preserving with axillary metastases: updated management. Arch Surg1990;125:210–4.
4. Kyokane T, Akashi-Tanaka S, Matsui T, Fukutomi T. Clinicopathological characteristics of non-palpable breast cancer presenting as an axillary mass. Breast Cancer 1995;2:105–12.
5. Edlow CW, Carter D. Heterotopic epithelium in axillary lymph nodes: report of a case and review of the literature. Am J Clin Pathol 1973;59:666–73.
6. Copeland EM, McBride CM. Axillary metastases from unknown primary sites.Ann Surg 1973;178:25–7.
7. Kemeny MM, Rivera DE, Terz JJ, Benfield JR. Occult primary adenocarcinoma with axillary metastases. Am J Surg 1986;152:43–7.
8. Iglehart JD, Ferguson BJ, Shinleton WW, Sabiston DC, Silva JS, Fetter BF, et al. An ultrastructual analysis of breast carcinoma presenting as isolated axillary adenopathy. Ann Surg 1982;196:8–13.
9. Bhatia SK, Saclarides TJ, Witt TR, Bonomi PD, Anderson KM, Economou SG. Hormone receptor studies in axillary metastases from occult breast cancers. Cancer1987;59:1170–2.
10. Grunfest S, Steiger E, Sebek B. Metastatic axillary adenopathy: use of estrogen receptor protein as an aid in diagnosis. Arch Surg 1978;113:1108–9.
11. Haupt HM, Rosen PP, Kinne DW. Breast carcinoma presenting with axillary lymph node metastases: an analysis of specific histopathologic features. Am J Surg Pathol 1985;9:165–75.
12. Patel J, Nemoto T, Rosner D, Dao TL, Pickren JW. Axillary lymph node metastasis from an occult breast cancer. Cancer 1981;47:2923–7.
13. Rosen PP. Axillary lymph node metastases in patients with occult noninvasive breast carcinoma. Cancer 1980;46:1298–306.
14. Ozzello L, Sanpitak P. Epithelial stromal junction of intraductal carcinoma of the breast. Cancer 1970;26:1186–98.
15. Ellerbroek N, Holmes F, Singietary E, Evans H, Oswald M, McNeese M. Treatment of patients with isolated axillary nodal metastases from an occult primary carcinoma consistent with breast origin. Cancer 1990;66:1461–7.
16. Vilcoq JR, Calle R, Ferme F, Veith F. Conservative treatment of axillary adenopathy due to probable subclinical breast cancer. Arch Surg 1982;117:1136–8.
17. Feuerman, MD, Attie, JN, Rosenberg B. Carcinoma in axillary lymph nodes as an indicator of breast cancer. Surg Gynecol & Obstet1962; 114: 5.
18. Westbrook KC, Gallager HS. Breast carcinoma presenting as an axillary mass. Am J Surg 1971; 122: 607.
19. Larsen RR, Sawyer KC, Sawyer RB, Torres RC. Occult carcinoma of the breast. Am J Surg 1964; 107: 553–555.
20. Osteen RT, Kopf G, Wilson RE. In pursuit of the unknown primary. Am J Surg 1978; 138: 494–498.
21. Fitts WT Jr, Steiner GC, Enterline HT. Prognosis of occult carcinoma of the breast. Am J Surg 1963; 106: 460.
22. Ashikari R, Rosen PP, Urban JA, Senoo T. Breast carcinoma presenting as an axillary mass. Ann Surg 1976; 183: 415–417.
23. Gershon-Cohen J, Ingleby H, Hermel MB. Occult carcinoma of the breast: Value of roentgenography. Arch Surg 1955; 70: 385.
Peri-operative hemodynamic stability in patients undergoing laparoscopic procedures using dexmedetomidine
Polycythemia vera (PV) is a chronic myeloproliferative disorder characterised by panmyelosis, splenomegaly, and predisposition to venous and arterial thrombosis. Our case was a 54 year male patient who presented with massive splenomegaly, eryhtrocytosis and bone marrow panmyelosis and positive JAK2V617F mutation. Sensitive and relatively cost effective test of JAK2V617F mutation helped in early diagnosis and treatment of PV with certainity. Patient responded well with phlebotomy. Polycythemia vera is a uncommon myeloproliferative neoplasm which is asymptomatic in majority of patients thus needs early identification and treatment to prevent serious complications of haemorrhage and thrombosis.
1. Thiele J, Kvasnicka HM, Orazi A, et al. Polycythemia vera. In: Swerdlow SH, Campo E, Harris NL, et al, eds. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. 4th ed. Lyon, France: IARC Press; 2008:40-43.
2. Mckenzie BS, Beglinger SS. Myeloproliferative disorders. In: Mckenzie BS, Williams LJ (Eds). Clinical Laboratory Hematology. 2nd edition. New Jersey: Pearson publishers;2010: 444-80.
3. Tefferi A. JAK and MPL mutations in myeloid malignancies. Leuk Lymphoma. 2008;49:388-397.
4. James C, Ugo V, Le Couedic JP, et al. A unique clonal JAK2 mutation leading to constitutive signaling causes polycythaemia vera. Nature. 2005; 434: 1144-1148.
5. Ross C, Vanamala N, Ramesh K. Polycythemia vera and essential thrombocythemia- A single institute experience. Indian J Med & Ped Oncol 2008;29(4):7-11.
6. Thiele JM, Kvasnicka HM. Diagnosis of polycythemia vera based on bone marrow pathology. Curr Hematol Rep. 2005; 4:218-223.
Survival of truncus arteriosus in 5th decade - a case report
Persistent Truncus arteriosus is congenital cyanotic heart disease characterised by a single great artery that leaves the base of heart and gives rise to coronary, pulmonary and systemic arteries. Majority of patients die of congestive heart failure before their first birthday .Only occasional patients survive in adulthood. We are presenting such a case
1. Lev M, Saphir O. Truncas arteriosus communis persistents Pediatr. 1942;20:74.
2. Calder L, van Praagh R, van Praagh S, et al. Truncus arteriosus communis. Clinical, angiographic and pathologic findings in 100 patients. Am Heart J.1976;92:23.
3. Tandon R, Hauck AJ, Nadas AS. Presistent truncus arteriosus A clinical, hemodynamic, and autopsy study of nineteen cases. Circulation. 1963;28:1050-60.
4. Wilson J.A description of a very unusual malformation of the human heart. Philos Trans R Soc London [Biol]. 1798;18:346.
5. Buchanan A. Malformation of the heart. Undivided truncas arteriosus. Heart otherwise double. Trans Pathol Soc London. 1864;15:89.
6. Collett RW, Edwards JE. Persistent truncas arteriosus. A classification according to anatomic types. Surgical Clinics of North America. 1949;29:1245.
7. Van Praagh R, van Praagh S. The anatomy of common aorticopulmonary trunk (Truncus arteriosus communis ) and its embryologic implications. Am J Cardiol.1965;16:406-25.
8. Van Praagh R. Editorial: classification of truncus arteriosus communis (TAC). Am Heart J. 1976;92:129-32.
9. Kirby ML. Contribution of neural crest to heart and vessel morphology. In: Richard P Harvey, Nadia Rosenthal (Eds). Heart development. San Diego, CA: Academic press. 199.pp.179-93.
10. Conway SJ, Henderson DJ, Copp AJ. Pax3 is required for neural crest migration in the mouse: evidence from the spolotch (Sp2H) mutant. Development.1997;124:505-14.
11. Momma K, AndoM, Mastsuoka R. Truncus arteriosus communis associated with 22q11 deletion. J Am Coll Cardiol. 1997;30:1067-71.
12. Goldmuntz E, Clark BJ, Mitchell LE, et al. Frequency of 22q11 deletions in patients with contruncal defects. J Am Coll Cardiol.1998;32:492-8.
13. Emanuel BS, Budarf ML, scamber PJ. The genetic basis of contruncal defects: The chromosome 22q11.2 deletion. In: Heart Development. (Eds). Richard P Harvey and nadia Rosenthal. San Diego, CA. Academic press. 1999.pp.463-78.
14. Goldmuntz E. Deciphering the genetic etiology of contruncal defects. In: Artman M, Woodrow Benson D, Srivatsava D, Nakazawa M. Malden. MA. Blackwell Futura. 2005.pp.238-41.
15. Mair D, Ritter D, Davis G selection of patients with truncus arteriosus for surgical correction: Anatomic and hemodynamic considerations. Circulation. 1974;49:144-51.
16. Butto F, Lucas R, Edwards J. Persistent truncus arteriosus: Pathologic anatomy in 54 cases. Pediatr Cardiol. 1989;7:95-101.
17. Thiene G, Bortolotti U, Gallucci V. Anatomical study of truncus arteriosus communis with embryological and surgical considerations. Br Heart J. 1976;38:1109-23.
18. Kirklin JW, Barratt- Boyes BG. Truncus arteriosus. In. Kirklin JW, Barratt- Boyes BG (Eds). Cardiac Surgery. 2nd edition. New York: Churchill livingstone. 1992.pp.1131-52.
19. Russell HM, Jacobs ML, Anderson RH, et al. A simplified categorization for common arterial trunk. J Thorc Cardiovasc Surg. 2011;141:645-53.
20. Bohuta L, Hussain A, Fricke TA, et al. Surgical repair of truncus arteriosus associated with interrupted aortic arch: Long-term outcomes. Ann Thorac Surg. 2011;91:1473-7.
21. Bharati S, McAllister HA Jr, Rosenquist GC, et al. The surgical anatomy of truncus arteriosus communis. J Thorac Cardiovasc Surg. 1974;67:501-10.
22. Jacobs ML. Congenital heart surgery nomenclature and database project: Truncus arteriosus. ATS. 2000;69:S50-S5.
23. Juaneda E, Haworth SG. Pulmonary vascular disease in children with truncus arteriosus. Am J Cardiol. 1984;54:1314.
24. Marcelleti C, McGoon DC, Mair DD. The natural histroy of truncus arteriosus. Circulation. 1976;54:108. Victorica BE, Krovetz LJ, Elliott CP, et al. Persistent truncus arteriosus in infancy. AM Heart J. 1969;77:13.
A study on contraceptive knowledge, attitude and practice (KAP) among women attending family planning clinic of a private hospital of Western INDIA
Background: The widespread adoption of family planning, in a society, is an integral component of modern development and is essential for the integration of women into social and economic life. Objectives: To assess the knowledge, attitude and practice regarding usage of contraceptive methods among women attending family planning clinic Material and Method: A cross sectional study was conducted in 100 urban women. They were allotted to two groups – Group A of 76 women consisted of those who came for Medical termination of pregnancy (MTP) and Group B of 24 women who came with incomplete abortion following induced abortion. A pretested semi structure questionnaire was used as study tool to assess the contraceptive knowledge, attitude and practices. The data was analyzed using appropriate statistical methods (SPSS ver. 20). Result: Though 82% women were aware of the existence of a contraceptive method, only 44% ever used one. The most commonly used contraceptive was condom (34%). 82% were willing to undergo tubectomy in future whereas only 20% were willing to accept an intrauterine contraceptive device. Conclusion(S): The study highlights that although there is high level of awareness, contraceptive use is not very high. New ways of motivating people to adopt contraceptives should be considered.
1. Trusell J. Contraceptive efficacy, in: Hatcher RA, Trusell J, Stewart Fet al. (eds). Contraceptive Technology, 17th ed. Irvington Publishers, New York, NY; 1998.
2. Kenny L. Contraception, sterilization and termination of pregnancy, in Luesley DM, Baker PN (eds), Obstetrics and Gynecology. An evidence-based text for MRCOG. Arnold, London, 1st edition 2004; 514-523.
3. Task force on post-ovulatory methods of fertility regulation. Randomized control trial of levonorgestrel versus the Yuzpe regimen of combined oral contraceptives for emergency contraception. Lancet1998; 352:428-33.
4. Young LK, Farguhar CM, Mc Cowan LME et al. The contraceptive practice of women seeking termination of pregnancy in an Aukland clinic. NZ Med J 1994; 107:189-91.
5. Aneblom G, Larsson M, Odlind V et al. Knowledge, use and attitudes towards emergency contraceptive pills among Swedish women presenting for induced abortion. BJOG 2002; 109:155-60.
6. Bromham DR, Cartmill RS. Knowledge and use of secondary contraception among patients requesting termination of pregnancy.BMJ 1993; 306; 556-7.
Digital and palmar dermatoglyphics patterns in myocardial infarction
Introduction: Dermatoglyhics is the scientific study of skin creases and lines and has formed an important part of surface anatomy. The development of dermatoglyphics occurs at much earlier embryonic stage. This is the same period when most of the organs and systems develop including the cardiovascular system. Hence in this study we evaluated the dermatoglyphics in patients of Myocardial Infarction as compared to normal counterparts. Materials and Methods: Study was carried out in Department of Anatomy, in D. Y. Patil medical college during January 2011 to June 2012. Finger prints and palm prints of 150 diagnosed cases of Myocardial Infarction 120 males (M) and 30 females (F) and 150 Control group120 males and 50 females were obtained. Materials required for standard ink method was collected and used for data collection of both the hands. Written consent of the patients was obtained. Results: It was observed in our present study that there was significant increase in whorls and decrease in percentage loops and arches in Myocardial Infarction as compared to controls. The frequency of total palmar pattern in Myocardial Infarction Group is decreased in both sexes and both sides as compared to the controls. There was increase in frequency of position of axial triradii at t’ and t’’ in both hands of myocardial Infarction group in both sexes. Conclusion: Dermatoglyphics in Myocardial Infarction showed significant variation as compare to normal. Presence of above dermatoglyphic features will help us to predict that these individuals may be susceptible for myocardial infarction. It warrants further research in the same direction.
1. Mescher AL. Junqueira's Basic Histology. 12th ed. USA: McGraw-Hill Companies Inc; 2010.p. CD Chapter-Skin.
2. Kumbnani H. K.: Dermatoglyphics- A Review. Anthropologist Special Volume No. 3: 2007: 285-295.
3. Dorland’s Illustrated Medical Dictionary. 28th ed. Philadelphia: Saunders W B; Dermatoglyphics; 1994; 449.
4. Penrose L. S.: and P. T. Ohara: The development of epidermal ridges: Journal of Medical Genetics, 10, (2), 1973, 201-208.
5. Kasey Wertheim.: Embryology and morphology of friction ridge skin. The Fingerprint sourcebook. Washington, D C: U S department of justice, office of justice programs. Published by NIJ (National institute of juctice).2011, 1-22.
6. Namouchi I: Anthropological significance of dermatoglyphic trait variation: an intra-Tunisian population analysis. International Journal of Modern Anthropology 2011; 4 : 12 – 27
7. Gupta UK and Prakash S: Dermatoglyphics: a study of finger tip patterns in bronchial asthma and its genetic disposition. Kathmandu University Medical Journal (2003) Vol. 1, No. 4, Issue 4, 267-271.
8. Pratibha Ramani, Ahilasha P. R., Herald Sherlin and others: Conventional Dermatoglyphics-Revived concept. International journal of pharma and bio sciences, Vol 2, issue 3 sep 2011, 446-458.
9. Fausi AS, Kasper DL, Longo DL, et al. Herrison's Principles of Internal Medicine Volume II. 17th ed. New York: McGraw-Hill; 2008.p.1532
10. Cummins H and Midlo. Finger Prints of palms and soles. An introduction to dermatoglyphics. 1961; Dover Pub. INC, New York.
11. Ashbaugh D. R.: Ridgeology. J. Forensic Ident: 1991, 41 (1), 1-64.
12. Dhall V, Rathee SK, Dhall A: Utility of finger prints in myocardial infarction patients. J Anatomical Society India, 2000; 49 (2): 153-154.
13. Rashad MN, Mi MP, Rhoads G: Dermatoglyphic studies of myocardial infarction patients. Abst Hum Hered 1978; 28:1–6.
14. Anderson MW, Haug PJ, Critchfield G: Dermatoglyphic features of Myocardial Infarction patients. abst Amer J Physl Anthropol, 1981; 55(4): 523-27.
15. Jalali F, KO Hajian-Tilaki: A Comparative Study of Dermatoglyphic Pattern in Patients with Myocardial Infarction and Control Group. Acta Medica Iranica, 2002, 40(3): 187-91.
Correlation between clinical and angiographic findings in patient underwent angiography
Pankaj Palange, Ravikant Patil, R B Kulkarni, Atul Jankar
Introduction: Cardiovascular diseases are account for approximately 12 million deaths annually and are commonest cause of death globally. The progressive evolution in cardiac catheterization technique coupled with the development of effective treatment options for coronary artery disease, diagnostic coronary angiography has become one of the primary components of cardiac catheterization. Objective: To study correlation between clinical and angiographic findings in patient underwent angiography. Material and Methods: A cross sectional study was carried out for the period of one Year in Department of Cardiology, Bharati Vidyapeeth Medical College and Hospital, Sangli. 100 patients above 20 years of age, symptomatic patient, asymptomatic patient with electrocardiogram changes, patients who are willfully opting for coronary angiography were included in the study. Patients with previously diagnosed ischemic heart disease and underwent PTCA or CABG are excluded. Coronary angiography either from femoral or radial artery was done. The results of coronary angiography were carefully interpreted. Patients were grouped as Single Vessels Disease (SVD), Double Vessel Disease (DVD) or Triple Vessel Disease (TVD). According to the percentage of stenosis; the patients were expressed as <50% and >50% stenosis. Statistical analysis was done using Microsoft excel and necessary statistical analysis software was used where necessary. Results: The majority of patients were male with mean age was 60.19± 11.73 years and 57.70± 9.19 years in females. The clinical characteristics showed that chest pain was common clinical feature (96%). The coronary angiography revealed that majority of patients were having SVD (36%) with involvement of LAD artery (82%). 15% showed normal coronary arteries. The correlation between clinical presentation and stenosis of coronary artery showed no statistical significant. Conclusion: The clinical assessment is a good predictor for CAD but it can’t be correlated directly to the coronary angiography findings.
1. Maskey A, Sayami A, Pamdey MR: coronary artery dieseae: An emerging epidemic in Nepal. J. Nepal Med Association 2003; 42:122-124.
2. Murry CJ, Lopez AD. Mortality by cause for eight regions of the world: Global burden of the disease study. Lancet 1997; 349: 1269-76.
3. Gaziano MJ, Manson JE, Ridker PM. Primary and secondary prevention of coronary heart disease. In: Libby P, Bonow RO. Mann DL, Zipes DP, editors. Braunwalds Heart disease. A text book of cardiovascular medicine. 8th ed. Saunders: Philadelphia; 2008. P. 1119-48.
4. Reddy KS, Yusuf S. Emerging epidemic of cardiovascular disease in developing countries. Circulation. 1998; 97: 596-601.
5. Jafary MH, Samad A, Ishaq M , Jawaid SA , Ahmad M, et al. Profile of Acute Myocardial Infarction (AMI) in Pakistan. Pak J Med Sci. 2007; 23:485-9.
6. Boden WE, O' rouke RA. COURAGE trial group. The evolving pattern of coronary artery disease in the US and Canada: Baseline characteristics of the clinical outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial. Am J Cadiol. 2007; 99: 208-12.
7. Jackson R, Chambless L, Higgins M. Sex differences in ischemic heart disease mortality and risk factors in 46 communities: an etiologic analysis. Cardiovascular Risk Factors 1997; 7: 43-54.
8. Mckeigue PM, Adelstein AM, Shipley MJ, Riemersma RA, Mamot MG, Hunt SP et al. Diet and risk factors for coronary heart disease in Asian in North west London Lancet 1985; 2:1086-90.
9. Nourjah P. National Hospital Ambulatory Care Survey: 1997 emergency department summary. Advance data from Vital and Health Statistics. Hyattsuille MD; National Statistics, 2001.
10. MAK Akanda, SY Ali, AEMM Islam, MM Rahman, A Parveen, MK Kabir, L Begum, RC Barman. Demographic Profile, Clinical Presentation and Angiographic Findings in 637 Patients with Coronary Heart Disease. Faridpur Med. Coll. J. 2011; 6(2):82-85.
Uncommon diffuse dense masses on X-ray mammogram, uncurtained by sonomammogram, confirmed on histopathology: A Case series
Unilateral enlargement of the breast can occur due to various diffuse infiltrative breast lesions, including normal physiological changes, infective, inflammatory, benign etiology and malignant tumors. In this article we present a series of cases with history of unilateral enlargement of breast and appearing as diffuse dense mass on x ray mammogram. Ultrasound findings made appropriate diagnoses which are confirmed on histopathology further.
1. Vuitch MF, Rosen PP, Erlandson RA. Pseudoangiomatous Hyperplasia Of Mammary Stroma. Hum pathology 1986;17:185-91.
2. Erin Bowman, MD,et al. Pseudoangiomatous Stromal Hyperplasia (PASH) of the Breast: A Series of 24 Patients. Breast Journal 2012 May-Jun; 8(3): 242–247.
3. Suhair Al-Saad, Sara Mathew George, Raja Al-Yusuf .Pseudo-angiomatous Stromal Hyperplasia: Benign Tumor of the Breast. Bahrain Medical Bulletin September 2009 ; 31: 3.
4. Navas Cañete A, et al. Pseudoangiomatous Stromal Hyperplasia: Magnetic Resonance Findings in Two Cases. Radiology 2007; 49(4): 275-8.
5. Salvador R, et al. Pseudo-angiomatous Stromal Hyperplasia Presenting as a Breast Mass: Imaging Findings in Three Patients. Breast 2004; 13(5): 431-5.
6. Mercado CL, et al. Pseudoangiomatous Stromal Hyperplasia of the Breast: Sonographic Features with Histopathologic Correlation. Breast J 2004; 10(5): 427-32.
7. AbidIrshad ,etal.Rare Breast Lesions: Correlation of Imaging and Histologic Features with WHO classification. Radiographics, September-October 2008;Volume 28, Issue 5.
