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Transient hepatopulmonary syndrome in a patient with acute hepatitis A[Note 1. Presented in the annual meeting of the American College ...]
Author(s) -
Regev A.,
Yeshurun M.,
Rodriguez M.,
Sagie A.,
Neff G. W.,
Molina E. G.,
Schiff E. R.
Publication year - 2001
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2001.00270.x
Subject(s) - hepatopulmonary syndrome , medicine , cirrhosis , asymptomatic , cardiology , hepatic encephalopathy , liver disease , gastroenterology , liver function , portal hypertension
The hepatopulmonary syndrome is defined as the triad of liver disease, hypoxaemia and intrapulmonary vascular dilatation. This syndrome has been described in patients with liver cirrhosis, noncirrhotic portal hypertension, and fulminant hepatic failure, however, there are no previous descriptions of hepatopulmonary syndrome in patients with acute nonfulminant viral hepatitis. We report a 47‐year‐old, previously healthy man that presented with acute hepatitis A, and developed progressive dyspnoea, platypnoea and orthodeoxia with no evidence of parenchymal or thromboembolic lung disease. PaO 2 on room air was 58 mmHg, O 2 saturation was 88% and alveolar‐arterial O 2 gradient was 62%. During his hospitalization serum albumin level decreased to 3.1 g/dl and prothrombin time was prolonged to 16.8 s, however, he remained alert with no signs of hepatic encephalopathy. Contrast echocardiography revealed left heart chamber opacification 3–4 cardiac cycles after the opacification of the right heart chamber, consistent with hepatopulmonary syndrome. During the following days there was a gradual improvement in the patient’s condition, with resolution of his dyspnoea and gradual increase of PaO 2. Repeat contrast echocardiography and PaO 2 determinations, 3 weeks later, were normal. On long‐term follow‐up the patient remained asymptomatic with normal liver function tests and normal O 2 saturation. This report indicates that hepatopulmonary syndrome may be a transient manifestation of acute hepatitis A in the absence of fulminant liver failure.