Our Current Issues

Background: AIS is an X-linked recessive disorder with an incidence of 1:20,000-64,000 male births. Point mutations in the androgen receptor gene are the most common cause of AIS. Patients most often present in late adolescence with primary amenorrhoea or infertility with labial or inguinal swellings. Case Presentation: A 30 years married lady presented to surgery OPD with complains of swelling in left groin for last four years. There was no pain at site and no history of obstruction. By history, she had not attended menarche and had no issues. USG showed an oval hypoechoic mass in left inguinal canal. Androgen Insensitivity Syndrome (AIS) is a DSD characterised by a problem with the androgen receptor (AR)3. AR gene is expressed in male embryos from 8 weeks of gestation. The condition is caused by a defect in androgenreceptors, which causes end-organ resistance to androgens. Vagina is a small tube that originates from the urogenital sinus and terminates blindly. Common associated genitalia abnormalities are hypospadias, micropenis, bifid scrotum and bilateral cryptorchidism. Androgen insensitivity syndrome has a low medical morbidity and mortality rate, whether it is complete or partial. Conclusion: AIS should be suspected when one encounters phenotypic female with primary amenorrhoea and inguinal or labial swelling. Such patients should be thoroughly evaluated clinically and radiologically. A diagnosis of AIS is established after correlating the clinical and radiological findings with histopathological features.

1. Tarafdar RunaLaila, Sheikh Salahuddin Ahmed. Androgen Insensitivity Syndrome- A Case Report. American Journal of Clinical and Experimental Medicine. Vol. 3, No. 4, 2015, pp. 133-136. doi: 10.11648/j.ajcem.20150304.11. 2. Nitsche EM, Hiort O. The molecular basis of androgen insensitivity. Horm Res 2000; 54:327-33. 3. Khan S, Craig LB (2013) A Review of Radiologic Im¬aging in Patients with Androgen Insensitivity. J GenitSystDisor S1.S1-003. 4. T Kemp. Three siblings with complete androgen in¬sensitivity syndrome. Journal of Endocrinology, Me¬tabolism and Diabetes of South Africa. Available from: http://cogentoa.tandfonline.com/loi/oemd20. 5. Pizzo A, Laganà AS, Borrielli I, DugoN. Complete an¬drogen insensitivity syndrome: a rare case of disorder of sex development. Case Rep Obstet Gynecol. 2013; 2013:232696. 6. Gottlieb B, Beitel LK, Lumbroso R, et al.: Update of the androgen receptorgene mutations database. Hum Mutat 14:103–114, 1999. 7. MandepudiGeethika, K. Mounika Reddy, K. Venkat Ramreddy, R.S.N. Moorthy. Complete Androgen Insen¬sitivity Syndrome in an Adult - A Rare Entity. International Journal of Contemporary Medical Research 2016; 3(4):1016-1018. 8. Deans R, Creighton SM, Liao LM, Conway GS. Timing of gonadectomy in adult women with complete androgeninsensitivity syndrome (CAIS): patient preferences and clinicalevidence. ClinEndocrinol (Oxf) 2012;76(6):894.

Background: A polyp is a grossly visible tumorous mass that protrudes from the mucosa or submucosa towards the lumen of the gut and is classified as neoplastic or non-neoplastic polyps. Polyps need to be excised upon detection during colonoscopy due to the risk of malignancy, irrespective of their size. Polyps that develop through the ‘adenoma–carcinoma pathway’ are considered neoplastic and may progress to invasive carcinoma; detection and removal decrease the morbidity and mortality. It is critical to diagnose and remove colorectal polyps as soon as they are discovered. Aims and objectives: To study incidence of colorectal polyps, age, sex wise and classification. Material and Methods: Observational and retrospective assessments of pathology reports for 8 years were analysed. Results: Incidences of colorectal polyp cases are in the ratio of 1:7536. This means that colorectal polyps are the rarest entity. 66.7% are in the neoplastic category of polyps. All cases are in the age range of 2–11 years of age. The maximum cases are in the age range of 6–10 years. The male to female gender ratio is 1:1. All cases were presented as bleeding per rectum. Results: All cases are in the paediatric age group. Juvenile polyps are the most common tumours in the colorectal region. In the present study, the maximum cases are in the 6–10 year age group, while in the Iranian study, the maximum cases are less than 6 years of age. The male to female ratio was 1.61:1.0 in the Iranian study, while the present Indian study shows 1:1. Conclusion: Polyps must be removed even if asymptomatic because of their probable neoplastic potential.

