ArticleClinical infectious diseases : an official publication of the Infectious Diseases Society of America2017
Reproductive Aging and Hepatic Fibrosis Progression in Human Immunodeficiency Virus/Hepatitis C Virus-Coinfected Women.
Article in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Association of cardiovascular disease risk with liver steatosis and fibrosis in people with HIV in low- and middle-income countries.AIDS (London, England) · 2025Article
- Sex differences in chronic liver disease and benign liver lesions.JHEP reports : innovation in hepatology · 2023Review
- Changes in liver steatosis in HIV-positive women are associated with the BMI, but not with biomarkers.Cytokine · 2021Article
- The Rate of Hepatic Fibrosis Progression in Patients Post-Fontan.Pediatric cardiology · 2020Article
- Beneficial and Deleterious Effects of Female Sex Hormones, Oral Contraceptives, and Phytoestrogens by Immunomodulation on the Liver.International journal of molecular sciences · 2019Review
- Testing for Hepatitis C in Pregnancy: the Time has Come for Routine Rather than Risk-based.Current hepatology reports · 2019Article
Corrections and comments
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Authors and funding
16 authors at 11 institutions in 2 countries.
Funding
Abstract
backgroundSeverity of hepatic fibrosis is greater in postmenopausal than in premenopausal women, perhaps owing to protective effects of estrogens. However, prior studies of estrogen and liver fibrosis lack serial fibrosis measures, adjustment for age, or longitudinal observations in coinfected populations.
methodsIn a longitudinal cohort of women coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV), we assessed fibrosis progression across reproductive age, using validated serum fibrosis markers, aminotransferase platelet ratio index (APRI) and fibrosis 4 (FIB-4). Fibrosis rate was evaluated within each woman as she transitioned from pre- to postmenopause, defined by a biomarker of ovarian function.
resultsThe median follow-up (n = 405) was 9.1 years (interquartile range, 5.0-15.2 years), with a median menopausal age of 49 years (47-52 years). When fully controlled for chronologic aging, the fibrosis progression rate was accelerated during perimenopause, as shown using FIB-4 (0.12 units per year faster than during premenopause; 95% confidence interval [CI], .02-.21; P = .01) and APRI (0.05 units per year faster; -.002 to .09; P = .06). Accelerated fibrosis was also observed during postmenopause compared with premenopause, for FIB-4 (0.14 units per year faster; 95% CI, -.01 to .29; P = .07) and APRI (0.07 units per year faster; -.003 to .15; P = .06). Accelerated fibrosis in perimenopause persisted after adjustment for Hispanic ethnicity, antiretroviral use, and alcohol (0.10 FIB-4 units per year faster than during premenopause; 95% CI, .008-.20; P = .03).
conclusionsIn HIV/HCV-coinfected women, hepatic fibrosis accelerates with reproductive aging. Accelerated fibrosis begins in perimenopause, highlighting a previously unrecognized group of women at increased risk for advanced fibrosis and associated complications. Longitudinal analyses of fibrosis rates across reproductive age should be conducted in non-HCV-related liver diseases, given potential implications in a broader spectrum of women.
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