A longer duration of estrogen deficiency increases fibrosis risk among postmenopausal women with nonalcoholic fatty liver disease.
A longer duration of estrogen deficiency increases fibrosis risk among postmenopausal women with nonalcoholic fatty liver disease.
Author information
- 1Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR.
- 2Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN.
- 3Gastroenterology and Hepatology, Duke University, Durham, NC.
- 4Dept. of Pathology, Duke University, Durham, NC.
- 5Dept. of Pathology, University of California San Francisco, San Francisco, CA.
- 6NASH CRN Data Coordinating Center, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
- 7Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
- 8Dept. of Pediatrics, Columbia University, New York, NY.
- 9Division of General Internal Medicine, Johns Hopkins Bloomberg School of Public, Health, Baltimore, MD.
- 10Gastroenterology, Central Arkansas Veterans Healthcare System, Little Rock, AR.
- 11Gastroenterology and Hepatology, University of Arkansas for Medical Sciences, Little Rock, AR.
Abstract
Post-menopausal women with nonalcoholic steatohepatitis (NASH) are at an increased risk of hepatic fibrosis when compared with premenopausal women. Whether duration of estrogen deficiency in postmenopausal state dictates individual’s fibrosis risk remains uninvestigated. We aimed to assess the associations of age at menopause and time from menopause with fibrosis severity in postmenopausal women with nonalcoholic fatty liver disease (NAFLD). Data from 488 post-menopausal women with 1) histologic diagnosis of NAFLD and 2) self-reported information on age at menopause were analyzed. The associations of premature menopause (age at menopause of <40 years) and time from menopause (age at study enrollment – age at menopause, years) with fibrosis severity (stage 0-4) were assessed using multiple ordinal logistic regression models with and without adjusting for clinical confounders. Among the participants (age at menopause: 43.7 ± 8.6 years), women with premature menopause (29.3%) were younger at enrollment (p<0.001) and used hormone replacement therapy (HRT) more often (p<0.003). After adjusting for age at enrollment, race, waist circumference standardized by body mass index, current smoking, current alcohol use, hypertension, diabetes/impaired fasting glucose, homeostatic model assessment of insulin resistance, and HRT, premature menopause was associated with an increased likelihood of having more severe fibrosis; adjusted cumulative odds ratio and 95% confidence interval (ACOR [95%CI]) was 1.9 [1.3-2.7], p=0.001, while time from menopause was directly associated with an increased likelihood of having more severe fibrosis (ACOR [95%CI] for 5-year unit=1.2 [1.1-1.3], p=0.002).
CONCLUSION:
Duration of estrogen deficiency in postmenopausal state confers fibrosis risk among post-menopausal women with NAFLD. This article is protected by copyright. All rights reserved.
© 2016 by the American Association for the Study of Liver Diseases.
KEYWORDS:
hepatic fibrosis; menopause; nonalcoholic fatty liver disease; nonalcoholic steatohepatitis; premature menopause
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