8. EunMiRyu In Yong Whang, Eun Deok Chang. Rapidly Growing Bilateral Pseudoangiomatous Stromal Hyperplasia of the Breast. Korean J Radiol 2010;11:355-358.
9. MerihGuray and Aysegul A. Sahin. Benign Breast Diseases: Classification, Diagnosis, and Management. The Oncologist 2006; 11:435-449.
10. Tavassoli FA, Devilee P, eds. Tumours of the breast: Pathology and genetics of tumours of the breast and female genital organs. World Health Organization Classification of Tumours.Lyon,France: IARC, 2003; 9–112.
11. Lee BJ, Pack GT. Giant Intracanalicular Myxoma of the Breast: The So-Called Cystosarcoma Phyllodes Mammae of Johannes Muller. Ann Surgery 1931;93(1):250-268.
12. Chua CL,Thomas A, Ng BK. Cystosarcomaphyllodes-Asian variations. Aust N Z J Surgery1988;58(4) :301–305.
13. Nielsen VT, Andreasen C. Phyllodestumour of themale breast. Histopathology 1987;11(7):761–762.
14. Barrio AV, et al. Clinicopathologic features and long-term outcomes of 293 phyllodestumours of the breast. Ann Surgery Oncology 2007;14(10):2961-2970.
15. Soumaya Ben Abdelkrima e, et al. PhyllodesTumours of the Breast: A Review of 26 Cases. World journal of oncology 2010,vol 1 number 3: 129-134 .
16. Karim RZ, Gerega SK, Yang YH, Spillane A, Carmalt H, Scolyer RA, Lee CS. Phyllodestumours of the breast: A clinicopathological analysis of 65 cases from a single institution. Breast 2009;18(3):165-170.
17. Korula A, Varghese J, Thomas M, Vyas F. Malignant phyllodestumour with intraductal and invasive carcinoma and lymph node metastasis. Singapore Med J 2008;49(11):e318-321.
18. S.Wurdinger, A. B. Herzog, D. R. Fischer et al.“Differentiationofphyllodes breast tumors from fibro adenomas on MRI,†American Journal of Roentgen ology, vol. 185,no. 5, pp. 1317–1321,2005
19. Shashi PrakashMishra, Satyendra Kumar Tiwary,ManjareeMishra, and Ajay Kumar Khanna .PhyllodesTumor of Breast: A Review Article. Department of Surgery, Institute of Medical Sciences, Banaras Hindu University:Volume 2013.
20. Gunhan-Bilgen et al. Inflammatory Breast Carcinoma: Mammographic, UltrasonographicClinical,andPathologicFindings in142 Cases.Radiology2002;223:829–838.
21. Dershaw DD, Moore MP, Liberman L, Deutch BM. Inflammatory breast carcinoma: mammographic findings.Radiology 1994; 190:831-834.
22. American Cancer Society.Inflammatory breast cancer.September 29, 2011. Available at: http: // www .cancer. org / acs / groups / cid / documents/web content/002298-pdf.
23. Anne C.et al. Primary Inflammatory Carcinoma of the Breast: Retrospective Review of Mammographic Findings,February 2000, Volume 174, Number 2.
24. Anne C. Kushwaha, Gary J. Whitman, Carol B. Stelling, Massimo Cristofanilli and Aman U. Buzdar.Primary Inflammatory Carcinoma of the Breast: Retrospective Review of Mammographic Findings. American Journal of Roentgenology. 2000;174: 535-538.
25. American Joint Commission on Cancer.AJCC Cancer Staging Manual, 7thedition , updated Cancer Staging Posters. Available http :// www. Cancerstaging.org/ staging /posters/ breast pdf.
Usefullness of dexmedetomidine as an adjuvant to local anaesthetics in infraclavicular brachial plexus block for prolongation of postoperative analgesia
Background and Objectives: The infraclavicular brachial plexus block is a safe and reliable approach to provide intraoperative and postoperative analgesia of upper limb. We evaluated the efficacy of dexmedetomidine added to local anaesthetics in infraclavicular brachial plexus block to hasten the onset of sensory and motor block and to prolong the postoperative analgesia. Methods: A prospective randomized double-blind study was carried out in 60 patients aged 18-60 years of ASA grade I and II, who were scheduled for various upper limb surgeries in orthopedics. The patients were divided into two groups of 30 each i.e. Control Group (group C) received 20 ml of inj. Bupivacaine + 10 ml of inj. Xylocaine + 10 ml of Normal Saline and Dexmedetomidine Group (group D) received 20 ml of inj. Bupivacaine + 10 ml of inj. Xylocaine + 10 ml of Normal Saline + 1 µg/kg of inj. Dexmedetomidine. Both groups were compared for the time of onset of sensory and motor blocks, postoperative analgesia and haemodynamic changes. Results: The onset of sensory and motor blockade (2.9 ± 1.0 Vs 8.8 ± 2.22 min and 5.23 ± 1.14 Vs 10.86 ± 2.41 min, respectively) were significantly more rapid in the D group than in the C group (p = 0.0001). The duration of sensory and motor blockade (825 ± 133.83 Vs 412 min ± 74.17 and 878.33 ± 166.23 Vs 409.33 ± 72.01 min respectively) were significantly longer in the D group than in the C group (p = 0.0001). The duration of analgesia (1448.66 ± 288.33 Vs 499 ± 78.79 min) was significantly longer in D group than in the C group (p = 0.0001). Systolic and diastolic blood pressure were lower in D group than C group during the period of anaesthesia from 30 to 120 minutes (in this period patients can be closely monitored and managed) (p < 0.05). Heart rate levels were also low in D group than C group during the period of anaesthesia from 15 to 120 minutes (p < 0.05). Conclusion: We conclude that the addition of dexmedetomidine to local anaesthetic mixture in infraclavicular brachial plexus block hastens the onset and prolong the duration of sensory and motor blocks, as well as the duration of postoperative analgesia.
1. Ertug Z, Yegin A, Ertem S, Sahin N, Hadimioglu N, Docemeci L, et al. Comparision of two different techniques for brachial plexus block: infraclavicular versus axillary technique. Acta Anaesthesiol Scand 2005; 49:1035-9.
2. Raj P, Montgomery SJ, Nettles D , Jenkins MT. infraclavicular Brachial plexus Block- A new approach. Anesth Analg 1973; 52:897-904.
3. Kilka HG, Geiger P, Mehrkens HH. Infraclavicular vertical brachial plexus blockade: A new technique of regional anesthesia. Anesthetist 1995; 44:339-44.
4. Lanz E, Thesiss D, Jancovic D. The extent of Blockade Following Various techniques of brachial plexus block. Anesth Analg 1983; 62:55-58.
5. McCartney CJ, brull R, Chan VW, et al. Early but no long term benefits of regional compared with general anesthesia for ambulatory hand surgery. Anesthesiology 2004; 101:461-7.
6. Cavino BJ, Wildsmith JA. Clinical pharmacology of local anesthetic agents. In:Cousins MJ, Bridenbaugh PO,eds. Neural Blackade in Clinical Anesthesia and Management of Pain. Philadelphia, PA:Lippincott-Raven, 1998;97-128.
7. Kuzma PJ, Kline MD, Calkins MD, Staats PS. Progress in the develepment of ultra-long- acting local anesthetics. Reg Anesth 1997; 22:534-51.
8. Yaksh TL, Ilfeld BM, Wiese AJ, perineural local anesthetic and adjuvant action: the meaning of ex-vivo data set for efficacy and safety. Reg Anesth Pain Med 2012; 37:366-8.
9. Candilo KD. Buprenorphine added to local anesthetic for axillary brachial plexus block prolongs postoperative analgesia. Reg Anesth Pain Med 2002; 27:162-7.
10. McCarteny CJ, Duggan E, Apatu E. Should we add clonidine to local anesthetic for peripheral nerve blockade? A qualitative systematic review of literature. Reg. Anesth Pain Med 2007; 32:330-8.
11. Parrington S, O’Donnell D, Chan VW, et.al Dexamethasone added to mepivacaine prolongs the duration of analgesia after supraclavicular brachial plexus blockade. Reg. Anesth Pain Med 2010; 35:422-6.
12. Buvanendran A, McCarthy RJ, Kroin JS, Leong W, Perry P, Tuman KJ. Intrathecal magnesium prolongs fentanyl analgesia: a prospective randomized, controlled trial. Anesth Analg 2002; 95:661-6.
13. Murali Krishna T, Panda NB, Batra YK, Rajeev S. Combination of low doses of intrathecal ketamine and midazolam with bupivacaine improves postoperative analgesia in orthopedic surgery. Eur J Anesthesiol 2008; 25:299-306.
14. Laiq N, Khan MN, Arif M, Khan S, Midazolam with bupivacaine for improving analgesia quality in brachial plexus block for upper limb surgeries.J Coll Physicin Surg Pak2008;18:674-8.
15. Gabriel JS, Gordin V. Alpha 2 agonist in regional anesthesia and anlgesia. Curr Opin Anesthesiol 2001; 14:751-3.
16. Panzer O, Moitra V, Sladen RN. Pharmacology of sedative-analgesic agents: Dexmedetomidine, remifentanyl, ketamine, volatile anesthetics, and the role of peripheral mu antagonists.Crit Care Clin 2009; 25:451-69.
17. Kanazi GE, Aouad MT, Jabbour-Khoury SI, AI Jazzar MD, Alameddine MM, AI-Yaman R, Bulbul M, Baraka AS. Effect of low dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block. Acta Anaesth Scand 2006; 50:222-7.
18. Congedo E, Sgreccia M, De Cosmo G. New drugs for epidural analgesia. Curr Drug Targets 2009; 10:696-706.
19. Memis D, Turan A, Karamanlioglu B, Pamukcu Z, Kurt I. Adding dexmedetomidine to lidocaine for Intravenous Regional Anaesthesia. Anesth Analg 2004; 98:835-40.
20. Esmaoglu A, Yegenoglu F, Akin A, Turk CY. Dexmedetomidine added to levobupivacaine prolongs axillary brachial plexus block. Anaesthe Analg 2010; 111:1548-51.
21. Obayah GM, Refaie A, Aboushanab O, Ibraheem N, Abdelazees M. Adding dexmedetomidine to bupivacaine for greater palatine nerve block prolongs postoperative analgesia after cleft palate repair. Eur J Anaesthesiol 2010; 27:280-4.
22. Jadon A, Panigrahi MR, Parida SS, Chakraborty S, Agrawal PS, Panda A. Buprenorphine improves the efficacy of bupivacaine in nerve plexus block: A double blind randomized evaluation in subclavian perivascular brachial block. J Anaesth Clin Pharmacol. 2009;25(2):207-10
23. Gaumann D, Forster A,Griessen M, Habre W, Poinsot O, Della Santa D. Comparision between clonidine and epinephrine admixture to lidocaine in brachial plexus block. Anesth Analg 1992; 75:69-74.
24. Gandhi R, Shah A, Patel I. Use of dexmedetomidine along with bupivacaine for brachial plexus block. National J Med Res 2012; 2:67-9.
25. Esmaoglu A, Mizrak A, Akin A, Turk Y, Boyaci A. Addition of dexmedetomidine to lidocaine for intravenous regional anesthesia. Eur J Anaesthesiol 2005; 22:447-51.
26. Eisenach JC, De Kock M, Klimscha W. Alpha (2) - Adrenergic agonists for regional anesthesia. A clinical review of Clonidine (1984-1995). Anesthesiology 1996; 85:655-74.
27. Guo TZ, Jiang JY, Buttermann AE, Maze M. Dexmedetomidine injection into the locus ceruleus produces Antinociception. Anesthesiology 1996; 84:873-81.
28. Abosedira MA. Adding Clonidine or dexmedetomidine to lidocaine during Bier’s block: a comparative study. J M Sci 2008; 8:660-4.
29. Brummet CM, Norat MA, Palmisano JM, Lydic R. Perineural administration of dexmedetomidine in combination with bupivacaine enhances sensory and motor blockade in Sciatic nerve block without inducing neurotoxicity in rat. Anesthesiology 2008; 109:502-11.
30. Hoffmen WE , Kochs E, Werner C, Thomas C, Albrecht RF. Dexmedetomidine improves neurologic outcome from incompelete ischaemia in rat reversal by the alpha 2- adrenergic antagonist atipamezol. Anesthesiology 1991; 75:328-32.
31. Maier C, Steinberg GK, Sun GH, Maze M. Neuroprotection by the aplha 2- adrenoceptor agonist dexmedetomidine in a focal model cerebral ischaemia Anesthesiology 1993;79:306-12.
32. Halonen T, Kotti T, Tuunanen J, Toppinen A, Miettinen R, Riekkinen PJ. Alpha 2- adrenoceptor agonist, dexmedetomidine protects against kainic acid- induced convulsions and neuronal damage. Brain Res 1995;693:217-24
33. Kuhmonen J, Pokorny J, Miettinen R, et. al. Neuroprotective effects of dexmedetomidine in the gerbill hippocampus after transient global ischaemia. Anesthesiology 1997; 87:371-7.
34. Jolkkonen J, Puurnen K, Koistinaho J, et al. Neuroprotection by the alpha-2 adrenoceptor agonist, dexmedetomidine, in rat focal cerebral ischaemia. Eur J Pharmacol 1999; 372:31-6.
35. Laudenbach V, Mantz J, Lagercrantz H, Desmonts JM, Evrard P, Gressens P. Effets of alpha-2 adrenoceptor agonist on perinatal excitotoxic brain injury: Comparison of clonidine and dexmedetomidine . Anesthesiology 2002; 96:134-41.
36. Ma D, Hossain M, Rajkumaraswamy N, et.al dexmedetomidine produces its neuroprotective effect via the α2-A adrenoceptor subtype. Eur J Pharmacol 2004; 502:87-97.
37. Konacki S, Adanir T, Yilmaz G, Rezanko T. The efficacy and neurotoxicity of dexmedetomidine administered via the epidural route. Eur J Anesthesiol 2008; 25:403-9.
38. Brummet CM, Padda AK, Amodeo FS, Welch KB, Lydic R. Perineural dexmedetomidine added to ropivacaine causes a dose dependant increase in the duration of thermal antinociception in sciatic nerve block in rat. Anesthesiology2009; 111:111-9.
39. Kosugi T, Mizuta K, Fujita T, Nakashima M, Kumamoto E. High concentration of dexmedetomidine inhibit compound action potential in frog sciatic nerve without α2 adrenoceptor activation. Br J Pharmacol. 2010; 160:1662-76.
40. Ammar AS, Mahmoud KM. Ultrasound-guided single injection infraclavicular brachial plexus block using bupivacaine alone or combined with dexmedetomidine for pain control in upper limb surgery: a prospective randomized controlled trial. Saudi J Anaesth 2012; 6:109-14.
41. Kaygusuz K. Effects of adding dexmedetomidine to levobupivacaine in axillary brachial plexus block. Curr Ther Res Clin Exp 2012; 73:103-11.
42. Talke P, Lobo E, Brown R. Systemically administered α2-agonist induced peripheral vasocostriction in humans. Anesthesiology 2003; 99:65-70.
43. Winnie AP, Radonjic R, Akkineki SR, et al Factors influencing distribution of local anesthetic injected into brachial plexus sheath. Anesth. Analg 1979; 58:225-234
Leiomyosarcoma of somatic soft tissue origin in the leg - a case report
Leiomyosarcoma of soft tissue is thought to arise from the smooth muscle cells lining small blood vessels. Most common site of involvement is retroperitoneum, accounting for approximately 50% of occurrences. Leiomyosarcoma of somatic soft tissues presents as an enlarging, painless mass. Although these tumours are generally associated with small blood vessels they usually do not present with signs or symptoms of vascular compression. However, when leiomyosarcoma arises from a major blood vessel, symptoms of vascular compromise or leg edema may be present, as well as neurologic symptoms such as numbness from compression of an adjacent nerve. We report a case of leiomyosarcoma of somatic soft tissue of the leg of a young male presented to us with swelling in the upper one-third of left leg which was associated with severe pain on extension of the joint. Patient was diagnosed as leiomyosarcoma of the somatic soft tissue origin by clinical, pathological and immunohistochemistry methods.
1. Gustafson P, Willen H, Baldetrop B, et al. Soft tissue leiomyosarcoma: a population-based epidemiologic and prognostic study of 48 patients, including cellular DNA content. Cancer 70:114, 1992.
2. Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors 4th Ed. Philadelphia: Mosby-Harcort, 2001.
3. De Saint Aubain Somerhausen N, Fletcher C. Leiomyosarcoma of Soft Tissue in Children: Clinicopathologic analysis of 20 cases. Am J Surg Pathol, 23(7):755, 1999.
4. McClain KL, Leach CT, Lenson HB, et al. Association of Epstein-Barr virus with leiomyosarcoma in young people with AIDS. New England Journal of Medicine 332:19, 1995.
5. Mankin, HJ, Casas-Ganem, J, Kim, JI, et al. Leiomyosarcoma of somatic soft tissues. Clin Orthop Relat Res. 2004 Apr ;( 421):225-31.
6. Golden T, Stout AP. Smooth muscle tumors of the gastrointestinal tract and retroperitoneal tissues. Surg Gynecol Obstet 73:784, 1941.
7. Fields JP, Helwig EB. Leiomyosarcoma of the skin and subcutaneous tissue. Cancer 47:156, 1981.
8. Jensen ML, Myhre Jensen O, Michalski W, et al. Intradermal and subcutaneous leiomyosarcoma: a clinicopathologic and immunohistochemical study. J Cutan Pathol 23:458, 1996.
9. Kevorkian J, Cento JP. Leiomyosarcoma of large arteries and veins. Surgery 73:39, 1973.
10. Burke AP, Virmani R. Sarcomas of the great vessels: a clinicopathologic study. Cancer 71:1761, 1993.
11. Farshid G, Goldblum J, Weiss SW. Leiomyosarcoma of soft tissue: a tumor of vascular origin with multivariate analysis of outcome. Mod Pathol. 2003 Aug; 16(8):778-85.
12. Fletcher CDM, Cin PD, Wever I, et al. Correlation between clinicopathological features and karyotype in spindle cell sarcomas: a report of 130 cases from the CHAP study group. Am J of Pathology 154:6, 1999
13. Rubin BP, Fletcher CDM. Myxoid leiomyosarcoma of soft tissue, an under recognized variant. Am J of Surg Pathol 24(7):927-936, 2000.
14. Hasimoto H, Daimaru Y, Tsuneyoshi M, et al. Leiomyosarcoma of the external soft tissues. Cancer 57:2077, 1986.
15. Templeton K. Leiomyosarcoma of bone. M J Orthop 34:55, 249-251, 2005.
16. Weiss SW. Smooth muscle tumors of soft tissue. Advances in Anatomic Pathology. 9(6):351-359 2002.
17. Iwata J, Fletcher CD. Immunohistochemical detection of cytokeratin and epithelial membrane antigen in leiomyosarcoma: a systematic study of 100 cases. Pathol Int 2000 Jan;50(1):7-14.
18. Adjuvant chemotherapy for localized respectable soft tissue sarcoma of adults: meta analysis of individual data. Sarcoma Meta-analysis Collaboration. Lancet 1997 350:1647.
Acrania is a rare lethal congenital anomaly characterised by an absence of the calvarium. Ultrasound allows early diagnosis of this anomaly. Although acrania associated with anencephaly is a well recognized entity with an incidence of about 10:10,000 births, isolated acrania is a rare anomaly, and its incidence is unknown. We report a 25 year old female patient referred to our ultrasound department for antenatal scan. The fetus was found to have a completely formed brain, base of the skull and facial structures but lacking a cranium.
1. Mannes EJ, Crelin ES, Hobbins JS et-al. Sonographic demonstration of fetal acrania. AJR Am J Roentgenol. 1982; 139 (1): 181-2.
2. Kaya H, Sezik M, Özkaya O, Aydin AR. Fetal acrania at term Perinatal Journal.2004;12(2):96–98.
3. Cincore V, Ninios AP, Pavlik J, Dong C. Prenatal Diagnosis of Acrania with amniotic band syndrome. Obstetrics and Gynecology. 2003; 102(5):1176–1178.
4. Fong KW, Toi A, Salem S, Hornberger LK, Chitayat D, Keating SJ, McAuliffe F, Johnson JA. Detection of fetal structural abnormalities with US during early pregnancy. Radiographics. 2004; 24:157-174.
5. Johnson SP, Sebire NJ, Snijders RJM, Tunkel S, Nicolaides KH. Ultrasound screening for anencephaly at 10–14 weeks of gestation. Ultrasound Obstet Gynecol. 1997; 9:14–16.
6. Liu I, Chang C, Yu C, Cheng Y, Chang F. Prenatal diagnosis of fetal acrania using three-dimensional ultrasound. Ultrasound in Medicine and Biology. 2009; 31(2):175–78.
7. Cafici D, Sepulveda W. First-trimester echogenic amniotic fluid in the acrania-anencephaly sequence. J Ultrasound Med. 2004; 22 (10): 1075-9.
8. Romero R, Pilu G, Jeanty J, et al. Prenatal Diagnosis of Congenital Anomalies. Appleton and Lange, Norwalk, Connecticut, 1988. pp 75-76.
A study of profile of poisoning cases in and around Hassan district, Karnataka
A study of profile of poisoning cases in and around Hassan district, Karnataka
1. Thomas WF, John HD, Willium RH. Stedman’s Medical dictionary.28th edition. Lippincott William and Wilkins, New York. 2000.
2. Gargi J, Tejpal HR. A retrospective autopsy study of poisoning in Northern region of Punjab. Journal of Punjab academy of Forensic medicine and toxicology. 2008;2:17-20.
3. Aaron R, Joseph A, Abraham S, Muliyil J, George K, Prasad J et.al . Suicides in young people in rural Southern India. Lancet.2004;363:1117-1118.
4. Eddleston M. Patterns and problems of deliberate self poisoning in the developing world. Q J Med, 2000;93:715-731.
5. Batra AK, Keoliya AN, Jadhav GU. Poisoning: An unnatural cause of morbidity and mortality in rural India. J Assoc Physicians India 2003;51:955-959.
