PLEURAL EFFUSION ASSOCIATED WITH ACUTE HEPATITIS A INFECTION

Abstract

Pleural effusion is a rare complication of acute viral hepatitis. The first case was reported in 1971,1 and thereafter 14 additional cases with similar conditions were reported.2-8 Among those, 5 were associated with hepatitis B4-7 and 2 had hepatitis A infection.8-11 Etiology could not be determined in the remaining 8 cases. Although pleural effusion associated with acute hepatitis A can be seen rarely in adults, there has been only one case recorded in a child.8 We here present the second and third childhood cases. Patient 1. A 12-year-old girl was admitted to the division of Pediatric Infectious Diseases of the Faculty of Medicine of Çukurova University with jaundice after 6 days of fever, anorexia, malaise and myalgia. She had been previously well. On examination the vital findings were normal, skin and sclera were icteric, there was a dullness to percussion at the base of the right lung and hepatomegaly was noted. All other physical examination findings were normal. The complete blood count was normal and the erythrocyte sedimentation rate was 40 mm/h. The blood urea nitrogen, electrolytes, calcium, phosphorus, glucose, urine analysis, bleeding time and coagulation tests were normal. Aspartate aminotransferase concentration was 166 units and alanine aminotransferase 567 units; total bilirubin was 6.1 mg/dl (direct bilirubin, 5.3 mg/dl); total protein was 7.1 g/dl and albumin was 3.7 g/dl. Hepatitis A virus (HAV) IgM was positive, whereas all other markers (HAV IgG, hepatitis B surface antigen, anti-hepatitis B surface antigen antibody, hepatitis B e antigen, anti-hepatitis B e antigen antibody, anti-hepatitis B core antigen antibody IgM, anti-hepatitis C virus, anti-hepatitis E virus) were negative. Epstein-Barr virus and cytomegalovirus serologies were negative. Chest radiograph showed consolidation of the right lower lobe, and a thorax ultrasound revealed a pleural effusion in the right chest. Abdominal ultrasonography revealed hepatomegaly only. A diagnostic thoracentesis yielded 10 ml of serous pleural fluid that contained no cells on microscopic examination. Glucose concentration was 95 mg/dl and protein was 4.2 g/dl. Cultures were sterile. Of the hepatitis markers tested for in the pleural fluid, only HAV IgM was positive. One week after the liver enzymes returned to normal, the pleural effusion resolved and the patient was discharged. Patient 2. A 5-year old boy was admitted to the hospital for jaundice, fever and malaise associated with dark urine and a light stool color. Two days before admission a chest radiograph revealed a pleural effusion. On physical examination the patient was febrile (38.8°C), the skin and sclera were icteric, there was a dullness to percussion at the base of the right lung and hepatomegaly was palpated 6 cm below the costal margin. The complete blood count was normal and the erythrocyte sedimentation rate was 62 mm/h. Blood urea nitrogen, electrolytes, calcium, phosphorus, glucose, urine analysis and coagulation tests were normal. Aspartate aminotransferase concentration was 890 units, and alanine aminotransferase was 1180 units; total bilirubin was 9.5 mg/dl (direct bilirubin, 8.2 mg/dl); total protein was 6.2 g/dl and albumin was 2.9 g/dl. Only hepatitis A virus IgM was positive. All other markers (HAV IgG, hepatitis B surface antigen, anti- hepatitis B surface antigen antibody, hepatitis B e antigen, anti- hepatitis B e antigen antibody, anti- hepatitis B core antigen antibody IgM, anti-hepatitis C virus and anti-hepatitis E virus) were negative. Thorax ultrasound revealed pleural effusion at the right base. Hepatomegaly was observed on the abdominal ultrasonography. In the serous fluid obtained by thoracentesis, no cells were found on direct microscopy; the glucose concentration was 85 mg/dl and protein 4.2 g/dl. In the pleural fluid HAV IgM was positive and cultures were sterile. Serology was negative for Epstein-Barr virus and cytomegalovirus. Three days after liver enzymes declined the pleural effusion decreased as determined by chest radiography and the patient was discharged from the hospital. Discussion. We present here the second and third pediatric patients who developed pleural effusion during the course of acute hepatitis A infection. Although the pathogenesis of the effusion is unknown, it seems likely that it relates to infectious inflammation of the liver rather than to immune complexes, because no other serosal surfaces were involved and there was no evidence of glomerular involvement. Pediatric physicians should be cognizant of pleural effusion developing during the course of acute viral hepatitis A and that this complication will resolve spontaneously. Emre Alhan, M.D. Dinçer Yıldızdaş, M.D. Hacer Yapıcıoğlu, M.D. Aksaray Necmi, M.D. Division of Pediatric Infectious Diseases (EA, AN); Faculty of Medicine (DY, HY); Çukurova University; Adana, Turkey