1. Ashtiani MTH, Monazemzadeh M, Farzaneh M, Tabriz HM, Mahjoub F, Karamian H, Sani MN, Khatami GR, Khodadad A, Farahmand F, Fallahi GH. Colorectal polyps: A clinical endoscopic and pathologic study in Iranian children Med Princ Pract 2009; 18:53-56.doi 10.1159/000163047. 2. Bas B, Dinc B, Oymaci E, Mayir B, Gunduz UR. What are the endoscopic and pathological characteristics of colorectal polyps? Asian Pac J Cancer Prev, 16(13), 5163-5167.doi: http://dx.doi.org/10.7314/APJCP.2015.16.13.5163. 3. Eshghi MJ, Fatemi R, Hashemi A,Aldulaimi D,Khodadoostan M. A retrospective study of patients with colorectal polyps: Gastroenterol Hepatol Bed Bench.2011; 4(1):17-22. 4. Jelsig AM.Hamartomatous polyps – A clinical and molecular genetic study: Dan Med J 2016; 63(8):B5280 (PhD thesis), 1-21. 5. Katsanos K, Rogalidou, M Siamopoulou, A and Tsianos, E (2011). Juvenile polyp presenting with rectal bleeding in a 2-year-old girl.Annals Of Gastroenterology, 24(1), 67.Retrieved from http://annalsgastro.gr/index.php/annalsgastro/article/view/898/650.

Background: Soft tissue tumours can occur at all ages at various sites in the body. There is a wide spectrum of benign and malignant tumours of soft tissue origin, though some are known to occur more frequently in childhood and some in the elderly. Aim of the study: to research the histomorphology of soft tissue cancers. Materials and Methods: Both prospective and retrospective research were conducted in the pathology department of Mallareddy Medical College for Women in Hyderabad, Telangana. 150 cases in total were examined for histopathology. Results: The total number of cases was 150. The age range was from 4 to 78 years. The majority of 70 (46.6%) were among those aged 31–40, followed by those aged 21–30, which showed 31 (20.6%) cases. Male patients were 80 (53.3%) and female patients were 70 (46.6%). Out! There were 120 cases (80%) of benign tumours and 30 cases (20.0%) were malignant tumors. Lipoma was the most common among benign soft tissue tumours, 69 (57.5%), and the next common was Hemangioma, 20 (16.6%). Among malignant tumours, 8 (26.6 %) cases were synovial sarcoma and 4 (13.3%) were fibrosacrcoma. Conclusion: Soft tissue tumours are more common in the fourth decade of life and have a slight male preponderance. The most common site for these tumours is the back region. Benign tumours are more common than malignant tumors, and those of intermediate malignancy are very rare. Among the benign tumours, lipoma and hamangioma are the most common, whereas among the malignant group, synovial sarcoma and liposarcomas are the most common.