6. Dash SK, Raju AS, Mohanty MK, Patnaik KK, Mohanty S. Sociodemographic profile of poisoning cases. JIAFM 2005;27(3):133-138.
7. Thomas M, Anandan S, Kuruvilla PS, Singh PR, David S. Profile of hospital admission following acute poisoning experiences from a major teaching hospital in South India. Adverse drug reaction and toxicology review. 2000; 19:313-317.
8. Zaheer MS, Aslam M, Gupta V, Sharma V, Khan SA. Profile of poisoning cases at a North Indian tertiary care hospital. Health and population: Perspectives and Issues.2009;32(4):176-183.
9. Maharani B, Vijayakumari N. Profile of poisoning cases in a tertiary care hospital, Tamil Nadu, India. Journal of Applied Pharmaceutical Science. 2013;3(1):91-94.
10. Kora SA, Doddamani GB, Halagali GR, Vijayamahantesh SN, Umakanth B. Socio demographic profile of the Organophosphorus poisoning cases in Southern India. Journal of Clinical and diagnostic research 2011; 5(5): 953-956.
A Comparative Study on Effect of Moderate and heavy Intensity Exercise Priscription in Moderate COPD Patients on Haemodynamics and Functional Capacity
Patients with COPD have reduced functional capacity due to deconditioning. Various studies have found that endurance exercise training is single most important aspect of rehabilitation for patients with chronic pulmonary disease. However, there are conflicting views about the intensity for exercise prescription in stable COPD patients. The optimal specific exercise prescription guidelines in terms of intensity prescription have not been well documented. The purpose of this study was to compare the effect of two training intensities in stable COPD patients, which would help in formulating a comfortable and efficient exercise program in this population. 60 male subjects with moderate COPD were selected through purposive sampling and randomly allocated into two groups, group A and group B, each group having 30 subjects (n=30). Group A subjects were trained with moderate intensity and Group B subjects with heavy intensity exercise. Subjects were trained with the prescribed intensity exercise for respective groups for 10 min per day, 4 times a week for 4 weeks of duration. Outcome of interest include Resting Heart rate, Respiratory rate, Distance covered in 6-min walk test, % predicted FEV1 value, % predicted FEV1/FVC ratio. Data were analysed using paired and unpaired t test. Group B showed significant improvement in RHR, RR. Improvement is found in both groups for 6-MWD, whereas group B subjects showed more significant improvement. However, there was no improvement found in FEV1 and FEV1/FVC ratio in either group. The result of this study revealed that heavy intensity exercise training provides benefits to patients with moderate COPD than moderate intensity exercise training in terms of improvements in functional status if done with permissible interval training during the training. There was 18% of improvement in 6-MWD in group B.
1. GOLD COPD 2007. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease.
2. World Health Organization, World Health Report 2002 Geneva: WHO 2002. www.who.int/whr/ 2002 /en/.
3. Christopher JL, Murray, Alan DL, Evidence-Based Health Policy-Lessons from the Global Burden of Disease Study Science. 1996; 274: 740-743.
4. Jindal SK, Aggrawal AN, Gupta D. A review of Population Study from India to Estimate National Burden of Chronic Obstructive Pulmonary Disease and Its Association with Smoking. Indian J Chest Dis Allied Sci 2001; 43 : -147.
5. Vigg Arul, Vigg Ajit, Vigg Avanti, and Mantri Sumanth. Prevalence Of Chronic Obstructive Pulmonary Disease In Patients Attending Chest Clinic In A Tertiary Care Hospital. CHEST / 128 / 4 / OCTOBER, 2005 SUPPLEMENT.
6. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th edition. Pp84.
7. Linda Nici; Claudio Donner; Emiel Wouters; Richard Zuwallack; et al. American Thoracic Society/European Respiratory Society Statement on Pulmonary rehabilitation. American Journal of Respiratory and Critical Care Medicine; Jun 15, 2006; 173, 12.
8. COOPER, C. B. Exercise in chronic pulmonary disease: aerobic exercise prescription. Med. Sci. Sports Exerc., Vol. 33, No. 7, Suppl., pp. S671–S679, 2001.
9. Frits M. E. Franssen, Roelinka Broekhuizen et.al. Effects of Whole-Body Exercise Training on Body Composition and Functional Capacity in Normal-Weight Patients with COPD. Chest 2004;125;2021-2028.
10. CRINER GERARD J., CORDOVA FRANCIS C et.al. Prospective Randomized Trial Comparing Bilateral Lung Volume Reduction Surgery to Pulmonary Rehabilitation in Severe Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med Vol 160. pp 2018–2027, 1999.
11. ACSM. ACSM’s Advanced Exercise Physiology. Mayland: Lippincott Williams and Wilkins, 2006. pp 4.
12. Durstine JL, Moore GE. ACSM’s Exercise Manegment for Persons with Chronic Diseases and Disabilities. 2nd ed. US Lippincott Williams and Wilkins. pp 92.
13. Wilmore JH, Costill DI. Physiology Sport and Exercise. 3rd ed. Champaign, IL: Human Kinetics, 1999, pp 279.
14. Kisner C, Colby LA. Therapeutic Exercise. 5th ed. Dariyaganj, New Delhi, J P Brothers. 2007. pp 241- 242.
15. Wilmore JH, Costill DI. Physiology Sport and Exercise. 3rd ed. Champaign, IL: Human Kinetics, 1999, pp 222.
16. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th edition.pp 415
17. Brooks GA, Fahey TD, White TP, et.al. Exercise Physiology. 2nd ed. Mountain View, CA: Mayfield, 2000. pp 545
18. Brooks GA, Fahey TD, White TP, et.al. Exercise Physiology. 2nd ed. Mountain View, CA: Mayfield, 2000. pp 214
19. McArdle WD, Katch FI, Katch VL. Exercise Physiology Energy, Nutrition & Human Performance. 5th ed. Mayland: Lippincott Williams and Wilkins, 2001. pp 950
20. ATS Statement: Guidelines for the Six-Minute Walk Test 2002
21. Enright Paul L., McBurnie Mary Ann. The 6-min Walk Test: A Quick Measure of Functional Status in Elderly Adults. Chest 2003;123;387-398.
22. ACSM. Acsm’s Guidelines for Exercise Testing and Prescription. 7th ed. Mayland: Lippincott Williams and Wilkins, 2006. pp 227
23. McArdle WD, Katch FI, Katch VL. Exercise Physiology Energy, Nutrition & Human Performance. 5th ed. Mayland: Lippincott Williams and Wilkins, 2001. pp 953
24. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 411
25. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 416.
26. Brooks GA, Fahey TD, White TP, et.al. Exercise Physiology. 2nd ed. Mountain View, CA: Mayfield, 2000. pp 545.
27. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 87
28. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 154
Influence of age, body fat distribution, alcohol consumption and smoking on liver enzymes activity in apparently healthy western Indian males
This prospective study was conducted to assess the effect of demographic and clinical parameters on liver enzymes in apparently healthy western Indian male population. The study population consisted of 669 males attending blood donation camps during 2011 to 2013. Anthropometric measurement was taken and history for alcohol consumption and smoking was noted. Biochemical parameters including AST, ALT, and GGT activities were determined using auto analyzer (AU-400 by Olympus). Mann-Whitney Test and Kruskal-Wallis One Way ANOVA on Ranks Test applied. P value of < 0.05 was considered to be statistically significant. All analyses were conducted using the SPSS-13.0. According to alcohol habit, 97 (14.5%) were alcoholic and 572 (85.5%) were non-alcoholic. According to smoking habits, 171 (25.6 %) were smokers and 498 (74.4 %) were non-smokers. Median activity of serum AST, ALT and GGT were 27.00 IU/L, 17.00 IU/L and 18.80 IU/L respectively. By univariate analyses, there were significant associations between increasing AST, ALT, or GGT tertiles and age, body mass index, and waist and hip circumferences, Waist-Hip ratio (p < 0.05). AST and GGT activity were significantly higher in alcoholic men compared to non alcoholic (p < 0.05). BMI, AST, ALT and GGT were significantly higher in smokers compared to non-smokers (p < 0.05). These data suggest that slight to moderate increase in BMI and light alcohol intake and smoking affected liver enzymes levels in apparently healthy western Indian males. These factors should be considered in the definition of normal limits for liver enzymes.
1. Jang ES1, Jeong SH, Hwang SH, Kim HY, Ahn SY, Lee J, Lee SH, Park YS, Hwang JH, Kim JW, Kim N, Lee DH: Effects of coffee, smoking, and alcohol on liver function tests: a comprehensive cross-sectional study. BMC Gastroenterol. 2012 Oct; 18(12):145.
2. Pratt DS, Kaplan MM: Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med. 2000; 342:1266–1271.
3. Giannini EG, Testa R, Savarino V: Liver enzyme alteration: a guide for clinicians. CMAJ. 2005; 172: 367–379.
4. Liu Z, Hu Y, Yang X, Tan A, Gao Y, Qin X, Liang Y, Mo Z, Peng T: Combinative analysis of factors influence serum alanine aminotransferase activity in adult male population from southern China. Clinical biochemistry. 2012; 45(18):1683-1688
5. Clark J M., Frederick L B, Anna M D: The prevalence and etiology of elevated aminotransferase levels in the United States. The American journal of gastroenterology. 2003; 98(5): 960-967.
6. Srikanthan, P, Seeman, T E, Karlamangla A S: Waist-hip-ratio as a predictor of all-cause mortality in high-functioning older adults. Annals of epidemiology.2009; 19(10): 724-731.
7. Hietala J, Puukka K, Koivisto H, Anttila P, Niemelä O: Serum gamma-glutamyl transferase in alcoholics, moderate drinkers and abstainers: effect on gt reference intervals at population level. Alcohol and Alcoholism. 2005; 40(6):511-514.
8. Alatalo P, Koivisto H, Puukka K, Hietala J, Anttila P, Bloigu R, Niemelä, O: Biomarkers of liver status in heavy drinkers, moderate drinkers and abstainers. Alcohol and alcoholism. 2009; 44(2):199-203.
9. Breitling LP, Raum E, Muller H, Rothenbacher D, Brenner H: Synergism between smoking and alcohol consumption with respect to serum gamma-glutamyltransferase. Hepatology. 2009; 49:802–808.
10. Khedmat H, Fallahian F, Abolghasemi H, Hajibeigi B, Attarchi Z, Alaeddini F, ... Zarei N: Serum gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase activity in Iranian healthy blood donor men. World Journal of Gastroenterology. 2007; 13(6): 889.
11. Abel E L, Kruger M L, Friedl J: How do physicians define “light,â€â€œmoderate,†and “heavy†drinking?. Alcoholism: Clinical and Experimental Research. 1998; 22(5): 979-984.
12. Robert L S: Clinical Reference Laboratory. 1999.
13. Ritchie RF, Palomaki G: Selecting clinically relevant populations for reference intervals. Clin Chem Lab Med. 2004; 42:702–709.
14. Piton A, Poynard T, Imbert-Bismut F, Khalil L, Delattre J, Pelissier E, Opolon P: Factors associated with serum alanine transaminase activity in healthy subjects: Consequences for the definition of normal values, for selection of blood donors, and for patients with chronic hepatitis C. Hepatology. 1998; 27(5): 1213–1219.
15. Lee J K, Shim J H, Lee H C, Lee S H, Kim K M, Lim Y S, ...Suh D J: Estimation of the healthy upper limits for serum alanine aminotransferase in Asian populations with normal liver histology.Hepatology. 2010; 51(5):1577-1583.
16. Stromme J H, Rustad P, Steensland H, Theodorsen L, Urdal P: Reference intervals for eight enzymes in blood of adult females and males measured in accordance with the International Federation of Clinical Chemistry reference system at 37 degrees C: part of the Nordic Reference Interval Project. Scandinavian Journal of Clinical and Laboratory Investigation. 2004; 64(4): 371–384.
17. Mohamadnejad M, Pourshams A, Malekzadeh R, Mohamadkhani A, Rajabiani A, Asgari A A, Mamar-Abadi M: Healthy ranges of serum alanine aminotransferase levels in Iranian blood donors. World journal of gastroenterology. 2003; 9(10): 2322-2324.
18. Burns CJ, Boswell JM, Olsen GW: Liver enzyme activity and body mass index. J Occup Environ Med. 1996; 38(12): 1248-1252.
19. Mala H, Zadak Z, Sobotka L, Maly J: Changes in selected biochemical parameters during a low-calorie reducing diet. Sb Lek. 2000; 101(1):105-108
20. Kumar S, Amarapurkar A, Amarapurkar D: Serum aminotransferase levels in healthy population from western India. The Indian journal of medical research. 2013; 138(6): 894.
21. Nakamura K, Motohashi Y, Kikuchi S, Tanaka M, Nakano S: Liver transferase activity in healthy Japanese employees aged 18–39 years. Ind Health.1998; 36: 218–22.
22. Lee D H., Ha M H, Christiani D C: Body weight, alcohol consumption and liver enzyme activity—a 4-year follow-up study. International journal of epidemiology. 2001; 30(4): 766-770.
23. Puukka K, Hietala J, Koivisto H, Anttila P, Bloigu R, Niemela O: Age-related changes on serum ggt activity and the assessment of ethanol intake. Alcohol and alcoholism. 2006; 41(5): 522-527.
24. Steffensen FH, Sorensen HT, Brock A, Vilstrup H, Lauritzen T: Alcohol consumption and serum liver-derived enzymes in a Danish population aged 30–50 years. Int J Epidemiol. 1997; 26: 92–99.
25. Lee DH, Lim JS, Yang JH, Ha MH, Jacobs DR Jr: Serum gammaglutamyltransferase within its normal range predicts a chronic elevation of alanine aminotransferase: a four year follow-up study. Free Radic Res. 2005; 39:589–593.
26. Chan-Yeung M, Ferreira P, Frohlich J, Schulzer M, Tan F:The effects of age, smoking, and alohol on routine laboratory tests. Am J Clin Pathol.1981; 75:320–326.
27. Whitehead TP, Robinson D, Allaway SL: The effects of cigarette smoking and alcohol consumption on serum liver enzyme activities: a dose-related study in men. Ann Clin Biochem. 1996; 33(6):530-535.
Antioxidants: the defense mechanism against free radicals
Introduction: Metabolism refers to biochemical processes that occur within any living organism - including humans - to maintain life. It is sum of all anabolic (synthesis) and catabolic (break down) reactions occurring in our body. Metabolism can also be aerobic (O2 dependent) or anaerobic (in absence of O2). These biochemical processes allow us to grow, reproduce, repair damage, and respond to our environment. Oxidants are formed as a normal product of aerobic metabolism. This aerobic metabolism does not come without cost. “Free radicals†are formed as a by product of this metabolism which is capable of attacking the healthy cells of the body. They are responsible for causation and progress of many diseases like Atherosclerosis, Cataract, Cancer, degenerative diseases, inflammatory diseases, etc. Antioxidants are the first line of defense for these free radicals and are vital in maintaining optimum health and well being. These anti oxidants can be obtained from natural dietary sources or can be taken as nutritional supplements.
1. SIES, H. (1985). Oxidative stress: introductory remarks. In Oxidative Stress, ed. SIES, H., pp. 1-8. Academic Press, London.
2. SIES, H. (1991). Oxidative stress: introduction. In Oxidative Stress: Oxidants and Antioxidants, ed. SIES, H., pp. xv-xxii. Academic Press, London.
3. Domenico P, Luigi L, Stefania E et al., Enhanced lipid peroxidation in hepatic cirrhosis, J Investig Med, Feb 46 (2) (1998) 51.
4. Beck M M and Levander O A, Fietary oxidative stress and the potentiation of viral infection, Annu Rev Nutr, 18 (1998) 93.
5. Peterhans E, Oxidants and antioxidants in viral diseases: Diseases mechanisms and metabolic regulation, J Nutr, 127 (1997) 962s.
6. Winterbourn CC. Reconciling the chemistry and biology of reactive oxygen species. Nature Chem Biol 2008; 4:278-286.
7. Lippincott W and Wilkins, Lippincott’s Illustrated Reviews: Biochemistry (V edition), 2011; 148
8. Herbert V. The antioxidant Supplement myth. Am J Clin Nutr 1994;60:157-168
9. Block, G. et al. Fruit, Vegetables, and Cancer Prevention: A Review of the Epidemiological Evidence, Nutr Cancer 1992; 18(1):1-29.
10. Hennekens, C.H. and Gaziano, J.M., Antioxidants and Heart Disease: Epidemiology and Clinical Evidence. Clin Cardiol 1993;16(suppl I):I-10, I-15).
11. SIES, H. (1993). Strategies of antioxidant defense. European Journal of Biochemistry 215, 213-219.
12. Reichard, P. and Ehrenberg, A. (1983) Science 221, 514-519
13. Anand P, Thomas SG, Kunnumakkara AB, et al. Biological activities of curcumin and its analogues (Congeners) made by man and mother nature. Biochem Pharmacol 2008; 76:1590–1611
14. Stampfer, M.J. et al., Vitamin E Consumption and the Risk of Coronary Disease in Women. N Eng J Med 1993; 328:1444-1449.
15. Hennekens, C.H. and Gaziano, J.M., Antioxidants and Heart Disease: Epidemiology and Clinical Evidence. Clin Cardiol 1993;16(suppl I):I-10, I-15).
16. American Dietetic Association, (2010). Retrieved June 1, 2010, from http://eatright.org
17. Amit K and Priyadarshani K.I., Free radicals, oxidative stress and importance of antioxidants in human health. J Med Allied Sci 2011; 1(2) : 53-60
18. Block, G. (1991) Am. J. Clin. Nutr. 53, 270S-282S.
19. Enstrom, J. E., Kanim, L. E. and Klein, M. A. (1992) Epidemiology 3, 194-202.
20. Byers, T. and Perry, G. (1992) Annu. Rev. Nutr. 12, 139-159.
Biochemical assessment of dysfunction of liver and brain in alcoholic liver disease patient
Bharati V Nalgirkar, Shubhangi S Pathak, Sanjeev Kale, Vivek V Nalgirkar
Total Serum Sialic acid has been suggested as a new marker of alcoholic liver disease. The synthesis and the catabolism of Sialic acid takes place in the liver and therefore the status of liver can influence the serum levels of Total Sialic acid (TSA). Increased capacity of transferrin deficient in SA to selectively deposit iron in the hepatocytes might be of significance for the development of hepatic siderosis observed in alcoholism. Estimation of serum sialic acid level may be of help in early diagnosis of alcoholic liver disease and prevents the progression of the disease to terminal stages and complications. However, the role of TSA as a marker of liver disease and its association with cognitive changes has not been clearly elucidated. Material and methods: A total of 68 cases and 50 age matched healthy controls were recruited. These patients were further categorized into 3 groups; fatty liver, alcoholic hepatitis and alcoholic cirrhosis. Enrolled patients were followed for 6 months. The study was approved by the institutional ethical committee. Global cognitive functions were assessed periodically with Mini Mental State Examination (MMSE).Serum TSA levels were determined by Biovision’s Sialic acid assay kit. Result: The serum TSA levels (34.74±11.25 nmol/µl) were significantly higher in the alcoholic liver disease than in the healthy controls (2.21±1.01 nmol/µl). Significantly higher TSA levels were observed in patients with alcoholic cirrhosis (36.46±7.66 nmol/µl, p<0.001) compared with alcoholic hepatitis (31.14±9.69 nmol/µl, p<0.001) and alcoholic fatty liver (35.17±10.9 nmol/µl, p<0.001). MMSE Scores were found to be lowest in alcoholic cirrhosis (10.60± 5.32) followed by hepatitis (12.36 ±5.48) and fatty liver (18.28±3.43). Conclusion: Serum TSA is significantly elevated in alcoholic cirrhosis. Serum TSA levels can be used as a marker of alcoholic liver disease and may correlate with cognitive dysfunction among ALD patients.
Objective: To evaluate acylated ghrelin and uric acid in prediabetic subjects and compare it with type 2 diabetics and healthy subjects and to examine the relationship between plasma acylated ghrelin and uric acid concentrations. Method: The study was conducted on 100 subjects: 50 subjects of prediabetes (Group - I) and 50 subjects of type 2 diabetes (Group - II). 50 healthy non-diabetic control subjects (Group-III) of same age of either sex were selected. All subjects with BMI > 30 kg/m2 were considered. Blood samples were analyzed for fasting blood glucose, insulin, HbA1c, uric acid and acylated ghrelin. Result: Acylated Ghrelin and uric acid increases in group -I when compared with group -III and decreases in group-II when compared to group –I. The strongest positive association of acylated ghrelin was observed between acylated ghrelin and Homa- β in prediabetic subjects while the strongest association of uric acid was observed between uric acid and acylated ghrelin in prediabetic subjects. Conclusion: Although the mean values of both acylated ghrelin and uric acid are high in prediabetic subjects as compared to obese control yet the mechanism related to prediabetes i.e. impaired insulin secretion has strong positive association with acylated ghrelin while it shows negative association with uric acid. Hence, acylated ghrelin and uric acid shows inverse relationship in prediabetic obese individuals.
1. Edmann J, Lipple F, Wagenpfeil S, et al: Differential association of basal and postprandial plasma ghrelin with leptin, insulin, and type 2 diabetes: Diabetes. 2005; 55:8–1371.
2. Dezaki K, Sone H, Yada T: Ghrelin is a physiological regulator of insulin release in pancreatic islets and glucose homeostasis:Pharmacol therapeutics. 2008; 118:239–249.
3. Al Massadi O, Tschöp MH, Tong J: Ghrelin acylation and metabolic control: Peptides. 2011; 32(11):8–2301.
4. Delhanty PJ, van der Lely AJ: Ghrelin and glucose homeostasis: Peptides. 2011; 32(11):18–2309.
5. Verhulst PJ, Depoortere I: Ghrelin's second life: from appetite stimulator to glucose regulator: World J Gastroenterol. 2012; 18(25):95–3183.
