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Prevalence and Risk Factors for Abnormal Liver Stiffness in HIV-infected Patients without Viral Hepatitis Coinfection: Role of Didanosine

2010; SAGE Publishing; Volume: 15; Issue: 5 Linguagem: Inglês

10.3851/imp1612

2040-2058

Nicolás Merchante, Inés Pérez‐Camacho, José Antonio López Mira, Antonio Rivero, Juan Macı́as, Ángela Camacho, Jesús Gómez‐Mateos, Milagros García-Lázaro, José Miguel Cisneros, Juan A. Pineda,

HIV/AIDS drug development and treatment

Background Unexpected cases of severe liver disease in HIV-infected patients have been reported and an association with didanosine (ddI) has been suggested. Transient elastography (TE) might detect patients harbouring such a condition. Our objective was to search for the presence of abnormal liver stiffness (LS) in a cohort of HIV-infected patients without HBV or HCV coinfection and to assess the related factors. Methods A cross-sectional prospective study was conducted. LS was assessed by TE in 258 HIV-infected patients without HBV or HCV coinfection and with no evidence of acute hepatotoxicity or other origins of liver disease. LS values ≥7.2 kPa were considered abnormal. Multivariate analyses were performed to identify factors associated with abnormal LS. Results Abnormal LS was observed in 29 (11.2%) patients. A total of 18 (16.4%) patients previously treated with ddI and 11 (7.4%) of those who never received ddI had LS values ≥7.2 kPa ( P=0.02). The prevalence of abnormal LS was higher in patients previously treated with abacavir than in those who had never received abacavir (15 [21.7%] versus 14 [7.4%]; P=0.001). After multivariate analyses, age (adjusted odds ratio [AOR] 1.05, 95% confidence interval [CI] 1.002-1.1; P=0.004) alcohol intake >50 g/day (AOR 7.2, 95% CI 2.6-19.7; P<0.0001), CD4 + T-cell count <200 cells/ml (AOR 3.4, 95% CI 1.06-11.007; P=0.03), time on ddI treatment (AOR 1.31, 95% CI 1.12-1.52; P=0.001) and previous abacavir exposure (AOR 3.01, 95% CI 1.18-7.67; P=0.02) were independently associated with abnormal LS. Conclusions The prevalence of abnormal LS in HIV-infected patients without HBV or HCV coinfection is substantial. Long-term exposure to ddI is a major cause of liver damage in these patients.