Taking postmenopausal hormone replacement therapy (HRT) increases the risk for ulcerative colitis (UC), but not Crohn's disease (CD), a study shows.
The study is the largest so far to explore the link between exogenous hormones and inflammatory bowel disease in postmenopausal women.
"Our results largely agree with prior work that has observed an association between oral contraceptive agents that contain estrogen and progestins on risk of UC among premenopausal women," say Andrew Chan (Harvard Medical School, Boston, Massachusetts, USA) and colleagues.
The authors used data from the Nurses' Health Study for 22,044 women who were postmenopausal at baseline and a further 86,800 who became postmenopausal during the course of the study. In all, 138 women developed UC, and 138 developed CD during the 32 years of the study.
Compared with those who had never used HRT, past and current users had a significantly increased risk for developing UC, the authors report in Gastroenterology. Those who currently used hormones had a 71% increased risk, and those who had previously taken hormones had a 65% increased risk.
Risk also seemed to increase with the duration of hormone use. For example, those who had taken HRT for 1-5 years had a 61% increased risk compared with those who had never taken HRT. In women who had taken hormones for over 10 years this risk increased to 80%.
But 5 years after stopping treatment, the risk for UC reduced, and was no longer statistically different from those who had never taken hormones.
Interestingly, the authors found no association between hormone use and CD, even though contraceptive use in premenopausal women is known to be associated with the condition. They suggest that this could be explained by different hormone dosages in contraceptives compared with HRT, or that the effect of hormones may be age-dependent.
The authors say that recent observations have shown that estrogen compounds modify colonic barrier function and estrogen is thought to be involved in the progression of other Type 2 helper T cell-related diseases, which could explain their effect in UC.
They conclude: "These findings provide novel insights into unique biological pathways related to estrogens that mediate the pathogenesis of UC. Further understanding of such mechanisms could eventually lead to elucidation of new targets for interventions that may modulate disease incidence or activity."
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