Published online Jul 7, 2015. doi: 10.3748/wjg.v21.i25.7613
Peer-review started: March 11, 2015
First decision: April 13, 2015
Revised: May 6, 2015
Accepted: May 27, 2015
Article in press: May 27, 2015
Published online: July 7, 2015
There are numerous physiologic and biochemical changes in menopause that can affect the function of the liver and mediate the development of liver disease. Menopause represents a state of growing estrogen deficiency, and this loss of estrogen in the setting of physiologic aging increases the likelihood of mitochondrial dysfunction, cellular senescence, declining immune responses to injury, and disarray in the balance between antioxidant formation and oxidative stress. The sum effect of these changes can contribute to increased susceptibility to development of significant liver pathology, particularly nonalcoholic fatty liver disease and hepatocellular carcinoma, as well as accelerated progression of fibrosis in liver diseases, as has been particularly demonstrated in hepatitis C virus liver disease. Recognition of the unique nature of these mediating factors should raise suspicion for liver disease in perimenopausal and menopausal women and offer an opportunity for implementation of aggressive treatment measures so as to avoid progression of liver disease to cirrhosis, liver cancer and liver failure.
Core tip: There is an interplay of hormonal issues and aging that create a unique path for development of liver disease in menopausal women. Reviewed in this article are the expected liver-related physiologic and biochemical features of menopause and the impact of menopause on the natural history of liver disease. The impact of an understanding of how menopause mediates liver disease is important as there are growing numbers of menopausal women worldwide.