1. Jain P, Shrivastava A, MallikR. Clinicomorphological Assessment of Soft Tissue Tumors.Sch J App Med Sci 2014; 2(2D):886-90. 2. Hassawi BA, Suliman AY, HasanIS.Soft tissue tumours – Histopathological study of 93 cases. Ann Coll Med Mosul 2010; 36 (1 and 2): 92-8. 3. Lavelle, S.M., PW Walton and Maura MhicLomhair: Effect of irradiation, asbestos and chemical carcinogenesis on incidence of sarcomas on implant. Technology and Health Care2004;12:217-223. 4. Sajjad M, Ahmad F, Khan ZA, Shah H. Histopathological pattern of soft tissues tumors and tumour like lesions in the pathology department of lady reading hospital Peshawar, Pakistan Medical College. J Ayub Med Coll Abbottabad 2016;28(3). 5. VahiniA Clinicopathological Study of Soft Tissue Tumours in Correlation with Immunohistochemistry. Journal of Dental and Medical Sciences 2015;14(1). 6. Harpal S, Richika, Ramesh K. Histopathological Pattern of Soft Tissue Tumours in 200 Cases. Annals of International Medical and Dental Research 2(6):6. 7. Natrajan. WL. Adult soft tissue sarcomas a pattern of case surgery of American college of surgeons. Ann. Sur 1987; 205:349. 8. Rosenberg A. In, Pathologic basis of disease, Soft tisuuetumors and tumor like lesions. Cotran, Kumar, Collins. WB Suanders Company, 6thed, Philadelphia, Pg 1259. 9. Gogoi G, Borgohain M, Saikia P, Patel B, Hazarika RK. Histomorphological Study of Soft Tissue Tumors and Review of Literature of Rarer Types.IntClinPathol J 2017; 4(6): 00113. 10. Umarani MK, Lakra PS, Bharathi M. Histopathological Spectrum of Soft Tissue Tumors in a Teaching Hospital IOSR Journal of Dental and Medical Sciences 2015;14(4):74-80. 11. Sharma BK, Singh UR. A Study of Different Patterns in Soft Tissue Tumors.Indian Journal of Pathology and Oncology 2016;3(1);23-25. 12. Chakrabarti PR, Chakrabarti S, Pandit A, Agrawal P, Dosi S, Jain MR. Histopathological study of soft tissue tumors: A three year experience in tertiary care centre. Indian Journal of Pathology and Oncology 2015; 2(3); 141-149.

Background: Systemic lupus erythematosus is a multi-systemic disorder which commonly affects the kidneys and remains the most dangerous life threatening complication. Renal manifestations are highly variable and patients present with a wide range of symptoms, ranging from asymptomatic proteinuria to renal insufficiency, which ends up on dialysis. Objective: To correlate the clinical, laboratory and histopathological findings in patients with different classes of lupus nephritis according to the WHO and the ISN/ RPS 2003 classifications. Materials and Methods: Patients from the Nephrology department, Government Medical College, Kottayam with a diagnosis of suspected Lupus Nephritis were detected on clinical and laboratory examinations. The study was an observational study conducted in the departments of Nephrology and Pathology, Medical College Hospital- Kottayam from 2010 to 2012. All diagnosed cases of Lupus Nephritis were included, while pregnant women with coagulopathy and those who were not willing to participate were excluded from the study. Results: The most common clinical symptom in these patients was Edema (67%) followed by Hematuria(51%). The mean systolic blood pressure (SBP) was highest for class IV+V (146.36 mm Hg), followed by class IV (140.63 mm Hg), with other classes (III,III+V,V,VI) having significantly lower SBP (128.10 mm Hg). The mean diastolic blood pressure (DBP) was highest for classes IV+V (87.5 mmHg). The mean serum creatinine levels were highest for class IV (1.88 mg/dl) followed by class IV+V (1.27 mg/ dl). The mean proteinuria for different classes was as follows: Class IV+V has the highest (5.10g/d).The mean activity indices of different classes of LN were assessed and found to be highest for class IV+V (8.68), followed by class IV (8.36). The mean chronicity indices of different classes of LN were assessed and found to be highest for class IV(1.16), followed by class IV +V(1.10). Conclusion: There was a strong positive correlation between clinical features as measured by proteinuria, systolic blood pressure, and histological findings in proliferative glomerulonephritis. Despite the positive results above, there was no strict correlation between the clinicobiological manifestations and the histological type of LN. This means that the clinical and biological picture can't be used to predict how bad the damage is.

