Gender Differences in Liver Fibrosis and Hepatitis C Virus-Related Parameters in Patients Coinfected with Human Immunodeficiency Virus
Julio Collazos, Jose Antonio Carton and Victor Asensi
Affiliation: Infectious Disease Unit, Hospital de Galdacano-Usansolo, 48960 Vizcaya, Spain.
Keywords: Antiretroviral therapy, female, gender differences, HCV infection, hepatic fibrosis, HIV infection, male, transient elastometry, cirrhosis
Objectives: To evaluate gender differences in liver fibrosis and hepatitis C virus-related parameters in patients coinfected with human immunodeficiency virus. Methods: Transversal study of 782 patients who underwent a complete clinical and laboratory evaluation. Fibrosis was measured by transient elastometry (TE) and by commonly used laboratory-derived fibrosis indexes. Results: Men were older, had higher rates of alcohol abuse, higher HCV viral load and liver tests, lower platelet values, poorer CDC clinical stages, longer duration of HCV infection, shorter time on successful antiretroviral therapy (ART) and had appreciably more advanced fibrosis than women. Multivariate analysis revealed that male gender (P < 0.0001), longer time since HCV acquisition (P < 0.0001), alcohol abuse (P < 0.0001), HCV genotype 3 (P=0.01), shorter time on successful ART (P=0.005) and worse CDC clinical stages (P=0.03) were independently associated with significant or higher stages of fibrosis. Male gender was also independently predictive of advanced or higher stages of fibrosis (P=0.06) or cirrhosis (P=0.02). In patients with no alcohol abuse, men had worse fibrosis parameters than women (P < 0.01 for each), but these differences decreased in patients with alcohol abuse and became non-significant. Conclusions: HIV-HCV-coinfected women have more favorable HCV virological and clinical profile than men and, particularly, lower degrees of fibrosis. Alcohol abuse seemed to result more deleterious in women than in men. The reportedly poorer outcomes of liver disease in HIV-HCV-coinfected patients, as compared with their HCV-monoinfected counterparts, could be ameliorated by addressing these cofactors, some of them preventable or treatable.
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