6. Gelling R, Overduin J, Morrison C, et al: Effect of uncontrolled diabetes on plasma ghrelin concentrations and ghrelin-induced feeding: Endocrinology. 2004; 145:82–4575.
7. Seppo M, Kellokoski M, Horkko S, et al: Low plasma ghrelin is associated with insulin resistance, hypertension, and the prevalence of type 2 Diabetes: Diabetes. 2003; 52:52–2546.
8. Wu J, Yan WH, Qiu L, Chen XQ, Guo XZ, Wu W, Xia LY, Qin XZ, Liu YH, Ding HT, et al: High prevalence of coexisting prehypertension and prediabetes among healthy adults in northern and northeastern China: BMC Publ Health. 2011; 11:794.
9. Vuorinen-Markkola H, Yki-Jarvinen H.: Hyperuricemia and insulin resistance: J Clin Endocrinol Metab. 1994; 78: 25–9.
10. C hen J, Wildman RP, Hamm LL, Muntner P, Reynolds K,Whelton PK et al.: Association between inflammation andinsulin resistance in U.S. nondiabetic adults. Results from the Third National Health and Nutrition Examination Survey: Diabetes Care. 2004; 27: 2960–5.
11. American Diabetes Association: Standards of medical care in diabetes—2014: Diabetes Care. 2014; 37(suppl 1):S14-S80.
12. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC.:Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man: Diabetologia. 1985; 28: 412–9.
13. Sharifi et al.: Acylated ghrelin and leptin concentrations in patients with type 2 diabetes mellitus, people with prediabetes and first degree relatives of patients with diabetes, a comparative study: Journal of Diabetes and Metabolic Disorders. 2013; 12:51.
14. L.Huang et al.: Increased acyl ghrelin but decreaded total ghrelin and unacyl ghrelin in Chinese Han people with impaired fasting glucose combined with impaired glucose tolerance :Peptides 2014;60:86-94.
15. H. K. Choi and E. S. Ford.: Haemoglobin A1c, fasting glucose, serum C peptide and insulin resistance in relation to serum uric acid levels—the Third National Health and Nutrition Examination Survey: Rheumatology. 2008; 47: 713–717.
16. Cook DG, Shaper AG, Thelle DS, Whitehead TP.: Serum uric acid, serum glucose and diabetes: relationships in a population study: Postgrad Med J. 1986; 62:1001–6.
17. Choi HK, Mount DB, Reginato AM. : Pathogenesis of gout: Ann Intern Med. 2005; 143:499–516.
18. Sudhindra Rao M. and Bino J.S.: A study of serum uric acid in diabetes mellitus and prediabetes in a south indian tertiary care hospital: NUJHS. June 2012; 2(2).
Study of biochemical parameters in beta thalassemia major patients
Children with thalassemia have various skeletal changes and effect on liver, lungs and kidneys. All these effect are due to ineffective erythropoiesis and hemochromatosis. All this leads to impairment of functions of various organs. The present study was conducted to assess the kidney functions with blood urea, serum creatinine, serum phosphates, serum sodium, serum potassium ,urinary total protein and urine specific gravity in children’s with beta thalassemia major.
1. Shinar E, Rachmilewitz EA: Oxidative denaturation of red blood cells in thalassemia Seminhematol 1990; 27: 70.
2. Weatherall DJ, Clegg JB: The thalassemia syndromes. 3rd ed. Blackwell Scientific Oxford, 1981.
3. Watanabe: Urinary protein as measured with a pyrogallol red molybdate complex, manually and in Hitachi 726 automated analyzer. Clin Chem 1986; 32:1551-54.
4. Teitz NW: Text Book of Clinical chemistry. W.B.Saunders Co 1986; 602-613.
5. Oktenli C, Bulucu F. Renal tubular dysfunction in a patient with beta thalassemia minor. Nephron 2002; 12:222-223.
6. Cetin T, Oktenli C, Ozgurtas T, Yenicesu M, Sanisoglu SY, Oguz Y, Yildiz O, Kurt I, Musabak U, Bulucu F, Kocar IH. Renal tubular dysfunction in beta- thalassemia minor. Am J Kidney Dis 2003 Dec. 42(6), 1164-8.
7. Aperia AC, Liebow AA, Roberts LE: Renal adaptation to anemia. Circ Res 1968; 22: 489-500.
8. Khalifa AS, Sheir S, El Magel LA, el Tayeb H, el Lamie C, Khalifa A, Mokhtar G: The kidney in Beta – Thalassemia Major: Acta haemat 1985; 74: 60.
9. Sumboonnanonda A, Malasit P, Tanphaichitr VS, Ong-ajyooth S, Sunthornchart S, Pattanakitsakul S, Petrarat S, Assateerawatt A, Vongjirad A. Renal tubular function in beta thalassemia. Pediatr Nephrol 1998 May: 12(4), 280-3.
10. Aldudak B, Karabay Bayazit A, Noyan A, Ozel A, Anarat A, Sasmaz I, Killinc Y, Gali E, Anarat R, Dikmen N: Renal function in pediatric patients with beta thalassemia major. Pediatr Nephrol 2000 Nov15; 15(1-2): 109-12.
11. Lapatsanis P, Sbyrakis S, Vertos C, Karaklis BA, Dosiadir S: Phosphaturia in thalassemia. Pediatrics 1976 Dec; 58(61), 885-92.
12. Lichtman AM, Miller DR, Cohen J, Waterhouse C: Reduced red cell glycoses, 2,3 diphosphoglycerate and adenosine tri phosphate concentration, and increased hemoglobin oxygen affinity caused by hypophosphatemia. Ann Inter Med 1971; 74: 562.
13. Jacob H, Amsden T: Acute hemolytic anemia with rigid red cells in hypophosphatemia. N Engl J Med 1971; 285: 1446.
14. Keitel HG, Thompson D, Itano HA: Hyposthenuria in sickle anemia A reversible renal defect. J Clin Invest 1956;35
15. Statius Van Eps LW, Schouten H, La Portiwusman LW, Struyker – Boudier AM: The influence of red blood cell transfusion on the hyposthenuria and renal hemodynamics of sickle cell anemia. Clin Chim Acta 1967; 17: 119-121.
16. Ong-ajyooth L, Malasit P, Ong-ajyooth S, Fucharoen S, Pootrakul P, Vasuvattakul S, Siritanaratkul N, Nilwarangkur S. Renal function in adult beta thalassemia / HBE disease. Nephron 1998; 78(2): 156-61.
17. Granner DK: Hormones that regulate calcium metabolism. In: Harpers Biochemistry. Murray RK, Granner DK, Mayes PA, Rodwell VW (eds). Lange Medical publications 25th edition 2002; 572-573.
18. Tenenehouse HS, Murer H: Disorders of renal tubular phosphate transport. J Am Soc Nephrol 2003; 14: 240-7.
19. Keitel HG, Thompson D, Itano HA: Hyposthenuria in sickle anemia A reversible renal defect. J Clin Invest 1956; 35.
20. Statius Van Eps LW, Schouten H, La Portiwusman LW, Struyker – Boudier AM: The influence of red blood cell transfusion on the hyposthenuria and renal hemodynamics of sickle cell anemia. Clin Chim Acta 1967; 17: 119-121.
21. Landing BH, Gonick HC, Nadorra RL, Hyman CB, Wells TR, Villarreal EG, Mersch J, Agness CL: Renal lesions and clinical findings in thalassemia major and other chronic anemias with hemosiderosis: Pediatr Pathol 1989; 9(5): 479-500.
22. Sonakul D, Pacharee P, Thakrenpol K: Pathologic findings in autopsy cases of thalassemia. Birth defect Orig Article 1988; 23: 157-156.
A statistical analysis of static water level trend and rainfall data in PTW-1watershed, Buldhana district, INDIA
Groundwater is a dynamic resource and it varies from place to place quantativaly and qualitatively. Its quantity is mostly depends on the rainfall data of that particular region, Geological terrain, Rock type i.e. Aquifer, Geomorphology and drainage pattern. In India especially in Maharashtra state drinking and irrigation water demand is rapidly increases last few years, to cope up this problem, it is necessary to evaluate the existing trend and availability of groundwater in time and space for proper planning in near future. Pre and post monsoon ground water record and its trend, rainfall pattern, and geological especially hydrological study is very useful technique for judicious future planning of groundwater utilization. Proper utilization of available surface water and Ground water quantity it is necessary to manage the watershed concept. For this manners, this paper discuss to analyze the long term (2002-2012) trend of pre- and post-monsoon water level of watershed PTW-1 of Malkapur and Motala Taluka of Buldhana district first time. Trend of Pre and Post Monsoon static Ground water level indicate that there is depletion of static ground water level with the passage of time.
1. Agashe R. M.. Hydrology of Maharashtra, Central Groundwater Board, Central region, Nagpur. 1994.
2. CGWB,Ground water information Buldhana district Maharashtra, ministry of water resources Central Ground Water Board, Central Region Nagpur, Government of India, Technival Report, 1565/OTH/2007,pp1-25.
3. Deshpande, S.M. and Aher, K.R., Quality of Groundwater from Tribakeswar-Peth area of Nashik District and its Suitability for Domestic and Irrigation Purpose, Gond. Geol. Mag.2011, v.26 (2), pp.157-162.
4. GSI Central Region, Buldhana District Resource Map, Buldhana District, Maharashtra 1990.
5. Jangle,P.P., The study of Hydro geomorphologic features in Buldhana district using IRS DATA, International research journal Shodh, Samiksha and Mulyakan,2010,V(2),14.
6. Patrikar G.M., Mitkari A.M. and Deshpande A.M., Unpublished Systematic hydrogeological survey report, GSDA, Maharashtra, 1987.
7. Purushtotham, D., Rao, A.N., Ravi Prakash, M., Shakeel Ahmed and G. Ashok Babu Environmental impact on groundwater of Maheshwaram watershed, Ranga Reddy district, Andhra Pradesh, Jour. Geol. Soc. India, 2011, v.77, pp 539-546.
8. RWSD, Annual Scarcity Report of Rural Water supply Department Dist Buldhana (2002 – 2012).
Pericolic abscess due to large bowel perforation by fish bone – a case report
A diagnosis of large-bowel perforation, caused by a sharp or pointed foreign body, is rarely made preoperatively because the clinical symptoms are usually nonspecific and can mimic other surgical conditions, such as appendicitis and diverticulitis. Less than 1% of ingested foreign body results in perforation from mouth to anus mostly by sharp objects. Of these sharp objects, chicken bone and fishbone account for half of the reported perforations. The most common sites are the ileo-caecal junction and sigmoid colon. In our case the patient presented late with pericolic abscess following the perforation by a fish bone in proximal ascending colon and the fish bone found extramurally making it as first case for that site of large bowel perforation by a fish bone with localized late presentation.
1. Hsu SD, Chan DC, Liu YC. Small-bowel perforation caused by fish bone. World J Gastroenterol 2005; 11(12): 1884-1885
2. Arif HS, Hakim IS, Asim MP, Fazl QP, Rubina L, Khurshid AW. Gastro Intestinal tract perforations due to ingested foreign bodies; a review of 21 cases. BJMP 2012;5(3):a529
3. Pinero MA, Fernandez Hernandez JA, Carrasco PM, Riquelme RJ, Parrilla PP. Intestinal perforation by foreign bodies. Eur J Surg 2000; 166: 307–309
4. Chu KM, Choi HK, Tuen HH, Law SYK, Branicki FJ, Wong J. A prospective randomized trial comparing the use of the flexible gastroscope versus the bronchoscope in the management of foreign body ingestion. Gastrointest Endosc 1998; 47:23–27
5. Chang JJ, Yen CL. Endoscopic retrieval of multiple fragmented gastric bamboo chopsticks by using a flexible overtube. World J Gastroenterol 2004; 10: 769–770
6. Webb WA. Management of foreign bodies of the upper gastrointestinal tract. Gastroenterology 1988; 94: 204-216
7. Hunter TB, Taljanovic MS. Foreign bodies. Radiographics. 2003 May Jun;23(3):731–57.
8. Eisen GM, Baron TH, Dominitz JA, et al. Guideline for the management of ingested foreign bodies. Gastrointestinal Endosc. 2002:55:802–6.
9. Stack LB, Munter DW. Foreign bodies in the gastrointestinal tract. Emerg Med Clin North Am. 1996 Aug; 14(3):493–521.
10. Eftaiha M, Hambrick E, Abcarian H. Principles of management of colorectal foreign bodies. Arch Surg. 1977:112:691–5.
11. Puia I.C, Puia V.R, Andreescu A, Cristea P.G. Ascending colon perforation by ingested fruit stones. Chirurgia (Bucur) 2011; 106(6):825-827.
12. Chiru J.J, Chen T.L, Zhan Y.L. Perforation of the transverse colon by a fish bone: case report. J Emerg Med 2009; 36(4):345-347.
13. Joglekar S, Rajput I, Kamat Sachin, Downey S. Sigmoid perforation caused by an ingested chicken bone presenting as right iliac fossa pain mimicking appendicitis: a case report. J Med Case Rep. 2009; 3:7385.
14. Ali F.E, Al-Busairi W.A, Esbaita E.Y, Al-Bustan M.A. Chronic perforation of the sigmoid colon by foreign body. Curr Surg. 2005; 62(4):419-422.
15. Ben Rejeb A, Gammoudi A, Ben Alaya M. Intestinal Perforation by Fish Bone. Apropos of a Case and Review of the Literature. Ann Chir 1993; 47(1): 86-70. (Abstract).
16. Chuvilkin AV. Case of Large Bowel Perforation by a Fish Bone. Wiad L ek 1973; 26(8): 761-3.
17. Chen CK, Su YJ, Lai YC, et al. Fish Bone-Related Intra-Abdominal Abscess in An Elderly Patient. Int J Infect Dis 2010; 14(2): e171-2.
Issue details
Bacterial colonization of endotracheal tubes in intubated patients
Mayuri K S, VinodKumar C S, Arun Kumar A, Jayasimha V L, Basavarajappa K G
Background: Ventilator associated pneumonia (VAP) is one of the most important form of hospital acquired infections which is associated with increased mortality and morbidity. VAP occurs in about 9 to 27% of all intubated patients. Intubation is associated with 3 to 10 fold increase in the incidence of VAP among all patients receiving mechanical ventilation. In contrast to other nosocomial infections, the crude mortality rate occurring due to VAP ranges from 24% to 76%. ICU patients with VAP have a 2 to 10-fold higher risk of death when compared with patients without pneumonia. Aim: The present study is undertaken to find out the frequency of occurrence of VAP in clinically suspected patients who are mechanically ventilated for more than 48 hours and the major pathogens causing VAP and their antibiotic sensitivity pattern. Methods: A total of 392 patients who are mechanically ventilated for more than 48 hours with clinical suspicion of VAP were included in the study. Endotracheal aspirate was collected and subjected to Grams stain and culture. Culture was performed by quantitative culture technique. Growth on the culture plate was identified by standard microbiological techniques and subjected to antibiotic sensitivity testing by Kirby Bauer disc diffusion method and CLSI guidelines. Results: Among the 392 clinically suspected VAP patients enrolled in the study 52.8% patients were diagnosed with VAP as per the CPIS score. The most common age group affected was 28- 40 years with male preponderance. 18% of the infections were categorized as early onset VAP while 72% as late onset VAP. Pseudomonas aeruginosa, Staphylococcus aureus and Acinetobacter baumannii were the most common isolates.78.5% of Gram negative bacteria were β lactamase producers.89.6% of the Pseudomonas aeruginosa and 96.2 % of Acinetobacter baumannii were meropenem and 84.6% of Staphylococcus aureus strains were methicillin resistant. Conclusion: Staphylococcus aureus was the most common organism causing early onset and Pseudomonas aeruginosa in late onset VAP.
1. Cristina M, Riccardo P, Nitin P et al Ventilator Associated Pneumonia: Evolving Definitions and Preventive Strategies. Respir Care 2013;58;6. 2. Apostolopoulou E, Bakakos P, Katostaras T, Gregorakos L. Incidence and risk factors for ventilator-associated pneumonia in multidisciplinary intensive care units in Athens, Greece. Respir Care 2003;48:681-88. 3. Steven M. K and Jonathon D. T. Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention. Clin Microbiol Rev 2006:19(4):637-9. 4. Niederman MS, Craven DE, Bonten MJ. American Thoracic Society and Infectious Diseases Society of America (ATS/IDSA). Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J RespirCrit Care Med 2005;171(4):388–416. 5. Zolfaghari PS and Wyncoll DL. The tracheal tube: gate way to ventilator-associated pneumonia. Crit Care 2011;15:310-12. 6. Rakshit P, Nagar VS, Deshpande AK. Incidence, clinical outcome, and risk stratification of ventilator associated pneumonia-a prospective cohort study. Indian J Crit Care Med 2005;9:211-16. 7. Fujitani S and Yuginton VL: Quantitative cultures for diagnosing ventilator- associated pneumonia: a critique. Clin Infect Dis 2006;43(2):106-113. 8. Bauer, Kirby, Sherri, Turek. Antibiotic susceptibility testing methods, Am.J.Clin Path 1966;45:493 -498. 9. Clinical and Laboratory Standards Institute (2006). Performance Standards for Antimicrobial Disk Susceptibility Tests, Approved Standard, 9th edn. Clinical and Laboratory Standards document M2-A9 [ISBN1-56238-586-0] Clinical and Laboratory Standards Institute: Wayne, PA, USA. 10. Coudron PE, Moland ES, Sanders CC. Occurrence and Detection of Extended-Spectrum ß-lactamases in members of the family Enterobacteriaceae at a Veterans Medical Center: Seek and You May Find. J ClinMicrobiol 1997; 35:2593-7. 11. Brun-Buisson C, Legrand P, Philippon A, Montravers F, Ansquer M, Duval J et al. Transferable enzymatic resistance to third-generation cephalosporins during a nosocomial outbreak of multi resistant Klebsiella pneumoniae. Lancet 1987;8:302-6. 12. French, G.L., Ling, J., Hui, Y.W. Determination of methicillin-resistance in Staphylococcus aureus by agar dilution and disc diffusion methods. Journal of Antimicrobial Chemotherapy 1987: 20; 599-608. 13. Gadani H, Vyas A, Kar AK. A study of ventilator-associated pneumonia:Incidence, outcome, risk factors and measures to be taken for prevention.Indian J Anaesth. 2010;54:535-40. 14. Ferrer R, Artigas A. Clinical review: Non- antibiotic strategies for preventing ventilator- associated pneumonia. Crit Care 2001;6(1): 45-51. 15. Porzecanski I and Bowton DL. Diagnosis and treatment of ventilator-associated pneumonia. Chest 2006;130:597-604. 16. Dey A, Bairy I. Incidence of multidrug-resistant organisms causing Ventilator associated pneumonia in a tertiary care hospital: A nine months’ prospective study. Ann Thorac Med. 2007;2:52–7. 17. Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J RespirCrit CareMed. 2002;165:867-903. 18. Rello J, Quintana E, Ausina V et al.Incidence, etiology, and outcome ofnosocomial pneumonia in mechanicallyventilated patients. Chest 1991;100(2):439–444 19. Fagon JY, Chastre J, Vuagnat A,Trouillet JL, Novara A, GibertC.Nosocomial pneumonia and mortalityamong patients in intensive care units.JAMA 1996;275(11):866–869. 20. Rahbar M, Monnavar KM, Vatan KK, Fadaei-haq A, Shakerian F. Carbapenemresistance in gram-negative bacilli isolates in an Iranian 1000-bed TertiaryHospital. Pak J Med Sci. 2008; 24(4):537-40. 21. Jakbrittu R.P, Boloor R. Characterisation of aerobic bacteria isolated fromendotracheal aspirate in adult patients suspected ventilator associatedpneumonia in a tertiary care center in Mangalore. Saudi J Anaesth. 2012;6(2):115–19. 22. Gupta A, Agrawal A, Mehrotra S, Singh A, Malik S, Khanna A. Incidence, risk stratification, antibiogram of pathogens isolated and clinical outcome of ventilator associated pneumonia. Indian J Crit Care Med. 2011;15:96-101.
Occult carcinoma of breast presenting as axillary nodal metastasis – a case report
Jawahar Krishnaswamy, Deivanayagam Shanmugam, Vijay Kalimuthu, Sanjai Venkatesh Somasukumar
We report the case of a 50-year-old woman with occult breast cancer who presented with a hard metastatic nodule in the left axilla. Histology identified a metastatic ductal carcinoma deposits in the lymph nodes, but mammography of left breast showed only diffuse thickening of skin and subcutaneous tissue.Left modified radical mastectomy was performed and histopathology revealed invasive ductal carcinoma 1mm x 1mm size with multiple axillary node metastasis.