1. Danchenko N, Satia JA, Anthony MS. Epidemiology of systemiclupus erythematosus: a comparison of worldwide diseaseburden. Lupus. 2006;15:308e318. 2. Bastian HM, Roseman JM, McGwin Jr G, et al. Systemic lupuserythematosus in three ethnic groups. XII. Risk factors forlupus nephritis after diagnosis. Lupus. 2002;11:152e160. 3. Singh S, Devidayal, Minz R, Nada R, Joshi K. Childhood lupusnephritis: 12 years experience from North India. Rhematol Int.2006;26:604e607. 4. Chakrabarti S, Ghosh AK, Bose J, De PK, Das K.Clinicopathologic study of lupus nephritis. J Indian Med Assoc.1998;96:268e271. 5. D. A. Charney, G. Nassar, L. Truong, and T. Nadasdy, “‘Pauciimmune’proliferative and necrotizing glomerulonephritis withthrombotic microangiopathy in patients with systemic lupuserythematosus and lupus-like syndrome,”TheAmerican Journalof Kidney Diseases, vol. 35, no. 6, pp. 1193–1206, 2000. 6. Manzi SM, Stark VE, Ramsey-Goldman R. Systemic lupus erythematosus: Epidemiology and classification of systemic lupus erythematosus. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt M,Weisman M., editors. Rheumatology. 3rd ed. St. Louis: CV Mosby; 2003. p. 1291-6. 7. Uramoto KM, Michet CJ Jr, Thumboo J, Sunku J, O’Fallon WM, Gabriel SE. Trends in the incidence and mortality of systemic lupus erythematosus, 1950-1992. Arthritis Rheum 1999;42(1):46-50. 8. Kumar A, Malaviya AN, Singh RR, Singh YN, Adya CM, Kakkar R. Survival in patients with systemic lupus erythematosus in India. Rheumatol Int 1992;12(3):107-9. 9. A. Fayaz, Y. Pirson, J. P. Cosyns, J. Yango, and M. Lambert, “Pauci-immune necrotizing and crescentic glomerulonephritis in a patient with systemic lupus erythematosus,” Clinical Nephrology, vol. 69, no. 4, pp. 290–293, 2008. 10. J. Weening, V. D. D'Agati, M. M. Schwartz et al., “The classification of glomerulonephritis in systemic lupus ereythematosus revisited,” Kidney International, vol. 65, pp. 521–530, 2004. 11. M. C. Hochberg, “Updating the American college of rheumatology revised criteria for the classification of systemic lupus erythematosus,” Arthritis and Rheumatism, vol. 40, no. 9, article 1725, 1997. 12. Andreea Munteanu, A. Caraba, Alina Pacurari, I. Romosan et al LupusNephritis: Correlation Of Clinicobiological Manifestation With HistologicalType Vol. XVII, Issue 1/2012. 13. Akbar Rajaee, Saeid Behzadi, Shabnam Bazmi, Morvarid Moayeri. TheClinical and Pathological Findings Among Patients with Lupus Nephritis inShiraz,Southern Iran. 14. Faurschou M, Dreyer L, Kamper AL, Starklint H, Jacobsen S. Long-term mortality and renal outcome in a cohort of 100 patients with lupus nephritis. Arthritis Care Res (Hoboken) 2010;62:873-80. 15. Singh S, Zhou XJ, Ahn C, Saxena R. A retrospective analysis of clinical presentation of lupus nephritis. Am J Med Sci 2011;342:467-73. 16. Mitjavila F, Pac V, Moga I, Poveda R, Vidaller A, Carrera M, Pujol RClinicopathological correlations and prognostic factors in lupus nephritis. 17. W. D. Bates, A.-M. Halland, R. D. Tribe, D. J. Rossouw Lupus NephritisPart I. Histopathological Classification, Activity And Chr~Nicity Scores S AirMed J 1991; 79: 256-259. 18. Stephen M. Korbet, MD, Edmund J. Lewis, MD, Melvin M. Schwartz, MD,Morris Reichlin, MD,Joni Evans, MS, and Richard D. Rohde, BS.FactorsPredictive of Outcome in Severe Lupus Nephritis. 19. Baldwin DS, Lowenstein J, Rothfield NF, Gallo G, McCluskey RT (1970).The clinical course of the proliferative and membranous forms of lupusnephritis. Ann Intern Med 73: 929-942.

