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Indian Journal of Medical Sciences, Vol. 59, No. 3, March, 2005, pp. 113-115 Case Report Acute viral E hepatitis with chronic liver disease (Autoimmune hepatitis) Desai H.G., Naik A.S. Gastroenterology, Jaslok Hospital & Research Center, Dr. G. Deshmukh Marg, Mumbai - 400 026 Code Number: ms05017 ABSTRACT A 36 years old male presented with anorexia, jaundice and ascites. He was suffering from acute viral E hepatitis. In view of ascites, he was investigated for associated asymptomatic chronic liver disease (CLD). The CLD was diagnosed as cirrhosis with autoimmune hepatitis and was treated with steroid with good response. He is maintaining good health with low dose steroid, on follow up for 1 year.KEYWORDS: Hepatitis E, chronic liver disease, autoimmune hepatitis INTRODUCTION In developing countries, faeco-orally transmitted virus infection, hepatitis A virus (HAV) or hepatitis E virus (HEV), is not uncommon below and above the age of 20 years respectively. Chronic liver disease (CLD) of hereditary etiology like Wilson′s disease or due to parenterally transmitted viruses hepatitis B virus (HBV) and hepatitis C virus (HCV), usually occurs below and above the age of 20 years respectively. A combination of acute HAV hepatitis with asymptomatic Wilson′s disease or acute HEV hepatitis with HBV or HCV asymptomatic cirrhosis is not uncommon in developing countries, below and above the age of 20 years respectively.[1],[2],[3],[4],[5] This case report from India describes the still rare occurrence of acute viral E hepatitis in a male patient with asymptomatic CLD, due to autoimmune hepatitis.CASE REPORT Thirty-six-years-old male was admitted in June 2001 with history of anorexia, nausea and jaundice of 6 weeks duration; ascites was noted 3 weeks after the onset of jaundice. On examination he had icterus, two finger palpable firm liver and moderate ascites.Laboratory findings were: Haemoglobin 11.5g%, WBC 3910, platelet count 2.19000, ESR 46(0-15), total bilirubin 23.1 mg%, direct 18.2 mg% SGPT : 452, SGOT : 280, alkaline phosphatase 276 U/L (normal 30-150U/L), Total protein 7.5 g%, serum albumin 3.1 g%, gamma globulin 2.7 g% (0.7-1.7 g%), PT 50 sec (control 16 sec). APTT 54 seconds (control 30 sec), HbsAg and Anti-HCV : negative. serum ceruloplasmin. 0.23 OD (normal: 0.2-0.5 OD) serum copper : 83 ug (75-160), 24 hour urinary copper excretion 625 ug/day (0-75). KF ring was absent. IgM Anti-HEV (ELISA) and smooth muscle antibody were positive. Ultra-sonography showed hepatosplenomegaly and ascites. Oesophagogastroscopy showed grade II varices. Isotope liver-spleen scan showed enlarged hot spleen suggestive of CLD. Liver biopsy was not done because of grossly abnormal PT and PTT. A diagnosis of acute HEV infection on an underlying CLD due to autoimmune hepatitis was made. The patient was started on 30mg prednisolone per day. He showed a good clinical and biochemical response to steroid therapy; azathioprine was later added to reduce maintenance dose of steroid. The bilirubin reduced to 1.1 mg%, SGPT 37 and SGOT 26, after 12 weeks of therapy. DISCUSSION Our patient had an asymptomatic CLD is suggested by presence of a firm liver, ascites, low albumin, raised gamma globulin, enlarged hot spleen on liver-spleen isotope scan and Grade II oesophageal varices on upper GI scopy. Markedly raised gamma globulin with a positive SMA, together with an immediate clinical and biochemical response to steroid therapy, indicated auto-immune hepatitis as a cause of CLD.The onset of sudden anorexia, nausea, with moderately raised transaminases together with IgM anti HEV positive test indicated acute viral E hepatitis. The patient was hence diagnosed as acute viral E hepatitis with CLD due to autoimmune hepatitis. Ascites was controlled with salt restriction and diuretic therapy (Spironolactone + Frusemide). Patient was started on prednisolone 30 mg / day which was gradually reduced; azathioprine was added to reduce the maintenance dose of steroid. The serum bilirubin, SGOT, SGPT and alkaline phosphatase gradually reduced to normal values and albumin increased to 4.0 g% in next 16 weeks. Patient is now asymptomatic on maintainence dose of 5 mg prednisolone and 50 mg azathioprine. In developing countries, a combination of acute viral hepatitis (HAV or HEV) on an asymptomatic CLD due to Wilson′s disease HBV, HCV, or autoimmune hepatitis (as in our patient) is likely to be misdiagnosed as subacute hepatic failure, in the absence of inadequate investigations.[6],[7],[8] A high degree of clinical suspicion of treatable CLD (Wilson′s disease or antoimmune hepatitis) in an asymptomatic stage, associated with acute viral hepatitis (HAV or HEV), could dramatically improve the prognosis of the patient (as observed in our patient). References
Copyright 2005 - Indian Journal of Medical Sciences |
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