1. Halsted WS. The result of radical operations for the cure of carcinoma of the breast. Ann Surg 1907;46:1–19. 2. Owen HW, Dockerty MB, Gray HK. Occult carcinoma of the breast. Surg Gynecol Obstet 1954;98:302–8. 3. Baron PL, Moore MP, Kinne DW, Candela FC, Osborne MP, Petrek JA. Occult breast cancer preserving with axillary metastases: updated management. Arch Surg1990;125:210–4. 4. Kyokane T, Akashi-Tanaka S, Matsui T, Fukutomi T. Clinicopathological characteristics of non-palpable breast cancer presenting as an axillary mass. Breast Cancer 1995;2:105–12. 5. Edlow CW, Carter D. Heterotopic epithelium in axillary lymph nodes: report of a case and review of the literature. Am J Clin Pathol 1973;59:666–73. 6. Copeland EM, McBride CM. Axillary metastases from unknown primary sites.Ann Surg 1973;178:25–7. 7. Kemeny MM, Rivera DE, Terz JJ, Benfield JR. Occult primary adenocarcinoma with axillary metastases. Am J Surg 1986;152:43–7. 8. Iglehart JD, Ferguson BJ, Shinleton WW, Sabiston DC, Silva JS, Fetter BF, et al. An ultrastructual analysis of breast carcinoma presenting as isolated axillary adenopathy. Ann Surg 1982;196:8–13. 9. Bhatia SK, Saclarides TJ, Witt TR, Bonomi PD, Anderson KM, Economou SG. Hormone receptor studies in axillary metastases from occult breast cancers. Cancer1987;59:1170–2. 10. Grunfest S, Steiger E, Sebek B. Metastatic axillary adenopathy: use of estrogen receptor protein as an aid in diagnosis. Arch Surg 1978;113:1108–9. 11. Haupt HM, Rosen PP, Kinne DW. Breast carcinoma presenting with axillary lymph node metastases: an analysis of specific histopathologic features. Am J Surg Pathol 1985;9:165–75. 12. Patel J, Nemoto T, Rosner D, Dao TL, Pickren JW. Axillary lymph node metastasis from an occult breast cancer. Cancer 1981;47:2923–7. 13. Rosen PP. Axillary lymph node metastases in patients with occult noninvasive breast carcinoma. Cancer 1980;46:1298–306. 14. Ozzello L, Sanpitak P. Epithelial stromal junction of intraductal carcinoma of the breast. Cancer 1970;26:1186–98. 15. Ellerbroek N, Holmes F, Singietary E, Evans H, Oswald M, McNeese M. Treatment of patients with isolated axillary nodal metastases from an occult primary carcinoma consistent with breast origin. Cancer 1990;66:1461–7. 16. Vilcoq JR, Calle R, Ferme F, Veith F. Conservative treatment of axillary adenopathy due to probable subclinical breast cancer. Arch Surg 1982;117:1136–8. 17. Feuerman, MD, Attie, JN, Rosenberg B. Carcinoma in axillary lymph nodes as an indicator of breast cancer. Surg Gynecol & Obstet1962; 114: 5. 18. Westbrook KC, Gallager HS. Breast carcinoma presenting as an axillary mass. Am J Surg 1971; 122: 607. 19. Larsen RR, Sawyer KC, Sawyer RB, Torres RC. Occult carcinoma of the breast. Am J Surg 1964; 107: 553–555. 20. Osteen RT, Kopf G, Wilson RE. In pursuit of the unknown primary. Am J Surg 1978; 138: 494–498. 21. Fitts WT Jr, Steiner GC, Enterline HT. Prognosis of occult carcinoma of the breast. Am J Surg 1963; 106: 460. 22. Ashikari R, Rosen PP, Urban JA, Senoo T. Breast carcinoma presenting as an axillary mass. Ann Surg 1976; 183: 415–417. 23. Gershon-Cohen J, Ingleby H, Hermel MB. Occult carcinoma of the breast: Value of roentgenography. Arch Surg 1955; 70: 385.
Peri-operative hemodynamic stability in patients undergoing laparoscopic procedures using dexmedetomidine
Sanjana Vinod, Maya Rose Jose
Peri-operative hemodynamic stability in patients undergoing laparoscopic procedures using dexmedetomidine
Peri-operative hemodynamic stability in patients undergoing laparoscopic procedures using dexmedetomidine
Polycythemia Vera with Janus Kinase2 mutation
N V Naren, P Giridhar, K P Rashmi, S N Sadia
Polycythemia vera (PV) is a chronic myeloproliferative disorder characterised by panmyelosis, splenomegaly, and predisposition to venous and arterial thrombosis. Our case was a 54 year male patient who presented with massive splenomegaly, eryhtrocytosis and bone marrow panmyelosis and positive JAK2V617F mutation. Sensitive and relatively cost effective test of JAK2V617F mutation helped in early diagnosis and treatment of PV with certainity. Patient responded well with phlebotomy. Polycythemia vera is a uncommon myeloproliferative neoplasm which is asymptomatic in majority of patients thus needs early identification and treatment to prevent serious complications of haemorrhage and thrombosis.
1. Thiele J, Kvasnicka HM, Orazi A, et al. Polycythemia vera. In: Swerdlow SH, Campo E, Harris NL, et al, eds. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. 4th ed. Lyon, France: IARC Press; 2008:40-43. 2. Mckenzie BS, Beglinger SS. Myeloproliferative disorders. In: Mckenzie BS, Williams LJ (Eds). Clinical Laboratory Hematology. 2nd edition. New Jersey: Pearson publishers;2010: 444-80. 3. Tefferi A. JAK and MPL mutations in myeloid malignancies. Leuk Lymphoma. 2008;49:388-397. 4. James C, Ugo V, Le Couedic JP, et al. A unique clonal JAK2 mutation leading to constitutive signaling causes polycythaemia vera. Nature. 2005; 434: 1144-1148. 5. Ross C, Vanamala N, Ramesh K. Polycythemia vera and essential thrombocythemia- A single institute experience. Indian J Med & Ped Oncol 2008;29(4):7-11. 6. Thiele JM, Kvasnicka HM. Diagnosis of polycythemia vera based on bone marrow pathology. Curr Hematol Rep. 2005; 4:218-223.
Survival of truncus arteriosus in 5th decade - a case report
Kalyan Munde, Nagesh Waghmare, Ashish Amaldi, Anil Kumar
Persistent Truncus arteriosus is congenital cyanotic heart disease characterised by a single great artery that leaves the base of heart and gives rise to coronary, pulmonary and systemic arteries. Majority of patients die of congestive heart failure before their first birthday .Only occasional patients survive in adulthood. We are presenting such a case
1. Lev M, Saphir O. Truncas arteriosus communis persistents Pediatr. 1942;20:74. 2. Calder L, van Praagh R, van Praagh S, et al. Truncus arteriosus communis. Clinical, angiographic and pathologic findings in 100 patients. Am Heart J.1976;92:23. 3. Tandon R, Hauck AJ, Nadas AS. Presistent truncus arteriosus A clinical, hemodynamic, and autopsy study of nineteen cases. Circulation. 1963;28:1050-60. 4. Wilson J.A description of a very unusual malformation of the human heart. Philos Trans R Soc London [Biol]. 1798;18:346. 5. Buchanan A. Malformation of the heart. Undivided truncas arteriosus. Heart otherwise double. Trans Pathol Soc London. 1864;15:89. 6. Collett RW, Edwards JE. Persistent truncas arteriosus. A classification according to anatomic types. Surgical Clinics of North America. 1949;29:1245. 7. Van Praagh R, van Praagh S. The anatomy of common aorticopulmonary trunk (Truncus arteriosus communis ) and its embryologic implications. Am J Cardiol.1965;16:406-25. 8. Van Praagh R. Editorial: classification of truncus arteriosus communis (TAC). Am Heart J. 1976;92:129-32. 9. Kirby ML. Contribution of neural crest to heart and vessel morphology. In: Richard P Harvey, Nadia Rosenthal (Eds). Heart development. San Diego, CA: Academic press. 199.pp.179-93. 10. Conway SJ, Henderson DJ, Copp AJ. Pax3 is required for neural crest migration in the mouse: evidence from the spolotch (Sp2H) mutant. Development.1997;124:505-14. 11. Momma K, AndoM, Mastsuoka R. Truncus arteriosus communis associated with 22q11 deletion. J Am Coll Cardiol. 1997;30:1067-71. 12. Goldmuntz E, Clark BJ, Mitchell LE, et al. Frequency of 22q11 deletions in patients with contruncal defects. J Am Coll Cardiol.1998;32:492-8. 13. Emanuel BS, Budarf ML, scamber PJ. The genetic basis of contruncal defects: The chromosome 22q11.2 deletion. In: Heart Development. (Eds). Richard P Harvey and nadia Rosenthal. San Diego, CA. Academic press. 1999.pp.463-78. 14. Goldmuntz E. Deciphering the genetic etiology of contruncal defects. In: Artman M, Woodrow Benson D, Srivatsava D, Nakazawa M. Malden. MA. Blackwell Futura. 2005.pp.238-41. 15. Mair D, Ritter D, Davis G selection of patients with truncus arteriosus for surgical correction: Anatomic and hemodynamic considerations. Circulation. 1974;49:144-51. 16. Butto F, Lucas R, Edwards J. Persistent truncus arteriosus: Pathologic anatomy in 54 cases. Pediatr Cardiol. 1989;7:95-101. 17. Thiene G, Bortolotti U, Gallucci V. Anatomical study of truncus arteriosus communis with embryological and surgical considerations. Br Heart J. 1976;38:1109-23. 18. Kirklin JW, Barratt- Boyes BG. Truncus arteriosus. In. Kirklin JW, Barratt- Boyes BG (Eds). Cardiac Surgery. 2nd edition. New York: Churchill livingstone. 1992.pp.1131-52. 19. Russell HM, Jacobs ML, Anderson RH, et al. A simplified categorization for common arterial trunk. J Thorc Cardiovasc Surg. 2011;141:645-53. 20. Bohuta L, Hussain A, Fricke TA, et al. Surgical repair of truncus arteriosus associated with interrupted aortic arch: Long-term outcomes. Ann Thorac Surg. 2011;91:1473-7. 21. Bharati S, McAllister HA Jr, Rosenquist GC, et al. The surgical anatomy of truncus arteriosus communis. J Thorac Cardiovasc Surg. 1974;67:501-10. 22. Jacobs ML. Congenital heart surgery nomenclature and database project: Truncus arteriosus. ATS. 2000;69:S50-S5. 23. Juaneda E, Haworth SG. Pulmonary vascular disease in children with truncus arteriosus. Am J Cardiol. 1984;54:1314. 24. Marcelleti C, McGoon DC, Mair DD. The natural histroy of truncus arteriosus. Circulation. 1976;54:108. Victorica BE, Krovetz LJ, Elliott CP, et al. Persistent truncus arteriosus in infancy. AM Heart J. 1969;77:13.
A study on contraceptive knowledge, attitude and practice (KAP) among women attending family planning clinic of a private hospital of Western INDIA
Rahul Rokade
Background: The widespread adoption of family planning, in a society, is an integral component of modern development and is essential for the integration of women into social and economic life. Objectives: To assess the knowledge, attitude and practice regarding usage of contraceptive methods among women attending family planning clinic Material and Method: A cross sectional study was conducted in 100 urban women. They were allotted to two groups – Group A of 76 women consisted of those who came for Medical termination of pregnancy (MTP) and Group B of 24 women who came with incomplete abortion following induced abortion. A pretested semi structure questionnaire was used as study tool to assess the contraceptive knowledge, attitude and practices. The data was analyzed using appropriate statistical methods (SPSS ver. 20). Result: Though 82% women were aware of the existence of a contraceptive method, only 44% ever used one. The most commonly used contraceptive was condom (34%). 82% were willing to undergo tubectomy in future whereas only 20% were willing to accept an intrauterine contraceptive device. Conclusion(S): The study highlights that although there is high level of awareness, contraceptive use is not very high. New ways of motivating people to adopt contraceptives should be considered.
1. Trusell J. Contraceptive efficacy, in: Hatcher RA, Trusell J, Stewart Fet al. (eds). Contraceptive Technology, 17th ed. Irvington Publishers, New York, NY; 1998. 2. Kenny L. Contraception, sterilization and termination of pregnancy, in Luesley DM, Baker PN (eds), Obstetrics and Gynecology. An evidence-based text for MRCOG. Arnold, London, 1st edition 2004; 514-523. 3. Task force on post-ovulatory methods of fertility regulation. Randomized control trial of levonorgestrel versus the Yuzpe regimen of combined oral contraceptives for emergency contraception. Lancet1998; 352:428-33. 4. Young LK, Farguhar CM, Mc Cowan LME et al. The contraceptive practice of women seeking termination of pregnancy in an Aukland clinic. NZ Med J 1994; 107:189-91. 5. Aneblom G, Larsson M, Odlind V et al. Knowledge, use and attitudes towards emergency contraceptive pills among Swedish women presenting for induced abortion. BJOG 2002; 109:155-60. 6. Bromham DR, Cartmill RS. Knowledge and use of secondary contraception among patients requesting termination of pregnancy.BMJ 1993; 306; 556-7.
Digital and palmar dermatoglyphics patterns in myocardial infarction
A V Salunkhe, N R Mudiraj
Introduction: Dermatoglyhics is the scientific study of skin creases and lines and has formed an important part of surface anatomy. The development of dermatoglyphics occurs at much earlier embryonic stage. This is the same period when most of the organs and systems develop including the cardiovascular system. Hence in this study we evaluated the dermatoglyphics in patients of Myocardial Infarction as compared to normal counterparts. Materials and Methods: Study was carried out in Department of Anatomy, in D. Y. Patil medical college during January 2011 to June 2012. Finger prints and palm prints of 150 diagnosed cases of Myocardial Infarction 120 males (M) and 30 females (F) and 150 Control group120 males and 50 females were obtained. Materials required for standard ink method was collected and used for data collection of both the hands. Written consent of the patients was obtained. Results: It was observed in our present study that there was significant increase in whorls and decrease in percentage loops and arches in Myocardial Infarction as compared to controls. The frequency of total palmar pattern in Myocardial Infarction Group is decreased in both sexes and both sides as compared to the controls. There was increase in frequency of position of axial triradii at t’ and t’’ in both hands of myocardial Infarction group in both sexes. Conclusion: Dermatoglyphics in Myocardial Infarction showed significant variation as compare to normal. Presence of above dermatoglyphic features will help us to predict that these individuals may be susceptible for myocardial infarction. It warrants further research in the same direction.
1. Mescher AL. Junqueira's Basic Histology. 12th ed. USA: McGraw-Hill Companies Inc; 2010.p. CD Chapter-Skin. 2. Kumbnani H. K.: Dermatoglyphics- A Review. Anthropologist Special Volume No. 3: 2007: 285-295. 3. Dorland’s Illustrated Medical Dictionary. 28th ed. Philadelphia: Saunders W B; Dermatoglyphics; 1994; 449. 4. Penrose L. S.: and P. T. Ohara: The development of epidermal ridges: Journal of Medical Genetics, 10, (2), 1973, 201-208. 5. Kasey Wertheim.: Embryology and morphology of friction ridge skin. The Fingerprint sourcebook. Washington, D C: U S department of justice, office of justice programs. Published by NIJ (National institute of juctice).2011, 1-22. 6. Namouchi I: Anthropological significance of dermatoglyphic trait variation: an intra-Tunisian population analysis. International Journal of Modern Anthropology 2011; 4 : 12 – 27 7. Gupta UK and Prakash S: Dermatoglyphics: a study of finger tip patterns in bronchial asthma and its genetic disposition. Kathmandu University Medical Journal (2003) Vol. 1, No. 4, Issue 4, 267-271. 8. Pratibha Ramani, Ahilasha P. R., Herald Sherlin and others: Conventional Dermatoglyphics-Revived concept. International journal of pharma and bio sciences, Vol 2, issue 3 sep 2011, 446-458. 9. Fausi AS, Kasper DL, Longo DL, et al. Herrison's Principles of Internal Medicine Volume II. 17th ed. New York: McGraw-Hill; 2008.p.1532 10. Cummins H and Midlo. Finger Prints of palms and soles. An introduction to dermatoglyphics. 1961; Dover Pub. INC, New York. 11. Ashbaugh D. R.: Ridgeology. J. Forensic Ident: 1991, 41 (1), 1-64. 12. Dhall V, Rathee SK, Dhall A: Utility of finger prints in myocardial infarction patients. J Anatomical Society India, 2000; 49 (2): 153-154. 13. Rashad MN, Mi MP, Rhoads G: Dermatoglyphic studies of myocardial infarction patients. Abst Hum Hered 1978; 28:1–6. 14. Anderson MW, Haug PJ, Critchfield G: Dermatoglyphic features of Myocardial Infarction patients. abst Amer J Physl Anthropol, 1981; 55(4): 523-27. 15. Jalali F, KO Hajian-Tilaki: A Comparative Study of Dermatoglyphic Pattern in Patients with Myocardial Infarction and Control Group. Acta Medica Iranica, 2002, 40(3): 187-91.
Correlation between clinical and angiographic findings in patient underwent angiography
Pankaj Palange, Ravikant Patil, R B Kulkarni, Atul Jankar
Introduction: Cardiovascular diseases are account for approximately 12 million deaths annually and are commonest cause of death globally. The progressive evolution in cardiac catheterization technique coupled with the development of effective treatment options for coronary artery disease, diagnostic coronary angiography has become one of the primary components of cardiac catheterization. Objective: To study correlation between clinical and angiographic findings in patient underwent angiography. Material and Methods: A cross sectional study was carried out for the period of one Year in Department of Cardiology, Bharati Vidyapeeth Medical College and Hospital, Sangli. 100 patients above 20 years of age, symptomatic patient, asymptomatic patient with electrocardiogram changes, patients who are willfully opting for coronary angiography were included in the study. Patients with previously diagnosed ischemic heart disease and underwent PTCA or CABG are excluded. Coronary angiography either from femoral or radial artery was done. The results of coronary angiography were carefully interpreted. Patients were grouped as Single Vessels Disease (SVD), Double Vessel Disease (DVD) or Triple Vessel Disease (TVD). According to the percentage of stenosis; the patients were expressed as <50% and >50% stenosis. Statistical analysis was done using Microsoft excel and necessary statistical analysis software was used where necessary. Results: The majority of patients were male with mean age was 60.19± 11.73 years and 57.70± 9.19 years in females. The clinical characteristics showed that chest pain was common clinical feature (96%). The coronary angiography revealed that majority of patients were having SVD (36%) with involvement of LAD artery (82%). 15% showed normal coronary arteries. The correlation between clinical presentation and stenosis of coronary artery showed no statistical significant. Conclusion: The clinical assessment is a good predictor for CAD but it can’t be correlated directly to the coronary angiography findings.
1. Maskey A, Sayami A, Pamdey MR: coronary artery dieseae: An emerging epidemic in Nepal. J. Nepal Med Association 2003; 42:122-124. 2. Murry CJ, Lopez AD. Mortality by cause for eight regions of the world: Global burden of the disease study. Lancet 1997; 349: 1269-76. 3. Gaziano MJ, Manson JE, Ridker PM. Primary and secondary prevention of coronary heart disease. In: Libby P, Bonow RO. Mann DL, Zipes DP, editors. Braunwalds Heart disease. A text book of cardiovascular medicine. 8th ed. Saunders: Philadelphia; 2008. P. 1119-48. 4. Reddy KS, Yusuf S. Emerging epidemic of cardiovascular disease in developing countries. Circulation. 1998; 97: 596-601. 5. Jafary MH, Samad A, Ishaq M , Jawaid SA , Ahmad M, et al. Profile of Acute Myocardial Infarction (AMI) in Pakistan. Pak J Med Sci. 2007; 23:485-9. 6. Boden WE, O' rouke RA. COURAGE trial group. The evolving pattern of coronary artery disease in the US and Canada: Baseline characteristics of the clinical outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial. Am J Cadiol. 2007; 99: 208-12. 7. Jackson R, Chambless L, Higgins M. Sex differences in ischemic heart disease mortality and risk factors in 46 communities: an etiologic analysis. Cardiovascular Risk Factors 1997; 7: 43-54. 8. Mckeigue PM, Adelstein AM, Shipley MJ, Riemersma RA, Mamot MG, Hunt SP et al. Diet and risk factors for coronary heart disease in Asian in North west London Lancet 1985; 2:1086-90. 9. Nourjah P. National Hospital Ambulatory Care Survey: 1997 emergency department summary. Advance data from Vital and Health Statistics. Hyattsuille MD; National Statistics, 2001. 10. MAK Akanda, SY Ali, AEMM Islam, MM Rahman, A Parveen, MK Kabir, L Begum, RC Barman. Demographic Profile, Clinical Presentation and Angiographic Findings in 637 Patients with Coronary Heart Disease. Faridpur Med. Coll. J. 2011; 6(2):82-85.
Uncommon diffuse dense masses on X-ray mammogram, uncurtained by sonomammogram, confirmed on histopathology: A Case series
Rajani Gorantla
Unilateral enlargement of the breast can occur due to various diffuse infiltrative breast lesions, including normal physiological changes, infective, inflammatory, benign etiology and malignant tumors. In this article we present a series of cases with history of unilateral enlargement of breast and appearing as diffuse dense mass on x ray mammogram. Ultrasound findings made appropriate diagnoses which are confirmed on histopathology further.