Background: Plasmapheresis, sometimes referred to as a therapeutic plasma exchange (TPE), is an extracorporeal technique that uses blood separation technology to remove certain plasma components that are toxic or blood cells from an organism. Therapeutic plasma exchange (PE) or plasmapheresis is the preferred treatment for a number of neurological and other disorders. even though it is secure in their hands. Aim: To examine the outcomes of plasmapheresis implementation at the Department of Immunohematology and Blood Transfusion, B.J. Medical College, Ahmedabad, Gujarat, India. Materials and Methods: A prospective evaluation of PE operations was carried out in a teaching hospital for tertiary care in west India over a six-month period from June to December 2016. All of the indications, clinical results, and technical factors are reviewed. Result: The main indication for PE was GBS (214 patients; 86.6%). The mean age of patients ranged from 7–71 years (mean =39 years). The most common complications were allergies with urticaria, fever with chills, thrombophlebitis, abdominal pain, etc. There was no mortality. Conclusion: The analysis of 247 cases of PE done in our department shows that the procedure is safe, with only minimal procedure-related complications and no mortality.

1.Woźniak K, Urbanowska E, Snarski E. Plasmapheresis in haematology. Wiad Lek. 2015; 68(2): 173-8. 2.Kes P. Indikacije. In: Kes P. Kontinuirano nadomještanje bubrežne funkcije. Hospal, Zagreb, 2002: 18-24. 3.Weinstein R. Therapeutic apheresis in neurological disorders. J Clin Apher 2000; 15:74-128. 4.Clark WF, Rock GA, Buskard N, Shumak KH, LeBlond P, Anderson D, et al. Therapeutic plasmma exchange: an update from the Canadian Apheresis Group. Ann Intern Med. 1999; 131:453–62. [PubMed]. 5.Korach JM, Berger P, Giraud C, Le Perff-Desman C, Chillet P. Role of replacement fluids in the immediate complications of plasma exchange. French Registry Cooperative Group. Intensive Care Med 1998; 24:452-8. 6.Shaz BH, Linenberger ML, Bandarenko N, Winters JL, Kim HC, Marques MB, et al. Category IV indications for therapeutic apheresis: ASFA fourth special issue. J Clin Apher. 2007; 22:176. [PubMed]. 7.Mian AN, Mendley SR. Acute dialysis in children. In: Henrich WL, editor. Principle and Practice of Dialysis. 3rd ed. Vol. 617. Philadelphia: Lippincott; 2004. p. 28. 8.Shariatmadar S, Nassiri M, Vincek V. Effect of plasma exchange on cytokines measured by multianalyte bead array in thrombotic thrombocytopenic purpura. Am J Haematol 2005; 79:83-8. 9.Couriel D, Weistein R. Complications of therapeutic plasma exchange: Recent assessment. J Clin Apher 1994; 9:1-5. 10.Mokryzicki MH, Kaplan AA. Therapeutic plasma exchange: Complications and management. Am J Kidney Dis 1994; 23: 817-27. 11.Bouget J, Chevret S, Chastang C, Raphael JC. Plasma exchange morbidity in GBS: Results from the French prospective, randomised, multicentre study. French Cooperative Group. Crit Care Med 1993; 21:651-8. 12.Hartung HP, Willison HJ, Keiseier BC. Acute immunoinflammatory neuropathy: Update on Guillain-Barre syndrome. Curr Opin Neurol 2002; 15:571-7. 13.Van der Meche FG, Schmitz PI. A randomised trial comparing intravenous immunoglobulin and plasma exchange in Guillain-Barre Syndrome. Dutch Guillain Barre Study Group. N Engl J Med 1992;326:1123-9. 14.Randomised Trial of Plasma exchange, Intravenous Immunoglobulin and Combined treatments in GuillainBarre Syndrome. Plasma exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group. Lancet 1997; 349:225-30. 15.Cortese I, Chaudhry V, So YT, Cantor F, Cornblath DR, Rae-Grant A. Evidence-based guideline update: Plasmapheresis in neurologic disorders: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2011;76:294-300. 16.Wong EC, Balogun RA. Therapeutic apheresis in pediatrics: Technique adjustments, indications and nonindications, a plasma exchange focus. J Clin Apher 2012; 27:132-7. 17.Basic-Jukic N, Brunetta B, Kes P. Plasma exchange in elderly patients. Ther Apher Dial 2010; 14:161-5.