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Articles by A Aravindan
Total Records ( 3 ) for A Aravindan
  B Asthana , P Sharma , R Ranjan , P Jain , A Aravindan , P Chandra Mishra and R. Saxena

Bleeding disorders constitute a large proportion of referrals to hematology departments. Worldwide, acquired causes of bleeding are commoner than inherited ones. To identify the spectrum of these disorders, we evaluated all referrals for bleeding encountered in this tertiary care centre over a one-year period. Of the total 1342 cases, 1040 (77.5%) had underlying exclusively acquired causes, whereas inherited causes constituted 302 cases (22.5%). Amongst acquired causes, disseminated intravascular coagulation was seen in 297 (28.6%), hepatic coagulopathy in 218 (20.9%), neurosurgical causes (intracranial bleeds) in 154 (14.8%), malignancy in 89 (8.6%), and miscellaneous multiple acquired causes including those due to anticoagulant drug overdose in 282 patients (27.1%). Referrals for isolated prolonged prothrombin time or thrombocytopenia were common, but were excluded from this study because not all presented with bleeding. Prompt laboratory work-up and precise identification of acquired causes of bleeding is the key to planning appropriate patient management including transfusion support.

  A Aravindan , J Yong , M Killingsworth , M Suranyi and J. Wong

Interferon beta is widely used for the treatment of relapsing and remitting multiple sclerosis. Renal side effects including nephrotic syndrome have been increasingly described with interferon beta treatment. We describe an illustrative case of a patient who developed severe nephrotic syndrome due to minimal change disease in association with interferon beta therapy and showed partial remission following cessation of interferon beta and treatment with cortico- steroids.

  A Aravindan , J Yong , M Killingsworth , S Strasser and M. Suranyi

Hepatitis B viral infection is usually a self-limiting disease in immunocompetent individuals. Chronic infection can be seen in up to 5% of infected patients. Renal manifestations of chronic HBV infection are usually glomerular. We describe here an uncommon presentation of a patient with chronic HBV infection with very high viral load and rapidly progressive renal failure. Renal biopsy showed features of tubulointerstitial nephritis and tubular epithelial inclusion bodies suggestive of HBV infection. Entecavir treatment slowed down the progression of his renal disease. Tubulointerstitial nephritis should be considered as a part of the differential diagnosis in patients with HBV infection. Early antiviral treatment may halt the progression of renal disease.

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