1. Vuitch MF, Rosen PP, Erlandson RA. Pseudoangiomatous Hyperplasia Of Mammary Stroma. Hum pathology 1986;17:185-91. 2. Erin Bowman, MD,et al. Pseudoangiomatous Stromal Hyperplasia (PASH) of the Breast: A Series of 24 Patients. Breast Journal 2012 May-Jun; 8(3): 242–247. 3. Suhair Al-Saad, Sara Mathew George, Raja Al-Yusuf .Pseudo-angiomatous Stromal Hyperplasia: Benign Tumor of the Breast. Bahrain Medical Bulletin September 2009 ; 31: 3. 4. Navas Cañete A, et al. Pseudoangiomatous Stromal Hyperplasia: Magnetic Resonance Findings in Two Cases. Radiology 2007; 49(4): 275-8. 5. Salvador R, et al. Pseudo-angiomatous Stromal Hyperplasia Presenting as a Breast Mass: Imaging Findings in Three Patients. Breast 2004; 13(5): 431-5. 6. Mercado CL, et al. Pseudoangiomatous Stromal Hyperplasia of the Breast: Sonographic Features with Histopathologic Correlation. Breast J 2004; 10(5): 427-32. 7. AbidIrshad ,etal.Rare Breast Lesions: Correlation of Imaging and Histologic Features with WHO classification. Radiographics, September-October 2008;Volume 28, Issue 5. 8. EunMiRyu In Yong Whang, Eun Deok Chang. Rapidly Growing Bilateral Pseudoangiomatous Stromal Hyperplasia of the Breast. Korean J Radiol 2010;11:355-358. 9. MerihGuray and Aysegul A. Sahin. Benign Breast Diseases: Classification, Diagnosis, and Management. The Oncologist 2006; 11:435-449. 10. Tavassoli FA, Devilee P, eds. Tumours of the breast: Pathology and genetics of tumours of the breast and female genital organs. World Health Organization Classification of Tumours.Lyon,France: IARC, 2003; 9–112. 11. Lee BJ, Pack GT. Giant Intracanalicular Myxoma of the Breast: The So-Called Cystosarcoma Phyllodes Mammae of Johannes Muller. Ann Surgery 1931;93(1):250-268. 12. Chua CL,Thomas A, Ng BK. Cystosarcomaphyllodes-Asian variations. Aust N Z J Surgery1988;58(4) :301–305. 13. Nielsen VT, Andreasen C. Phyllodestumour of themale breast. Histopathology 1987;11(7):761–762. 14. Barrio AV, et al. Clinicopathologic features and long-term outcomes of 293 phyllodestumours of the breast. Ann Surgery Oncology 2007;14(10):2961-2970. 15. Soumaya Ben Abdelkrima e, et al. PhyllodesTumours of the Breast: A Review of 26 Cases. World journal of oncology 2010,vol 1 number 3: 129-134 . 16. Karim RZ, Gerega SK, Yang YH, Spillane A, Carmalt H, Scolyer RA, Lee CS. Phyllodestumours of the breast: A clinicopathological analysis of 65 cases from a single institution. Breast 2009;18(3):165-170. 17. Korula A, Varghese J, Thomas M, Vyas F. Malignant phyllodestumour with intraductal and invasive carcinoma and lymph node metastasis. Singapore Med J 2008;49(11):e318-321. 18. S.Wurdinger, A. B. Herzog, D. R. Fischer et al.“Differentiationofphyllodes breast tumors from fibro adenomas on MRI,†American Journal of Roentgen ology, vol. 185,no. 5, pp. 1317–1321,2005 19. Shashi PrakashMishra, Satyendra Kumar Tiwary,ManjareeMishra, and Ajay Kumar Khanna .PhyllodesTumor of Breast: A Review Article. Department of Surgery, Institute of Medical Sciences, Banaras Hindu University:Volume 2013. 20. Gunhan-Bilgen et al. Inflammatory Breast Carcinoma: Mammographic, UltrasonographicClinical,andPathologicFindings in142 Cases.Radiology2002;223:829–838. 21. Dershaw DD, Moore MP, Liberman L, Deutch BM. Inflammatory breast carcinoma: mammographic findings.Radiology 1994; 190:831-834. 22. American Cancer Society.Inflammatory breast cancer.September 29, 2011. Available at: http: // www .cancer. org / acs / groups / cid / documents/web content/002298-pdf. 23. Anne C.et al. Primary Inflammatory Carcinoma of the Breast: Retrospective Review of Mammographic Findings,February 2000, Volume 174, Number 2. 24. Anne C. Kushwaha, Gary J. Whitman, Carol B. Stelling, Massimo Cristofanilli and Aman U. Buzdar.Primary Inflammatory Carcinoma of the Breast: Retrospective Review of Mammographic Findings. American Journal of Roentgenology. 2000;174: 535-538. 25. American Joint Commission on Cancer.AJCC Cancer Staging Manual, 7thedition , updated Cancer Staging Posters. Available http :// www. Cancerstaging.org/ staging /posters/ breast pdf.
Usefullness of dexmedetomidine as an adjuvant to local anaesthetics in infraclavicular brachial plexus block for prolongation of postoperative analgesia
Prashant Lomate, Divakar Patil, Vasudha Jadhav, Trupti Deshpande, Manisha Patil
Background and Objectives: The infraclavicular brachial plexus block is a safe and reliable approach to provide intraoperative and postoperative analgesia of upper limb. We evaluated the efficacy of dexmedetomidine added to local anaesthetics in infraclavicular brachial plexus block to hasten the onset of sensory and motor block and to prolong the postoperative analgesia. Methods: A prospective randomized double-blind study was carried out in 60 patients aged 18-60 years of ASA grade I and II, who were scheduled for various upper limb surgeries in orthopedics. The patients were divided into two groups of 30 each i.e. Control Group (group C) received 20 ml of inj. Bupivacaine + 10 ml of inj. Xylocaine + 10 ml of Normal Saline and Dexmedetomidine Group (group D) received 20 ml of inj. Bupivacaine + 10 ml of inj. Xylocaine + 10 ml of Normal Saline + 1 µg/kg of inj. Dexmedetomidine. Both groups were compared for the time of onset of sensory and motor blocks, postoperative analgesia and haemodynamic changes. Results: The onset of sensory and motor blockade (2.9 ± 1.0 Vs 8.8 ± 2.22 min and 5.23 ± 1.14 Vs 10.86 ± 2.41 min, respectively) were significantly more rapid in the D group than in the C group (p = 0.0001). The duration of sensory and motor blockade (825 ± 133.83 Vs 412 min ± 74.17 and 878.33 ± 166.23 Vs 409.33 ± 72.01 min respectively) were significantly longer in the D group than in the C group (p = 0.0001). The duration of analgesia (1448.66 ± 288.33 Vs 499 ± 78.79 min) was significantly longer in D group than in the C group (p = 0.0001). Systolic and diastolic blood pressure were lower in D group than C group during the period of anaesthesia from 30 to 120 minutes (in this period patients can be closely monitored and managed) (p < 0.05). Heart rate levels were also low in D group than C group during the period of anaesthesia from 15 to 120 minutes (p < 0.05). Conclusion: We conclude that the addition of dexmedetomidine to local anaesthetic mixture in infraclavicular brachial plexus block hastens the onset and prolong the duration of sensory and motor blocks, as well as the duration of postoperative analgesia.
1. Ertug Z, Yegin A, Ertem S, Sahin N, Hadimioglu N, Docemeci L, et al. Comparision of two different techniques for brachial plexus block: infraclavicular versus axillary technique. Acta Anaesthesiol Scand 2005; 49:1035-9. 2. Raj P, Montgomery SJ, Nettles D , Jenkins MT. infraclavicular Brachial plexus Block- A new approach. Anesth Analg 1973; 52:897-904. 3. Kilka HG, Geiger P, Mehrkens HH. Infraclavicular vertical brachial plexus blockade: A new technique of regional anesthesia. Anesthetist 1995; 44:339-44. 4. Lanz E, Thesiss D, Jancovic D. The extent of Blockade Following Various techniques of brachial plexus block. Anesth Analg 1983; 62:55-58. 5. McCartney CJ, brull R, Chan VW, et al. Early but no long term benefits of regional compared with general anesthesia for ambulatory hand surgery. Anesthesiology 2004; 101:461-7. 6. Cavino BJ, Wildsmith JA. Clinical pharmacology of local anesthetic agents. In:Cousins MJ, Bridenbaugh PO,eds. Neural Blackade in Clinical Anesthesia and Management of Pain. Philadelphia, PA:Lippincott-Raven, 1998;97-128. 7. Kuzma PJ, Kline MD, Calkins MD, Staats PS. Progress in the develepment of ultra-long- acting local anesthetics. Reg Anesth 1997; 22:534-51. 8. Yaksh TL, Ilfeld BM, Wiese AJ, perineural local anesthetic and adjuvant action: the meaning of ex-vivo data set for efficacy and safety. Reg Anesth Pain Med 2012; 37:366-8. 9. Candilo KD. Buprenorphine added to local anesthetic for axillary brachial plexus block prolongs postoperative analgesia. Reg Anesth Pain Med 2002; 27:162-7. 10. McCarteny CJ, Duggan E, Apatu E. Should we add clonidine to local anesthetic for peripheral nerve blockade? A qualitative systematic review of literature. Reg. Anesth Pain Med 2007; 32:330-8. 11. Parrington S, O’Donnell D, Chan VW, et.al Dexamethasone added to mepivacaine prolongs the duration of analgesia after supraclavicular brachial plexus blockade. Reg. Anesth Pain Med 2010; 35:422-6. 12. Buvanendran A, McCarthy RJ, Kroin JS, Leong W, Perry P, Tuman KJ. Intrathecal magnesium prolongs fentanyl analgesia: a prospective randomized, controlled trial. Anesth Analg 2002; 95:661-6. 13. Murali Krishna T, Panda NB, Batra YK, Rajeev S. Combination of low doses of intrathecal ketamine and midazolam with bupivacaine improves postoperative analgesia in orthopedic surgery. Eur J Anesthesiol 2008; 25:299-306. 14. Laiq N, Khan MN, Arif M, Khan S, Midazolam with bupivacaine for improving analgesia quality in brachial plexus block for upper limb surgeries.J Coll Physicin Surg Pak2008;18:674-8. 15. Gabriel JS, Gordin V. Alpha 2 agonist in regional anesthesia and anlgesia. Curr Opin Anesthesiol 2001; 14:751-3. 16. Panzer O, Moitra V, Sladen RN. Pharmacology of sedative-analgesic agents: Dexmedetomidine, remifentanyl, ketamine, volatile anesthetics, and the role of peripheral mu antagonists.Crit Care Clin 2009; 25:451-69. 17. Kanazi GE, Aouad MT, Jabbour-Khoury SI, AI Jazzar MD, Alameddine MM, AI-Yaman R, Bulbul M, Baraka AS. Effect of low dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block. Acta Anaesth Scand 2006; 50:222-7. 18. Congedo E, Sgreccia M, De Cosmo G. New drugs for epidural analgesia. Curr Drug Targets 2009; 10:696-706. 19. Memis D, Turan A, Karamanlioglu B, Pamukcu Z, Kurt I. Adding dexmedetomidine to lidocaine for Intravenous Regional Anaesthesia. Anesth Analg 2004; 98:835-40. 20. Esmaoglu A, Yegenoglu F, Akin A, Turk CY. Dexmedetomidine added to levobupivacaine prolongs axillary brachial plexus block. Anaesthe Analg 2010; 111:1548-51. 21. Obayah GM, Refaie A, Aboushanab O, Ibraheem N, Abdelazees M. Adding dexmedetomidine to bupivacaine for greater palatine nerve block prolongs postoperative analgesia after cleft palate repair. Eur J Anaesthesiol 2010; 27:280-4. 22. Jadon A, Panigrahi MR, Parida SS, Chakraborty S, Agrawal PS, Panda A. Buprenorphine improves the efficacy of bupivacaine in nerve plexus block: A double blind randomized evaluation in subclavian perivascular brachial block. J Anaesth Clin Pharmacol. 2009;25(2):207-10 23. Gaumann D, Forster A,Griessen M, Habre W, Poinsot O, Della Santa D. Comparision between clonidine and epinephrine admixture to lidocaine in brachial plexus block. Anesth Analg 1992; 75:69-74. 24. Gandhi R, Shah A, Patel I. Use of dexmedetomidine along with bupivacaine for brachial plexus block. National J Med Res 2012; 2:67-9. 25. Esmaoglu A, Mizrak A, Akin A, Turk Y, Boyaci A. Addition of dexmedetomidine to lidocaine for intravenous regional anesthesia. Eur J Anaesthesiol 2005; 22:447-51. 26. Eisenach JC, De Kock M, Klimscha W. Alpha (2) - Adrenergic agonists for regional anesthesia. A clinical review of Clonidine (1984-1995). Anesthesiology 1996; 85:655-74. 27. Guo TZ, Jiang JY, Buttermann AE, Maze M. Dexmedetomidine injection into the locus ceruleus produces Antinociception. Anesthesiology 1996; 84:873-81. 28. Abosedira MA. Adding Clonidine or dexmedetomidine to lidocaine during Bier’s block: a comparative study. J M Sci 2008; 8:660-4. 29. Brummet CM, Norat MA, Palmisano JM, Lydic R. Perineural administration of dexmedetomidine in combination with bupivacaine enhances sensory and motor blockade in Sciatic nerve block without inducing neurotoxicity in rat. Anesthesiology 2008; 109:502-11. 30. Hoffmen WE , Kochs E, Werner C, Thomas C, Albrecht RF. Dexmedetomidine improves neurologic outcome from incompelete ischaemia in rat reversal by the alpha 2- adrenergic antagonist atipamezol. Anesthesiology 1991; 75:328-32. 31. Maier C, Steinberg GK, Sun GH, Maze M. Neuroprotection by the aplha 2- adrenoceptor agonist dexmedetomidine in a focal model cerebral ischaemia Anesthesiology 1993;79:306-12. 32. Halonen T, Kotti T, Tuunanen J, Toppinen A, Miettinen R, Riekkinen PJ. Alpha 2- adrenoceptor agonist, dexmedetomidine protects against kainic acid- induced convulsions and neuronal damage. Brain Res 1995;693:217-24 33. Kuhmonen J, Pokorny J, Miettinen R, et. al. Neuroprotective effects of dexmedetomidine in the gerbill hippocampus after transient global ischaemia. Anesthesiology 1997; 87:371-7. 34. Jolkkonen J, Puurnen K, Koistinaho J, et al. Neuroprotection by the alpha-2 adrenoceptor agonist, dexmedetomidine, in rat focal cerebral ischaemia. Eur J Pharmacol 1999; 372:31-6. 35. Laudenbach V, Mantz J, Lagercrantz H, Desmonts JM, Evrard P, Gressens P. Effets of alpha-2 adrenoceptor agonist on perinatal excitotoxic brain injury: Comparison of clonidine and dexmedetomidine . Anesthesiology 2002; 96:134-41. 36. Ma D, Hossain M, Rajkumaraswamy N, et.al dexmedetomidine produces its neuroprotective effect via the α2-A adrenoceptor subtype. Eur J Pharmacol 2004; 502:87-97. 37. Konacki S, Adanir T, Yilmaz G, Rezanko T. The efficacy and neurotoxicity of dexmedetomidine administered via the epidural route. Eur J Anesthesiol 2008; 25:403-9. 38. Brummet CM, Padda AK, Amodeo FS, Welch KB, Lydic R. Perineural dexmedetomidine added to ropivacaine causes a dose dependant increase in the duration of thermal antinociception in sciatic nerve block in rat. Anesthesiology2009; 111:111-9. 39. Kosugi T, Mizuta K, Fujita T, Nakashima M, Kumamoto E. High concentration of dexmedetomidine inhibit compound action potential in frog sciatic nerve without α2 adrenoceptor activation. Br J Pharmacol. 2010; 160:1662-76. 40. Ammar AS, Mahmoud KM. Ultrasound-guided single injection infraclavicular brachial plexus block using bupivacaine alone or combined with dexmedetomidine for pain control in upper limb surgery: a prospective randomized controlled trial. Saudi J Anaesth 2012; 6:109-14. 41. Kaygusuz K. Effects of adding dexmedetomidine to levobupivacaine in axillary brachial plexus block. Curr Ther Res Clin Exp 2012; 73:103-11. 42. Talke P, Lobo E, Brown R. Systemically administered α2-agonist induced peripheral vasocostriction in humans. Anesthesiology 2003; 99:65-70. 43. Winnie AP, Radonjic R, Akkineki SR, et al Factors influencing distribution of local anesthetic injected into brachial plexus sheath. Anesth. Analg 1979; 58:225-234
Leiomyosarcoma of somatic soft tissue origin in the leg - a case report
Jawahar Krishnaswamy, Deivanayagam Shanmugam, Vijay Kalimuthu, Vinod Balaji Baskar
Leiomyosarcoma of soft tissue is thought to arise from the smooth muscle cells lining small blood vessels. Most common site of involvement is retroperitoneum, accounting for approximately 50% of occurrences. Leiomyosarcoma of somatic soft tissues presents as an enlarging, painless mass. Although these tumours are generally associated with small blood vessels they usually do not present with signs or symptoms of vascular compression. However, when leiomyosarcoma arises from a major blood vessel, symptoms of vascular compromise or leg edema may be present, as well as neurologic symptoms such as numbness from compression of an adjacent nerve. We report a case of leiomyosarcoma of somatic soft tissue of the leg of a young male presented to us with swelling in the upper one-third of left leg which was associated with severe pain on extension of the joint. Patient was diagnosed as leiomyosarcoma of the somatic soft tissue origin by clinical, pathological and immunohistochemistry methods.
1. Gustafson P, Willen H, Baldetrop B, et al. Soft tissue leiomyosarcoma: a population-based epidemiologic and prognostic study of 48 patients, including cellular DNA content. Cancer 70:114, 1992. 2. Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors 4th Ed. Philadelphia: Mosby-Harcort, 2001. 3. De Saint Aubain Somerhausen N, Fletcher C. Leiomyosarcoma of Soft Tissue in Children: Clinicopathologic analysis of 20 cases. Am J Surg Pathol, 23(7):755, 1999. 4. McClain KL, Leach CT, Lenson HB, et al. Association of Epstein-Barr virus with leiomyosarcoma in young people with AIDS. New England Journal of Medicine 332:19, 1995. 5. Mankin, HJ, Casas-Ganem, J, Kim, JI, et al. Leiomyosarcoma of somatic soft tissues. Clin Orthop Relat Res. 2004 Apr ;( 421):225-31. 6. Golden T, Stout AP. Smooth muscle tumors of the gastrointestinal tract and retroperitoneal tissues. Surg Gynecol Obstet 73:784, 1941. 7. Fields JP, Helwig EB. Leiomyosarcoma of the skin and subcutaneous tissue. Cancer 47:156, 1981. 8. Jensen ML, Myhre Jensen O, Michalski W, et al. Intradermal and subcutaneous leiomyosarcoma: a clinicopathologic and immunohistochemical study. J Cutan Pathol 23:458, 1996. 9. Kevorkian J, Cento JP. Leiomyosarcoma of large arteries and veins. Surgery 73:39, 1973. 10. Burke AP, Virmani R. Sarcomas of the great vessels: a clinicopathologic study. Cancer 71:1761, 1993. 11. Farshid G, Goldblum J, Weiss SW. Leiomyosarcoma of soft tissue: a tumor of vascular origin with multivariate analysis of outcome. Mod Pathol. 2003 Aug; 16(8):778-85. 12. Fletcher CDM, Cin PD, Wever I, et al. Correlation between clinicopathological features and karyotype in spindle cell sarcomas: a report of 130 cases from the CHAP study group. Am J of Pathology 154:6, 1999 13. Rubin BP, Fletcher CDM. Myxoid leiomyosarcoma of soft tissue, an under recognized variant. Am J of Surg Pathol 24(7):927-936, 2000. 14. Hasimoto H, Daimaru Y, Tsuneyoshi M, et al. Leiomyosarcoma of the external soft tissues. Cancer 57:2077, 1986. 15. Templeton K. Leiomyosarcoma of bone. M J Orthop 34:55, 249-251, 2005. 16. Weiss SW. Smooth muscle tumors of soft tissue. Advances in Anatomic Pathology. 9(6):351-359 2002. 17. Iwata J, Fletcher CD. Immunohistochemical detection of cytokeratin and epithelial membrane antigen in leiomyosarcoma: a systematic study of 100 cases. Pathol Int 2000 Jan;50(1):7-14. 18. Adjuvant chemotherapy for localized respectable soft tissue sarcoma of adults: meta analysis of individual data. Sarcoma Meta-analysis Collaboration. Lancet 1997 350:1647.
Acrania: a case report
Satish Prasad B S, Lakshmi Paragannavar
Acrania is a rare lethal congenital anomaly characterised by an absence of the calvarium. Ultrasound allows early diagnosis of this anomaly. Although acrania associated with anencephaly is a well recognized entity with an incidence of about 10:10,000 births, isolated acrania is a rare anomaly, and its incidence is unknown. We report a 25 year old female patient referred to our ultrasound department for antenatal scan. The fetus was found to have a completely formed brain, base of the skull and facial structures but lacking a cranium.
1. Mannes EJ, Crelin ES, Hobbins JS et-al. Sonographic demonstration of fetal acrania. AJR Am J Roentgenol. 1982; 139 (1): 181-2. 2. Kaya H, Sezik M, Özkaya O, Aydin AR. Fetal acrania at term Perinatal Journal.2004;12(2):96–98. 3. Cincore V, Ninios AP, Pavlik J, Dong C. Prenatal Diagnosis of Acrania with amniotic band syndrome. Obstetrics and Gynecology. 2003; 102(5):1176–1178. 4. Fong KW, Toi A, Salem S, Hornberger LK, Chitayat D, Keating SJ, McAuliffe F, Johnson JA. Detection of fetal structural abnormalities with US during early pregnancy. Radiographics. 2004; 24:157-174. 5. Johnson SP, Sebire NJ, Snijders RJM, Tunkel S, Nicolaides KH. Ultrasound screening for anencephaly at 10–14 weeks of gestation. Ultrasound Obstet Gynecol. 1997; 9:14–16. 6. Liu I, Chang C, Yu C, Cheng Y, Chang F. Prenatal diagnosis of fetal acrania using three-dimensional ultrasound. Ultrasound in Medicine and Biology. 2009; 31(2):175–78. 7. Cafici D, Sepulveda W. First-trimester echogenic amniotic fluid in the acrania-anencephaly sequence. J Ultrasound Med. 2004; 22 (10): 1075-9. 8. Romero R, Pilu G, Jeanty J, et al. Prenatal Diagnosis of Congenital Anomalies. Appleton and Lange, Norwalk, Connecticut, 1988. pp 75-76.
