DOI: 10.1097/QAD.0b013e3280fa81cb
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PMID: 17457112
Issn Print: 0269-9370
Publication Date: 2007/05/11
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Excerpt
A 27-year-old white homosexual man presented to the HIV clinic and complained of generalized weakness, upper abdominal pain/distension, daily heartburn, non-bloody diarrhea and excessive flatulence that had its onset 3 days after starting nevirapine, and exacerbated further when the dose of nevirapine was increased from 200 to 400 mg a day. He was previously doing well on a triple nucleoside analogue regimen including didanosine 250 mg and emtricitabine 200 mg/tenofovir 300 mg a day, with an undetectable HIV viral load and a CD4 cell count of 249 cells/μl, but nevirapine was substituted for didanosine 4 weeks before his current presentation in order to give diversity to his antiretroviral regimen. His past medical history was significant for gastroesophageal reflux disease, psoriasis and bipolar disorder. Besides the antiretroviral drugs, he used over-the-counter omeperazole, dovonex 0.005% ointment and fluocinolone 0.01% cream as needed. He had used alcohol in moderate amounts during the past 6 years, using up to 13 units of alcohol on a weekly basis. He did not have any history of intravenous drug use. His physical examination revealed stable vital signs and moderate diffuse upper abdominal tenderness and no rashes.
His complete blood count, albumin and prothrombin time were normal. His liver function tests showed an alkaline phosphatase level of 165 U/ml (38–126), an aspartate aminotransferase level of 126 U/ml (14–36), an alanine aminotransferase level of 109 U/ml (9–52) and a total bilirubin level of 0.6 mg/dl (0.2–1.3). Before starting nevirapine, his alkaline phosphatase level was 110 IU/ml, the aspartate aminotransferase level was 75 IU/ml, the alanine aminotransferase level was 79 IU/ml and the bilirubin level was 0.3 mg/dl. The hepatic viral serologies, hepatitis C virus RNA, hepatitis B virus DNA, antinuclear antibody, antimitochondrial antibody and anti-liver–kidney microsomal antibody were all negative. The F actin antibody was weakly positive, whereas ceruloplasmin and iron saturation were within the normal limits.
He underwent a computed tomography scan of the abdomen after the administration of oral and intravenous contrast that showed splenomegaly, perisplenic varices and no ascites. An upper gastrointestinal endosocopy showed grade two esophageal varices and minimal portal gastropathy. Biopsies of the antrum and duodenum showed mild inflammation. A transvenous liver biopsy performed a month after his initial presentation showed mild zone III sinusoidal dilation, patchy hepatocellular necrosis and congestion. His free hepatic venous pressure was 9 mmHg, wedged hepatic venous pressure was 17 mmHg and the hepatovenous gradient was 8 mm. An echocardiogram showed normal heart function. A magnetic resonance angiography of the abdomen showed no evidence of portal, splenic, superior mesenteric or hepatic venous obstruction.
Upon his initial presentation to the HIV clinic, nevirapine was stopped for a week, with some improvement of his symptoms, and was restarted again. Finally, because of persistent and worsening abdominal pain requiring narcotic analgesics, all antiretroviral agents, including nevirapine, were stopped 8 weeks after his initial presentation, and a second liver biopsy was performed that showed progressive changes of sinusoidal dilatation, hepatocellular congestion, patchy hepatocyte atrophy and reticulin compression, as well as hepatocellular necrosis without fibrosis compared with his previous biopsy (Fig. 1a and b). Four months after his initial presentation and 2 months after being off antiretroviral drugs, his abdominal pain had improved significantly and he had stopped using narcotic analgesics.
The present case is similar to case number 3 reported by Mallet et al.
