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Chronic hepatitis C virus (HCV) is an independent risk factor for antiretroviral-related hepatotoxicity, but little is known about the frequency of severe liver toxicity in patients with HIV-HCV coinfection first treated for HCV (pretreated). The aim of this prospective study of 105 patients was to compare the incidence of progression to severe antiretroviral-related liver toxicity in 66 patients pretreated (36 with interferon-alpha [IFNalpha], 30 with IFNalpha plus ribavirin), and 39 patients not pretreated. The subjects could choose whether to receive anti-HCV therapy. Severe liver toxicity was defined as alanine aminotransferase (ALT) level > or =5-times the upper limit of normal in patients with normal baseline levels and > or =3.5-times in those with increased baseline levels. The authors also estimated the hepatotoxicity-related risk of discontinuing antiretroviral therapy. During antiretroviral therapy, 10 subjects (9.5%) experienced severe hepatotoxicity: 4 of 66 pretreated patients and 6 of 39 untreated patients (24-month survival: 94% +/- 2.9% vs. 85% +/- 5.8%). After adjusting for baseline CD4 cell counts, ALT levels, histologic scores, HCV and HIV viremia, HCV genotype (genotype 1 in 29% of pretreated patients and 20% of patients not pretreated), and previous anti-HCV therapy, the risk of discontinuing anti-HIV treatment was significantly higher in the anti-HCV untreated patients (RR = 10.4; 95% CI: 1.6-66; p =.0127) and in those with increased baseline ALT levels (RR = 1.014; 95% CI: 1.006-1.021; p =.0005). The authors' data suggest that previous treatment of chronic active HCV is an independent factor associated with a decrease of severe liver toxicity as the result of a subsequent antiretroviral regimen. The authors also confirm that the baseline level of ALT is an important prognostic factor for increased liver damage during antiretroviral therapy.

We performed polymerase chain reaction (PCR) for detection of cytomegalovirus (CMV), varicella-zoster virus (VZV), herpes simplex virus (HSV), and Toxoplasma gondii DNA in aqueous humor from 15 patients who were infected with human immunodeficiency virus (HIV) and who had retinitis of unclear origin; these patients were selected from among 820 patients evaluated by ophthalmoscopic examination. On the basis of the final response to treatment, CMV, VZV, and T. gondii retinitis was diagnosed in 5, 2, and 4 of the 15 patients, respectively. No final etiologic diagnosis was reached for four patients. All 5 patients with CMV retinitis were CMV DNA-positive. 1 of 2 patients with VZV retinopathy were VZV DNA-positive, and 3 of 4 patients with T. gondii retinitis were T. gondii DNA-positive. All PCR assays of aqueous humor from the four patients without infectious retinitis were negative. PCR assay of aqueous humor is helpful in the etiologic diagnosis of retinitis of unclear origin in HIV-infected patients.

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