A study of profile of poisoning cases in and around Hassan district, Karnataka
Shivakumar K T, Deepak P
A study of profile of poisoning cases in and around Hassan district, Karnataka
1. Thomas WF, John HD, Willium RH. Stedman’s Medical dictionary.28th edition. Lippincott William and Wilkins, New York. 2000. 2. Gargi J, Tejpal HR. A retrospective autopsy study of poisoning in Northern region of Punjab. Journal of Punjab academy of Forensic medicine and toxicology. 2008;2:17-20. 3. Aaron R, Joseph A, Abraham S, Muliyil J, George K, Prasad J et.al . Suicides in young people in rural Southern India. Lancet.2004;363:1117-1118. 4. Eddleston M. Patterns and problems of deliberate self poisoning in the developing world. Q J Med, 2000;93:715-731. 5. Batra AK, Keoliya AN, Jadhav GU. Poisoning: An unnatural cause of morbidity and mortality in rural India. J Assoc Physicians India 2003;51:955-959. 6. Dash SK, Raju AS, Mohanty MK, Patnaik KK, Mohanty S. Sociodemographic profile of poisoning cases. JIAFM 2005;27(3):133-138. 7. Thomas M, Anandan S, Kuruvilla PS, Singh PR, David S. Profile of hospital admission following acute poisoning experiences from a major teaching hospital in South India. Adverse drug reaction and toxicology review. 2000; 19:313-317. 8. Zaheer MS, Aslam M, Gupta V, Sharma V, Khan SA. Profile of poisoning cases at a North Indian tertiary care hospital. Health and population: Perspectives and Issues.2009;32(4):176-183. 9. Maharani B, Vijayakumari N. Profile of poisoning cases in a tertiary care hospital, Tamil Nadu, India. Journal of Applied Pharmaceutical Science. 2013;3(1):91-94. 10. Kora SA, Doddamani GB, Halagali GR, Vijayamahantesh SN, Umakanth B. Socio demographic profile of the Organophosphorus poisoning cases in Southern India. Journal of Clinical and diagnostic research 2011; 5(5): 953-956.
A Comparative Study on Effect of Moderate and heavy Intensity Exercise Priscription in Moderate COPD Patients on Haemodynamics and Functional Capacity
Virendra K Meshram
Patients with COPD have reduced functional capacity due to deconditioning. Various studies have found that endurance exercise training is single most important aspect of rehabilitation for patients with chronic pulmonary disease. However, there are conflicting views about the intensity for exercise prescription in stable COPD patients. The optimal specific exercise prescription guidelines in terms of intensity prescription have not been well documented. The purpose of this study was to compare the effect of two training intensities in stable COPD patients, which would help in formulating a comfortable and efficient exercise program in this population. 60 male subjects with moderate COPD were selected through purposive sampling and randomly allocated into two groups, group A and group B, each group having 30 subjects (n=30). Group A subjects were trained with moderate intensity and Group B subjects with heavy intensity exercise. Subjects were trained with the prescribed intensity exercise for respective groups for 10 min per day, 4 times a week for 4 weeks of duration. Outcome of interest include Resting Heart rate, Respiratory rate, Distance covered in 6-min walk test, % predicted FEV1 value, % predicted FEV1/FVC ratio. Data were analysed using paired and unpaired t test. Group B showed significant improvement in RHR, RR. Improvement is found in both groups for 6-MWD, whereas group B subjects showed more significant improvement. However, there was no improvement found in FEV1 and FEV1/FVC ratio in either group. The result of this study revealed that heavy intensity exercise training provides benefits to patients with moderate COPD than moderate intensity exercise training in terms of improvements in functional status if done with permissible interval training during the training. There was 18% of improvement in 6-MWD in group B.
1. GOLD COPD 2007. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. 2. World Health Organization, World Health Report 2002 Geneva: WHO 2002. www.who.int/whr/ 2002 /en/. 3. Christopher JL, Murray, Alan DL, Evidence-Based Health Policy-Lessons from the Global Burden of Disease Study Science. 1996; 274: 740-743. 4. Jindal SK, Aggrawal AN, Gupta D. A review of Population Study from India to Estimate National Burden of Chronic Obstructive Pulmonary Disease and Its Association with Smoking. Indian J Chest Dis Allied Sci 2001; 43 : -147. 5. Vigg Arul, Vigg Ajit, Vigg Avanti, and Mantri Sumanth. Prevalence Of Chronic Obstructive Pulmonary Disease In Patients Attending Chest Clinic In A Tertiary Care Hospital. CHEST / 128 / 4 / OCTOBER, 2005 SUPPLEMENT. 6. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th edition. Pp84. 7. Linda Nici; Claudio Donner; Emiel Wouters; Richard Zuwallack; et al. American Thoracic Society/European Respiratory Society Statement on Pulmonary rehabilitation. American Journal of Respiratory and Critical Care Medicine; Jun 15, 2006; 173, 12. 8. COOPER, C. B. Exercise in chronic pulmonary disease: aerobic exercise prescription. Med. Sci. Sports Exerc., Vol. 33, No. 7, Suppl., pp. S671–S679, 2001. 9. Frits M. E. Franssen, Roelinka Broekhuizen et.al. Effects of Whole-Body Exercise Training on Body Composition and Functional Capacity in Normal-Weight Patients with COPD. Chest 2004;125;2021-2028. 10. CRINER GERARD J., CORDOVA FRANCIS C et.al. Prospective Randomized Trial Comparing Bilateral Lung Volume Reduction Surgery to Pulmonary Rehabilitation in Severe Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med Vol 160. pp 2018–2027, 1999. 11. ACSM. ACSM’s Advanced Exercise Physiology. Mayland: Lippincott Williams and Wilkins, 2006. pp 4. 12. Durstine JL, Moore GE. ACSM’s Exercise Manegment for Persons with Chronic Diseases and Disabilities. 2nd ed. US Lippincott Williams and Wilkins. pp 92. 13. Wilmore JH, Costill DI. Physiology Sport and Exercise. 3rd ed. Champaign, IL: Human Kinetics, 1999, pp 279. 14. Kisner C, Colby LA. Therapeutic Exercise. 5th ed. Dariyaganj, New Delhi, J P Brothers. 2007. pp 241- 242. 15. Wilmore JH, Costill DI. Physiology Sport and Exercise. 3rd ed. Champaign, IL: Human Kinetics, 1999, pp 222. 16. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th edition.pp 415 17. Brooks GA, Fahey TD, White TP, et.al. Exercise Physiology. 2nd ed. Mountain View, CA: Mayfield, 2000. pp 545 18. Brooks GA, Fahey TD, White TP, et.al. Exercise Physiology. 2nd ed. Mountain View, CA: Mayfield, 2000. pp 214 19. McArdle WD, Katch FI, Katch VL. Exercise Physiology Energy, Nutrition & Human Performance. 5th ed. Mayland: Lippincott Williams and Wilkins, 2001. pp 950 20. ATS Statement: Guidelines for the Six-Minute Walk Test 2002 21. Enright Paul L., McBurnie Mary Ann. The 6-min Walk Test: A Quick Measure of Functional Status in Elderly Adults. Chest 2003;123;387-398. 22. ACSM. Acsm’s Guidelines for Exercise Testing and Prescription. 7th ed. Mayland: Lippincott Williams and Wilkins, 2006. pp 227 23. McArdle WD, Katch FI, Katch VL. Exercise Physiology Energy, Nutrition & Human Performance. 5th ed. Mayland: Lippincott Williams and Wilkins, 2001. pp 953 24. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 411 25. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 416. 26. Brooks GA, Fahey TD, White TP, et.al. Exercise Physiology. 2nd ed. Mountain View, CA: Mayfield, 2000. pp 545. 27. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 87 28. Frownfelter Donna. Cardiovascular and Pulmonary Physical Therapy (Evidence and Practice). 4th ed. pp 154
Influence of age, body fat distribution, alcohol consumption and smoking on liver enzymes activity in apparently healthy western Indian males
Shalini N Maksane, Sucheta P Dandekar
This prospective study was conducted to assess the effect of demographic and clinical parameters on liver enzymes in apparently healthy western Indian male population. The study population consisted of 669 males attending blood donation camps during 2011 to 2013. Anthropometric measurement was taken and history for alcohol consumption and smoking was noted. Biochemical parameters including AST, ALT, and GGT activities were determined using auto analyzer (AU-400 by Olympus). Mann-Whitney Test and Kruskal-Wallis One Way ANOVA on Ranks Test applied. P value of < 0.05 was considered to be statistically significant. All analyses were conducted using the SPSS-13.0. According to alcohol habit, 97 (14.5%) were alcoholic and 572 (85.5%) were non-alcoholic. According to smoking habits, 171 (25.6 %) were smokers and 498 (74.4 %) were non-smokers. Median activity of serum AST, ALT and GGT were 27.00 IU/L, 17.00 IU/L and 18.80 IU/L respectively. By univariate analyses, there were significant associations between increasing AST, ALT, or GGT tertiles and age, body mass index, and waist and hip circumferences, Waist-Hip ratio (p < 0.05). AST and GGT activity were significantly higher in alcoholic men compared to non alcoholic (p < 0.05). BMI, AST, ALT and GGT were significantly higher in smokers compared to non-smokers (p < 0.05). These data suggest that slight to moderate increase in BMI and light alcohol intake and smoking affected liver enzymes levels in apparently healthy western Indian males. These factors should be considered in the definition of normal limits for liver enzymes.
1. Jang ES1, Jeong SH, Hwang SH, Kim HY, Ahn SY, Lee J, Lee SH, Park YS, Hwang JH, Kim JW, Kim N, Lee DH: Effects of coffee, smoking, and alcohol on liver function tests: a comprehensive cross-sectional study. BMC Gastroenterol. 2012 Oct; 18(12):145. 2. Pratt DS, Kaplan MM: Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med. 2000; 342:1266–1271. 3. Giannini EG, Testa R, Savarino V: Liver enzyme alteration: a guide for clinicians. CMAJ. 2005; 172: 367–379. 4. Liu Z, Hu Y, Yang X, Tan A, Gao Y, Qin X, Liang Y, Mo Z, Peng T: Combinative analysis of factors influence serum alanine aminotransferase activity in adult male population from southern China. Clinical biochemistry. 2012; 45(18):1683-1688 5. Clark J M., Frederick L B, Anna M D: The prevalence and etiology of elevated aminotransferase levels in the United States. The American journal of gastroenterology. 2003; 98(5): 960-967. 6. Srikanthan, P, Seeman, T E, Karlamangla A S: Waist-hip-ratio as a predictor of all-cause mortality in high-functioning older adults. Annals of epidemiology.2009; 19(10): 724-731. 7. Hietala J, Puukka K, Koivisto H, Anttila P, Niemelä O: Serum gamma-glutamyl transferase in alcoholics, moderate drinkers and abstainers: effect on gt reference intervals at population level. Alcohol and Alcoholism. 2005; 40(6):511-514. 8. Alatalo P, Koivisto H, Puukka K, Hietala J, Anttila P, Bloigu R, Niemelä, O: Biomarkers of liver status in heavy drinkers, moderate drinkers and abstainers. Alcohol and alcoholism. 2009; 44(2):199-203. 9. Breitling LP, Raum E, Muller H, Rothenbacher D, Brenner H: Synergism between smoking and alcohol consumption with respect to serum gamma-glutamyltransferase. Hepatology. 2009; 49:802–808. 10. Khedmat H, Fallahian F, Abolghasemi H, Hajibeigi B, Attarchi Z, Alaeddini F, ... Zarei N: Serum gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase activity in Iranian healthy blood donor men. World Journal of Gastroenterology. 2007; 13(6): 889. 11. Abel E L, Kruger M L, Friedl J: How do physicians define “light,â€â€œmoderate,†and “heavy†drinking?. Alcoholism: Clinical and Experimental Research. 1998; 22(5): 979-984. 12. Robert L S: Clinical Reference Laboratory. 1999. 13. Ritchie RF, Palomaki G: Selecting clinically relevant populations for reference intervals. Clin Chem Lab Med. 2004; 42:702–709. 14. Piton A, Poynard T, Imbert-Bismut F, Khalil L, Delattre J, Pelissier E, Opolon P: Factors associated with serum alanine transaminase activity in healthy subjects: Consequences for the definition of normal values, for selection of blood donors, and for patients with chronic hepatitis C. Hepatology. 1998; 27(5): 1213–1219. 15. Lee J K, Shim J H, Lee H C, Lee S H, Kim K M, Lim Y S, ...Suh D J: Estimation of the healthy upper limits for serum alanine aminotransferase in Asian populations with normal liver histology.Hepatology. 2010; 51(5):1577-1583. 16. Stromme J H, Rustad P, Steensland H, Theodorsen L, Urdal P: Reference intervals for eight enzymes in blood of adult females and males measured in accordance with the International Federation of Clinical Chemistry reference system at 37 degrees C: part of the Nordic Reference Interval Project. Scandinavian Journal of Clinical and Laboratory Investigation. 2004; 64(4): 371–384. 17. Mohamadnejad M, Pourshams A, Malekzadeh R, Mohamadkhani A, Rajabiani A, Asgari A A, Mamar-Abadi M: Healthy ranges of serum alanine aminotransferase levels in Iranian blood donors. World journal of gastroenterology. 2003; 9(10): 2322-2324. 18. Burns CJ, Boswell JM, Olsen GW: Liver enzyme activity and body mass index. J Occup Environ Med. 1996; 38(12): 1248-1252. 19. Mala H, Zadak Z, Sobotka L, Maly J: Changes in selected biochemical parameters during a low-calorie reducing diet. Sb Lek. 2000; 101(1):105-108 20. Kumar S, Amarapurkar A, Amarapurkar D: Serum aminotransferase levels in healthy population from western India. The Indian journal of medical research. 2013; 138(6): 894. 21. Nakamura K, Motohashi Y, Kikuchi S, Tanaka M, Nakano S: Liver transferase activity in healthy Japanese employees aged 18–39 years. Ind Health.1998; 36: 218–22. 22. Lee D H., Ha M H, Christiani D C: Body weight, alcohol consumption and liver enzyme activity—a 4-year follow-up study. International journal of epidemiology. 2001; 30(4): 766-770. 23. Puukka K, Hietala J, Koivisto H, Anttila P, Bloigu R, Niemela O: Age-related changes on serum ggt activity and the assessment of ethanol intake. Alcohol and alcoholism. 2006; 41(5): 522-527. 24. Steffensen FH, Sorensen HT, Brock A, Vilstrup H, Lauritzen T: Alcohol consumption and serum liver-derived enzymes in a Danish population aged 30–50 years. Int J Epidemiol. 1997; 26: 92–99. 25. Lee DH, Lim JS, Yang JH, Ha MH, Jacobs DR Jr: Serum gammaglutamyltransferase within its normal range predicts a chronic elevation of alanine aminotransferase: a four year follow-up study. Free Radic Res. 2005; 39:589–593. 26. Chan-Yeung M, Ferreira P, Frohlich J, Schulzer M, Tan F:The effects of age, smoking, and alohol on routine laboratory tests. Am J Clin Pathol.1981; 75:320–326. 27. Whitehead TP, Robinson D, Allaway SL: The effects of cigarette smoking and alcohol consumption on serum liver enzyme activities: a dose-related study in men. Ann Clin Biochem. 1996; 33(6):530-535.
Antioxidants: the defense mechanism against free radicals
Runki
Introduction: Metabolism refers to biochemical processes that occur within any living organism - including humans - to maintain life. It is sum of all anabolic (synthesis) and catabolic (break down) reactions occurring in our body. Metabolism can also be aerobic (O2 dependent) or anaerobic (in absence of O2). These biochemical processes allow us to grow, reproduce, repair damage, and respond to our environment. Oxidants are formed as a normal product of aerobic metabolism. This aerobic metabolism does not come without cost. “Free radicals†are formed as a by product of this metabolism which is capable of attacking the healthy cells of the body. They are responsible for causation and progress of many diseases like Atherosclerosis, Cataract, Cancer, degenerative diseases, inflammatory diseases, etc. Antioxidants are the first line of defense for these free radicals and are vital in maintaining optimum health and well being. These anti oxidants can be obtained from natural dietary sources or can be taken as nutritional supplements.
1. SIES, H. (1985). Oxidative stress: introductory remarks. In Oxidative Stress, ed. SIES, H., pp. 1-8. Academic Press, London. 2. SIES, H. (1991). Oxidative stress: introduction. In Oxidative Stress: Oxidants and Antioxidants, ed. SIES, H., pp. xv-xxii. Academic Press, London. 3. Domenico P, Luigi L, Stefania E et al., Enhanced lipid peroxidation in hepatic cirrhosis, J Investig Med, Feb 46 (2) (1998) 51. 4. Beck M M and Levander O A, Fietary oxidative stress and the potentiation of viral infection, Annu Rev Nutr, 18 (1998) 93. 5. Peterhans E, Oxidants and antioxidants in viral diseases: Diseases mechanisms and metabolic regulation, J Nutr, 127 (1997) 962s. 6. Winterbourn CC. Reconciling the chemistry and biology of reactive oxygen species. Nature Chem Biol 2008; 4:278-286. 7. Lippincott W and Wilkins, Lippincott’s Illustrated Reviews: Biochemistry (V edition), 2011; 148 8. Herbert V. The antioxidant Supplement myth. Am J Clin Nutr 1994;60:157-168 9. Block, G. et al. Fruit, Vegetables, and Cancer Prevention: A Review of the Epidemiological Evidence, Nutr Cancer 1992; 18(1):1-29. 10. Hennekens, C.H. and Gaziano, J.M., Antioxidants and Heart Disease: Epidemiology and Clinical Evidence. Clin Cardiol 1993;16(suppl I):I-10, I-15). 11. SIES, H. (1993). Strategies of antioxidant defense. European Journal of Biochemistry 215, 213-219. 12. Reichard, P. and Ehrenberg, A. (1983) Science 221, 514-519 13. Anand P, Thomas SG, Kunnumakkara AB, et al. Biological activities of curcumin and its analogues (Congeners) made by man and mother nature. Biochem Pharmacol 2008; 76:1590–1611 14. Stampfer, M.J. et al., Vitamin E Consumption and the Risk of Coronary Disease in Women. N Eng J Med 1993; 328:1444-1449. 15. Hennekens, C.H. and Gaziano, J.M., Antioxidants and Heart Disease: Epidemiology and Clinical Evidence. Clin Cardiol 1993;16(suppl I):I-10, I-15). 16. American Dietetic Association, (2010). Retrieved June 1, 2010, from http://eatright.org 17. Amit K and Priyadarshani K.I., Free radicals, oxidative stress and importance of antioxidants in human health. J Med Allied Sci 2011; 1(2) : 53-60 18. Block, G. (1991) Am. J. Clin. Nutr. 53, 270S-282S. 19. Enstrom, J. E., Kanim, L. E. and Klein, M. A. (1992) Epidemiology 3, 194-202. 20. Byers, T. and Perry, G. (1992) Annu. Rev. Nutr. 12, 139-159.
Biochemical assessment of dysfunction of liver and brain in alcoholic liver disease patient
Bharati V Nalgirkar, Shubhangi S Pathak, Sanjeev Kale, Vivek V Nalgirkar
Total Serum Sialic acid has been suggested as a new marker of alcoholic liver disease. The synthesis and the catabolism of Sialic acid takes place in the liver and therefore the status of liver can influence the serum levels of Total Sialic acid (TSA). Increased capacity of transferrin deficient in SA to selectively deposit iron in the hepatocytes might be of significance for the development of hepatic siderosis observed in alcoholism. Estimation of serum sialic acid level may be of help in early diagnosis of alcoholic liver disease and prevents the progression of the disease to terminal stages and complications. However, the role of TSA as a marker of liver disease and its association with cognitive changes has not been clearly elucidated. Material and methods: A total of 68 cases and 50 age matched healthy controls were recruited. These patients were further categorized into 3 groups; fatty liver, alcoholic hepatitis and alcoholic cirrhosis. Enrolled patients were followed for 6 months. The study was approved by the institutional ethical committee. Global cognitive functions were assessed periodically with Mini Mental State Examination (MMSE).Serum TSA levels were determined by Biovision’s Sialic acid assay kit. Result: The serum TSA levels (34.74±11.25 nmol/µl) were significantly higher in the alcoholic liver disease than in the healthy controls (2.21±1.01 nmol/µl). Significantly higher TSA levels were observed in patients with alcoholic cirrhosis (36.46±7.66 nmol/µl, p<0.001) compared with alcoholic hepatitis (31.14±9.69 nmol/µl, p<0.001) and alcoholic fatty liver (35.17±10.9 nmol/µl, p<0.001). MMSE Scores were found to be lowest in alcoholic cirrhosis (10.60± 5.32) followed by hepatitis (12.36 ±5.48) and fatty liver (18.28±3.43). Conclusion: Serum TSA is significantly elevated in alcoholic cirrhosis. Serum TSA levels can be used as a marker of alcoholic liver disease and may correlate with cognitive dysfunction among ALD patients.
