Pleural effusion associated with acute hepatitis A infection.

Abstract

To The Editors: Alhan et al.1 in the December, 1999, issue of the Pediatric Infectious Disease Journal® report on pleural effusion during acute hepatitis A infection in children. Pleural effusion is a rare and benign complication of hepatitis A, and its appearance does not seem to correlate with seriousness of illness in children.1, 2 In all published pediatric cases with exception of case presented by Willner et al.3 in which pleural effusion was accompanied by pericarditis, pleurisy associated with hepatitis A resolved spontaneously.1, 2 All children with effusions had good outcome of hepatic illness.1–3 We present a case of severe hepatitis A complicated by pleural effusion and resulting in death in a 3-year-old boy. A 3-year-old boy, refugee from Kosovo, was admitted to the Department of Pediatric Infectious Diseases at Zagreb with a 2-day history of fever, vomiting and jaundice. His past medical history was unremarkable. On physical examination the patient was febrile (38.5°C) and icteric. His vital signs were normal. There was a dullness to percussion at the base of the right lung and hepatomegaly 4 cm below the costal margin. Thorax ultrasound revealed a pleural effusion in the right chest. Abdominal ultrasonography yielded normal findings except hepatomegaly. Blood chemistry studies yielded the following: total bilirubin, 52.9 μmol/l; direct bilirubin, 44.5 μmol/l; alanine aminotransferase (ALT), 1430 units/l; aspartate aminotransferase (AST), 1190 units/l; gamma-glutamyltransferase, 80 units/l; alkaline phosphatase, 667 units/l. Total protein was 73 g/l and albumin was 40 g/l. Prothrombin time was 19.1 s. Thoracocentesis yielded pleural fluid with no cells and with biochemical characteristics of transudate. Bacteriologic culture of pleural fluid remained sterile. The patient was strongly positive for hepatitis A virus IgM antibody in serum and pleural fluid. All other viral markers (hepatitis B, hepatitis C, hepatitis E, Epstein-Barr virus, cytomegalovirus and human herpesvirus 6) were negative. Erythrocyte sedimentation rate was 12 mm/h and all other hematologic and biochemical variables were normal. Seven days after admission liver function tests were more impaired: total bilirubin, 198.1 μmol/l, ALT 1790 units/l, AST 3290 units/l. Prothrombin time was 27.9 s. Although liver disease worsened, thorax ultrasonography revealed total resolution of the pleural effusion. Two weeks after admission the patient went into a coma caused by fulminant hepatic failure, resulting in death from refractory increased intracranial pressure. Discussion. We present a patient with acute hepatitis A who developed pleural effusion early in the course of illness. Like patients reported by Alhan et al.,1 there was no evidence of other serous membrane or glomerular involvement, thus suggesting parainflammatory effusion. The most interesting event in our patient is spontaneous resolution of effusion, despite progression of the liver disease, which resulted in fulminant hepatic failure and death. A possible conclusion is that pleural effusion is a benign and early complication of acute hepatitis A infection that resolves spontaneously regardless of illness outcome. Goran Tesovic M.D. Dalibor Vukelic M.D. Branka Vukovic M.D. Branka Benic M.D. Dragomir Božinovic M.D., Ph.D. Department of Pediatric Infectious Diseases University of Zagreb School of Medicine Zagreb, Croatia Accepted for publication March 8, 2000. Address for reprints: Dr. Goran Tesovic, Department of Pediatric Infectious Diseases, Mirogojska c.8, 10 000 Zagreb, Croatia. Fax 385 1 46 78 235; E-mail [email protected].