The hepatitis A virus (HAV) is a common infectious etiology of acute hepatitis worldwide. HAV is most commonly transmitted through the oral-fecal route via exposure to contaminated food, water, or close physical contact with an infectious person. According to the World Health Organization (WHO), infection rates in developed countries are low. However, high-risk groups include injection-drug users, men who have sex with men, people traveling to endemic areas, and isolated communities. HAV does not cause chronic liver disease unlike hepatitis B or C. Acute hepatitis usually presents as a self-limited illness; development of fulminant hepatitis is rare. Typical symptoms of acute infection include nausea, vomiting, abdominal pain, fatigue, malaise, poor appetite, and fever; management is with supportive care. Alternate clinical patterns include cholestatic, prolonged, and relapsing disease. Vaccination against HAV is recommended for children 12 months or older and adults with the risk of exposure including travellers to endemic countries, men who have sex with men, illicit drug users, potential occupational exposure, and/or chronic liver disease [1-4].

A 26-year-old male, previously well, presented with abdominal pain, loss of appetite, low-grade intermittent fever, nausea, vomiting. There was history of yellowish discoloration of eye and skin.There was no history of bleeding or previous history of jaundice, urinary complaints, and change in urine or stool colour. He had no history of contact with chronic cough or with tuberculosis-diagnosed patients.

On examination: Blood pressure 110/70mmHg, pulse rate 88/minute, respiratory rate 20/minute, and temperature 37°C. There was decreased air entry and dullness in the lower lung field bilaterally.The liver was palpable 6cm below the right costal margin, total liver span 15cm, and tender. There was some palmar pallor, otherwise normal. On investigations, hepatitis A antibody IgM was reactive. Other viral markers (hepatitis B, hepatitis C, and human immunodeficiency virus test was negative). Other investigations are listed in Table 1.

Table 1: Investigations of the Patient at Presentation and During Follow-Up

Ultrasonography examination revealed minimal ascites, hepatosplenomegaly, and small bilateral pleural effusion. Ultrasound guided-pleural tap revealed no cells and is transudative, gene Xpert for tuberculosis was negative and Gastric aspirate was also done for gene Xpert and found to be negative.

Atypical extra-hepatic manifestations of acute hepatitis A are not frequent and include rash, pancreatitis, mono-neuritis, Guillain-Barré syndrome, acute kidney injury including glomerulonephritis, as well as interstitial nephritis and renal failure following haemolysis, dehydration or liver failure, pneumonitis, myocarditis, pleural or pericardial effusion, arthritis, haemolysis (especially in patients with glucose-6 phosphate dehydrogenase deficiency) [5-6].

The exact mechanism of pleural effusion in hepatitis A infection is not well known but the following mechanisms have been postulated. Transport of fluid from diaphragmatic lymphatics or leakage from a diaphragmatic defect to the pleural cavity from coexistent ascites. The second postulated mechanism is a virus-induced infection of the liver, with unknown mechanisms results in effusion. Pleural effusion may also result from immune complex deposition, or direct effect of viral on pleura. Pleural effusion secondary to hepatitis A resolves spontaneously even though liver damage progresses [7]. Although the mechanism of pleural effusion in hepatitis A infection patient is speculated by the above mechanisms, there may not be different mechanisms for icteric hepatitis A infection associated with pleural effusion.

Documented case reports of HAV infection with pleural effusions showed that the presence of effusion with HAV infection did not signify poor outcome and it resolves with supportive treatment alone [8-9].

Pleural effusion and ascitis has not been reported previously to be associated with icteric hepatitis A viral infection. We would like to stress that although pleural effusion and ascitis is rarely seen during icteric hepatitis A, hepatitis A infection should be considered in the differential diagnosis in patients with pleural effusions and ascitis, especially in developing countries. Pleural effusion is a benign and early extrahepatic complication of icteric acute hepatitis A infection that resolves spontaneously.

1. Alberts, C.J. et al. “Hepatitis A incidence, seroprevalence, and vaccination decision among msm in Amsterdam, the Netherlands.” Vaccine, vol. 37, no. 21, 2019, pp. 2849–56.

2. Johnson, K.D. et al. “adherence to hepatitis a and hepatitis b multi-dose vaccination schedules among adults in the United Kingdom: A Retrospective Cohort Study.” BMC Public Health, vol. 19, no. 1, 2019, pp. 1–9.

3. Brennan, J. et al. “Notes from the field: Acute hepatitis A virus infection among previously vaccinated persons with hiv infection—tennessee, 2018.” Morbidity and Mortality Weekly Report, vol. 68, no. 14, 2019, pp. 328–29.

4. Wilson, E. et al. “Notes from the field: Hepatitis A outbreak associated with drug use and homelessness—west Virginia, 2018.” Morbidity and Mortality Weekly Report, vol. 68, no. 14, 2019, p. 330.

5. Abid, S. et al. “Severe hemolysis and renal failure in glucose-6-phosphate dehydrogenase deficient patients with hepatitis E.” The American Journal of Gastroenterology, vol. 97, no. 6, 2002, pp. 1544–47.

6. Jeong, S.H. and H.S. Lee. “Hepatitis A: Clinical manifestations and management.” Intervirology, vol. 53, no. 1, 2010, pp. 15–19.

7. Tesovic, G. et al. “Pleural effusion associated with acute hepatitis A infection.” The Pediatric Infectious Disease Journal, vol. 19, no. 6, 2000, pp. 585–86.

8. Gürkan, F. “Ascites and pleural effusion accompanying hepatitis A infection in a child.” Clinical Microbiology and Infection, vol. 6, no. 5, 2000, pp. 286–87.

9. Erdem, E. et al. “Hepatitis a with pleural effusion, ascites and acalculous cholecystitis.” Iranian Journal of Pediatrics, vol. 20, no. 4, 2010, pp. 479.