1. Global status report on alcohol and health. World Health Organization (WHO) 2002. 2. Sarkar AP, Sen S, Mondal S, Singh OP, Chakraborty A, Swaika B. Study on socio-demographic characteristics of alcoholics attending the de-addiction center at Burdwan medical college and hospital in West Bengal Indian J Public Health 2013;57:33-5. 3. Rao R. Endotoxemia and gut barrier dysfunction in alcoholic liver disease. Hepatology.2009; 50:638–644. 4. Charles S Lieber .CYP2E1: from ASH to NASH. Hepatology Research 2004; 28:1–11. 5. Sillanaukee P1, Pönniö M, Jääskeläinen IP. Occurrence of sialic acids in healthy humans and different disorders. Eur J Clin Invest. 1999; 29(5):413-425. 6. Pönniö M1, Alho H, Heinälä P, Nikkari ST, Sillanaukee P. Serum and saliva levels of sialic acid are elevated in alcoholics Alcohol Clin Exp Res. 1999; 23(6):1060-4. 7. Ajit Varki and Roland Schauer. Sialic Acids. Varki A, Cummings RD, Esko JD, et al. editors. Essentials of Glycobiology. 2nd edition. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 2009. Chapter 14. 8. Kloppel TM, Morré DJ. Characteristics of transplantable tumors induced in the rat by N-2- fluorenylacetamide: elevations in tissue and serum sialic acid. Natl Cancer Inst. 1980; 64(6):1401-11. 9. Anttila, P., Järvi, K., Latvala, J., Romppanen, J., Punnonen, K., Niemela, O. “Biomarkers of alcohol consumption in patients classified according to the degree of liver disease severity†Scand. J. Clin. Lab. Invest2005; 65:141-151. 10. Ewa Gruszewska, 1 Bogdan Cylwik, 2 Anatol Panasiuk, 3 Maciej Szmitkowski, 1 Robert Flisiak, 3 and Lech Chroste. Total and Free Serum Sialic Acid Concentration in Liver Diseases BioMed Research International 2014 (2014).5 pages. 11. Folstein, M., Folstein, S.E., McHugh, P.R. “Mini-Mental State†a Practical Method for Grading the Cognitive State of Patients for the Clinician. Journal of Psychiatric Research. 1975; 12(3): 189-198. 12. Kanwaljit Chopra and Vinod Tiwari. Alcoholic neuropathy: possible mechanisms and future treatment possibilities. Br J Clin Pharmacol. 2012; 73(3): 348–362. 13. Neafsey EJ, Collins MA. Moderate alcohol consumption and cognitive risk. Neuropsychiatry Dis Treat 2011; 7:465-84. 14. I Diamond and R O Messing. Neurologic effects of alcoholism. West J Med.1994; 161(3): 279–287. 15. Savolainen VT, Liesto K, Männikkö A, Penttilä A, Karhunen PJ. Alcohol Consumption and Alcoholic Liver Disease: Evidence of a Threshold Level of Effects of Ethanol.Alcohol clin Exp Res.1993; 17(5):1112-7. 16. Mads Kamper-Jørgensen1, Morten Grønbæk1, Janne Tolstrup1, Ulrik Becker2.Alcohol and cirrhosis: dose –response or threshold effect? Journal of Hepatology. 2004; 41: 25-30. 17. Katherine M. Conigrave1, Peter Davies2, Paul Haber1 and John B. Whitfield3.Traditional markers of excessive alcohol uses. Addiction 2003:98 (Suppl. 2), 31–43. 18. Ewa Gruszewska, 1 Bogdan Cylwik,2 Anatol Panasiuk,3 Maciej Szmitkowski,1 Robert Flisiak,3 and Lech Chroste. Total and Free Serum Sialic Acid Concentration in Liver Diseases BioMed Research International 2014 (2014).5 pages. 19. Santhosh Kumar*1, K. Balu Mahendran 2, Mohammad Anwar 3, K.N. Kalaivanam 1, R. Bheemasen 1 and E. Gnana Desigan 4 Kumar et al .Role of Acute Phase Proteins Status in Chronic Alcoholic liver diseases. IJPSR 2013; 4(9): 3471-3476. 20. Cylwik B, Krawiec A, Chrostek L, Supronowicz Z, Szmitkowski M. The effect of chronic alcohol drinking on the total concentration of sialic acid and lipid-bound sialic acid. Pol Merkur Lekarski 2009; 27(158):101-4. 21. Dr. C. Selva Kumar *, R. Kalaivani. Study of Adenosine Deaminase and Serum Protein Bound Sialic Acid Levels in Alcoholic Liver Disease. Int J Biol Med Res. 2011; 2(3): 754-756. 22. Chrostek L1, Cylwik B, Szmitkowski M, Korcz W. The diagnostic accuracy of carbohydrate-deficient transferrin, sialic acid and commonly used markers of alcohol abuse during abstinence. Clin Chim Acta. 2006; 364(1-2):167-71. 23. N. Stefenelli, H. Klotz, A. Engel, P. Bauer. Serum sialic acid in malignant tumors, bacterial infections and chronic liver diseases. Journal of Cancer Research and Clinical Oncology1985; 109:55-59. 24. Arif, S., Najeeb-ul-Haq, Hanif, R., Khan, A.S., Jamil-ur-Rehman, Mufti, T.A.Variations of serum sialic acid level in liver cirrhosis Journal of Ayub Medical College, Abbottabad : JAMC. 2005; 17:54-57. 25. David Edwin, 1 Laura Flynn, 1 Andrew Klein,2 and paul J.Thuluvath 3 .Cognitive Impairment in Alcoholic and Nonalcoholic Cirrhotic Patients. Hepatology 1999; 30, No. 6. 26. Zhou H, Deng J, Li J, Wang Y, Zhang M, He H. Study of the relationship between cigarette smoking, alcohol drinking and cognitive impairment among elderly people in China. Age Ageing. 2003; 32(2):205-10. 27. Ka Kin King Chan1 et al. Association between alcohol consumption and cognitive impairment in Southern Chinese older adults. Int J Geriatr Psychiatry. 2010; 25(12):1272-9. 28. Edwin D, Flynn L, Klein A, et al. Cognitive impairment in alcoholic and nonalcoholic cirrhotic patients. Hepatology 1999; 30: 1363–7. 29. Tarter R E, Hegedus AM, VanThiel D H, et al. Hepatic dysfunction and neuropsychological test performance in alcoholics with cirrhosis. J Stud Alcohol 1986; 47: 74–7. 30. Tarter RE1, Arria AM, Van Thiel DH Hepatic encephalopathy coexistent with alcoholism Recent Dev Alcohol. 1991; 9:205-24. 31. Irwin M, Smith TL, Butters N, Brown S, Baird S, Grant I, Schuckit MA. Graded neuropsychological impairment and elevated gamma-glutamyl transferase in chronic alcoholic men. Alcohol Clin Exp Res. 1989 Feb; 13(1):99-103. 32. Wang B. Sialic acid is an essential nutrient for brain development and cognition. Annu Rev Nutr.2009; 29:177-222. 33. Lech Chrostek, Bogdan Cylwik, Agnieszka Krawiec, Walenty Korcz and Maciej Szmitkowski. Relationship between serum sialic acid and sialyted glycoproteins in alcoholics. Alcohol and Alcoholism 2007; 42(6):588-592. 34. Ewa Gruszewska, 1 Bogdan Cylwik, 2 Anatol Panasiuk, 3 Maciej Szmitkowski,1 Robert Flisiak,3 and Lech Chroste. Total and Free Serum Sialic Acid Concentration in Liver Diseases BioMed Research International 2014 (2014).5 pages
Relationship between acylated ghrelin and uric acid in prediabetic obese individuals
Ankita Sharma, G G Kaushik, Sonali Sharma, J S Broca
Objective: To evaluate acylated ghrelin and uric acid in prediabetic subjects and compare it with type 2 diabetics and healthy subjects and to examine the relationship between plasma acylated ghrelin and uric acid concentrations. Method: The study was conducted on 100 subjects: 50 subjects of prediabetes (Group - I) and 50 subjects of type 2 diabetes (Group - II). 50 healthy non-diabetic control subjects (Group-III) of same age of either sex were selected. All subjects with BMI > 30 kg/m2 were considered. Blood samples were analyzed for fasting blood glucose, insulin, HbA1c, uric acid and acylated ghrelin. Result: Acylated Ghrelin and uric acid increases in group -I when compared with group -III and decreases in group-II when compared to group –I. The strongest positive association of acylated ghrelin was observed between acylated ghrelin and Homa- β in prediabetic subjects while the strongest association of uric acid was observed between uric acid and acylated ghrelin in prediabetic subjects. Conclusion: Although the mean values of both acylated ghrelin and uric acid are high in prediabetic subjects as compared to obese control yet the mechanism related to prediabetes i.e. impaired insulin secretion has strong positive association with acylated ghrelin while it shows negative association with uric acid. Hence, acylated ghrelin and uric acid shows inverse relationship in prediabetic obese individuals.
1. Edmann J, Lipple F, Wagenpfeil S, et al: Differential association of basal and postprandial plasma ghrelin with leptin, insulin, and type 2 diabetes: Diabetes. 2005; 55:8–1371. 2. Dezaki K, Sone H, Yada T: Ghrelin is a physiological regulator of insulin release in pancreatic islets and glucose homeostasis:Pharmacol therapeutics. 2008; 118:239–249. 3. Al Massadi O, Tschöp MH, Tong J: Ghrelin acylation and metabolic control: Peptides. 2011; 32(11):8–2301. 4. Delhanty PJ, van der Lely AJ: Ghrelin and glucose homeostasis: Peptides. 2011; 32(11):18–2309. 5. Verhulst PJ, Depoortere I: Ghrelin's second life: from appetite stimulator to glucose regulator: World J Gastroenterol. 2012; 18(25):95–3183. 6. Gelling R, Overduin J, Morrison C, et al: Effect of uncontrolled diabetes on plasma ghrelin concentrations and ghrelin-induced feeding: Endocrinology. 2004; 145:82–4575. 7. Seppo M, Kellokoski M, Horkko S, et al: Low plasma ghrelin is associated with insulin resistance, hypertension, and the prevalence of type 2 Diabetes: Diabetes. 2003; 52:52–2546. 8. Wu J, Yan WH, Qiu L, Chen XQ, Guo XZ, Wu W, Xia LY, Qin XZ, Liu YH, Ding HT, et al: High prevalence of coexisting prehypertension and prediabetes among healthy adults in northern and northeastern China: BMC Publ Health. 2011; 11:794. 9. Vuorinen-Markkola H, Yki-Jarvinen H.: Hyperuricemia and insulin resistance: J Clin Endocrinol Metab. 1994; 78: 25–9. 10. C hen J, Wildman RP, Hamm LL, Muntner P, Reynolds K,Whelton PK et al.: Association between inflammation andinsulin resistance in U.S. nondiabetic adults. Results from the Third National Health and Nutrition Examination Survey: Diabetes Care. 2004; 27: 2960–5. 11. American Diabetes Association: Standards of medical care in diabetes—2014: Diabetes Care. 2014; 37(suppl 1):S14-S80. 12. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC.:Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man: Diabetologia. 1985; 28: 412–9. 13. Sharifi et al.: Acylated ghrelin and leptin concentrations in patients with type 2 diabetes mellitus, people with prediabetes and first degree relatives of patients with diabetes, a comparative study: Journal of Diabetes and Metabolic Disorders. 2013; 12:51. 14. L.Huang et al.: Increased acyl ghrelin but decreaded total ghrelin and unacyl ghrelin in Chinese Han people with impaired fasting glucose combined with impaired glucose tolerance :Peptides 2014;60:86-94. 15. H. K. Choi and E. S. Ford.: Haemoglobin A1c, fasting glucose, serum C peptide and insulin resistance in relation to serum uric acid levels—the Third National Health and Nutrition Examination Survey: Rheumatology. 2008; 47: 713–717. 16. Cook DG, Shaper AG, Thelle DS, Whitehead TP.: Serum uric acid, serum glucose and diabetes: relationships in a population study: Postgrad Med J. 1986; 62:1001–6. 17. Choi HK, Mount DB, Reginato AM. : Pathogenesis of gout: Ann Intern Med. 2005; 143:499–516. 18. Sudhindra Rao M. and Bino J.S.: A study of serum uric acid in diabetes mellitus and prediabetes in a south indian tertiary care hospital: NUJHS. June 2012; 2(2).
Study of biochemical parameters in beta thalassemia major patients
Vinita Belsare, Hrishikesh Belsare, Sandip Lambe
Children with thalassemia have various skeletal changes and effect on liver, lungs and kidneys. All these effect are due to ineffective erythropoiesis and hemochromatosis. All this leads to impairment of functions of various organs. The present study was conducted to assess the kidney functions with blood urea, serum creatinine, serum phosphates, serum sodium, serum potassium ,urinary total protein and urine specific gravity in children’s with beta thalassemia major.
1. Shinar E, Rachmilewitz EA: Oxidative denaturation of red blood cells in thalassemia Seminhematol 1990; 27: 70. 2. Weatherall DJ, Clegg JB: The thalassemia syndromes. 3rd ed. Blackwell Scientific Oxford, 1981. 3. Watanabe: Urinary protein as measured with a pyrogallol red molybdate complex, manually and in Hitachi 726 automated analyzer. Clin Chem 1986; 32:1551-54. 4. Teitz NW: Text Book of Clinical chemistry. W.B.Saunders Co 1986; 602-613. 5. Oktenli C, Bulucu F. Renal tubular dysfunction in a patient with beta thalassemia minor. Nephron 2002; 12:222-223. 6. Cetin T, Oktenli C, Ozgurtas T, Yenicesu M, Sanisoglu SY, Oguz Y, Yildiz O, Kurt I, Musabak U, Bulucu F, Kocar IH. Renal tubular dysfunction in beta- thalassemia minor. Am J Kidney Dis 2003 Dec. 42(6), 1164-8. 7. Aperia AC, Liebow AA, Roberts LE: Renal adaptation to anemia. Circ Res 1968; 22: 489-500. 8. Khalifa AS, Sheir S, El Magel LA, el Tayeb H, el Lamie C, Khalifa A, Mokhtar G: The kidney in Beta – Thalassemia Major: Acta haemat 1985; 74: 60. 9. Sumboonnanonda A, Malasit P, Tanphaichitr VS, Ong-ajyooth S, Sunthornchart S, Pattanakitsakul S, Petrarat S, Assateerawatt A, Vongjirad A. Renal tubular function in beta thalassemia. Pediatr Nephrol 1998 May: 12(4), 280-3. 10. Aldudak B, Karabay Bayazit A, Noyan A, Ozel A, Anarat A, Sasmaz I, Killinc Y, Gali E, Anarat R, Dikmen N: Renal function in pediatric patients with beta thalassemia major. Pediatr Nephrol 2000 Nov15; 15(1-2): 109-12. 11. Lapatsanis P, Sbyrakis S, Vertos C, Karaklis BA, Dosiadir S: Phosphaturia in thalassemia. Pediatrics 1976 Dec; 58(61), 885-92. 12. Lichtman AM, Miller DR, Cohen J, Waterhouse C: Reduced red cell glycoses, 2,3 diphosphoglycerate and adenosine tri phosphate concentration, and increased hemoglobin oxygen affinity caused by hypophosphatemia. Ann Inter Med 1971; 74: 562. 13. Jacob H, Amsden T: Acute hemolytic anemia with rigid red cells in hypophosphatemia. N Engl J Med 1971; 285: 1446. 14. Keitel HG, Thompson D, Itano HA: Hyposthenuria in sickle anemia A reversible renal defect. J Clin Invest 1956;35 15. Statius Van Eps LW, Schouten H, La Portiwusman LW, Struyker – Boudier AM: The influence of red blood cell transfusion on the hyposthenuria and renal hemodynamics of sickle cell anemia. Clin Chim Acta 1967; 17: 119-121. 16. Ong-ajyooth L, Malasit P, Ong-ajyooth S, Fucharoen S, Pootrakul P, Vasuvattakul S, Siritanaratkul N, Nilwarangkur S. Renal function in adult beta thalassemia / HBE disease. Nephron 1998; 78(2): 156-61. 17. Granner DK: Hormones that regulate calcium metabolism. In: Harpers Biochemistry. Murray RK, Granner DK, Mayes PA, Rodwell VW (eds). Lange Medical publications 25th edition 2002; 572-573. 18. Tenenehouse HS, Murer H: Disorders of renal tubular phosphate transport. J Am Soc Nephrol 2003; 14: 240-7. 19. Keitel HG, Thompson D, Itano HA: Hyposthenuria in sickle anemia A reversible renal defect. J Clin Invest 1956; 35. 20. Statius Van Eps LW, Schouten H, La Portiwusman LW, Struyker – Boudier AM: The influence of red blood cell transfusion on the hyposthenuria and renal hemodynamics of sickle cell anemia. Clin Chim Acta 1967; 17: 119-121. 21. Landing BH, Gonick HC, Nadorra RL, Hyman CB, Wells TR, Villarreal EG, Mersch J, Agness CL: Renal lesions and clinical findings in thalassemia major and other chronic anemias with hemosiderosis: Pediatr Pathol 1989; 9(5): 479-500. 22. Sonakul D, Pacharee P, Thakrenpol K: Pathologic findings in autopsy cases of thalassemia. Birth defect Orig Article 1988; 23: 157-156.
A statistical analysis of static water level trend and rainfall data in PTW-1watershed, Buldhana district, INDIA
P V Kathane, Suryakant M Patil, K R Aher
Groundwater is a dynamic resource and it varies from place to place quantativaly and qualitatively. Its quantity is mostly depends on the rainfall data of that particular region, Geological terrain, Rock type i.e. Aquifer, Geomorphology and drainage pattern. In India especially in Maharashtra state drinking and irrigation water demand is rapidly increases last few years, to cope up this problem, it is necessary to evaluate the existing trend and availability of groundwater in time and space for proper planning in near future. Pre and post monsoon ground water record and its trend, rainfall pattern, and geological especially hydrological study is very useful technique for judicious future planning of groundwater utilization. Proper utilization of available surface water and Ground water quantity it is necessary to manage the watershed concept. For this manners, this paper discuss to analyze the long term (2002-2012) trend of pre- and post-monsoon water level of watershed PTW-1 of Malkapur and Motala Taluka of Buldhana district first time. Trend of Pre and Post Monsoon static Ground water level indicate that there is depletion of static ground water level with the passage of time.
1. Agashe R. M.. Hydrology of Maharashtra, Central Groundwater Board, Central region, Nagpur. 1994. 2. CGWB,Ground water information Buldhana district Maharashtra, ministry of water resources Central Ground Water Board, Central Region Nagpur, Government of India, Technival Report, 1565/OTH/2007,pp1-25. 3. Deshpande, S.M. and Aher, K.R., Quality of Groundwater from Tribakeswar-Peth area of Nashik District and its Suitability for Domestic and Irrigation Purpose, Gond. Geol. Mag.2011, v.26 (2), pp.157-162. 4. GSI Central Region, Buldhana District Resource Map, Buldhana District, Maharashtra 1990. 5. Jangle,P.P., The study of Hydro geomorphologic features in Buldhana district using IRS DATA, International research journal Shodh, Samiksha and Mulyakan,2010,V(2),14. 6. Patrikar G.M., Mitkari A.M. and Deshpande A.M., Unpublished Systematic hydrogeological survey report, GSDA, Maharashtra, 1987. 7. Purushtotham, D., Rao, A.N., Ravi Prakash, M., Shakeel Ahmed and G. Ashok Babu Environmental impact on groundwater of Maheshwaram watershed, Ranga Reddy district, Andhra Pradesh, Jour. Geol. Soc. India, 2011, v.77, pp 539-546. 8. RWSD, Annual Scarcity Report of Rural Water supply Department Dist Buldhana (2002 – 2012).
Pericolic abscess due to large bowel perforation by fish bone – a case report
Vijay Kalimuthu, Jawahar Krishnaswamy, Anitha Samraj, Ravishankar Jayavelu
A diagnosis of large-bowel perforation, caused by a sharp or pointed foreign body, is rarely made preoperatively because the clinical symptoms are usually nonspecific and can mimic other surgical conditions, such as appendicitis and diverticulitis. Less than 1% of ingested foreign body results in perforation from mouth to anus mostly by sharp objects. Of these sharp objects, chicken bone and fishbone account for half of the reported perforations. The most common sites are the ileo-caecal junction and sigmoid colon. In our case the patient presented late with pericolic abscess following the perforation by a fish bone in proximal ascending colon and the fish bone found extramurally making it as first case for that site of large bowel perforation by a fish bone with localized late presentation.
1. Hsu SD, Chan DC, Liu YC. Small-bowel perforation caused by fish bone. World J Gastroenterol 2005; 11(12): 1884-1885 2. Arif HS, Hakim IS, Asim MP, Fazl QP, Rubina L, Khurshid AW. Gastro Intestinal tract perforations due to ingested foreign bodies; a review of 21 cases. BJMP 2012;5(3):a529 3. Pinero MA, Fernandez Hernandez JA, Carrasco PM, Riquelme RJ, Parrilla PP. Intestinal perforation by foreign bodies. Eur J Surg 2000; 166: 307–309 4. Chu KM, Choi HK, Tuen HH, Law SYK, Branicki FJ, Wong J. A prospective randomized trial comparing the use of the flexible gastroscope versus the bronchoscope in the management of foreign body ingestion. Gastrointest Endosc 1998; 47:23–27 5. Chang JJ, Yen CL. Endoscopic retrieval of multiple fragmented gastric bamboo chopsticks by using a flexible overtube. World J Gastroenterol 2004; 10: 769–770 6. Webb WA. Management of foreign bodies of the upper gastrointestinal tract. Gastroenterology 1988; 94: 204-216 7. Hunter TB, Taljanovic MS. Foreign bodies. Radiographics. 2003 May Jun;23(3):731–57. 8. Eisen GM, Baron TH, Dominitz JA, et al. Guideline for the management of ingested foreign bodies. Gastrointestinal Endosc. 2002:55:802–6. 9. Stack LB, Munter DW. Foreign bodies in the gastrointestinal tract. Emerg Med Clin North Am. 1996 Aug; 14(3):493–521. 10. Eftaiha M, Hambrick E, Abcarian H. Principles of management of colorectal foreign bodies. Arch Surg. 1977:112:691–5. 11. Puia I.C, Puia V.R, Andreescu A, Cristea P.G. Ascending colon perforation by ingested fruit stones. Chirurgia (Bucur) 2011; 106(6):825-827. 12. Chiru J.J, Chen T.L, Zhan Y.L. Perforation of the transverse colon by a fish bone: case report. J Emerg Med 2009; 36(4):345-347. 13. Joglekar S, Rajput I, Kamat Sachin, Downey S. Sigmoid perforation caused by an ingested chicken bone presenting as right iliac fossa pain mimicking appendicitis: a case report. J Med Case Rep. 2009; 3:7385. 14. Ali F.E, Al-Busairi W.A, Esbaita E.Y, Al-Bustan M.A. Chronic perforation of the sigmoid colon by foreign body. Curr Surg. 2005; 62(4):419-422. 15. Ben Rejeb A, Gammoudi A, Ben Alaya M. Intestinal Perforation by Fish Bone. Apropos of a Case and Review of the Literature. Ann Chir 1993; 47(1): 86-70. (Abstract). 16. Chuvilkin AV. Case of Large Bowel Perforation by a Fish Bone. Wiad L ek 1973; 26(8): 761-3. 17. Chen CK, Su YJ, Lai YC, et al. Fish Bone-Related Intra-Abdominal Abscess in An Elderly Patient. Int J Infect Dis 2010; 14(2): e171-2.