Testing a hypothesis that pelvic organ prolapse (POP) is a focal manifestation of disordered connective tissue, we evaluated whether there is an association between POP and history of fracture.
This was a case-control study. Baseline data were from postmenopausal women aged 60 years or older enrolled in the Women's Health Initiative Estrogen Plus Progestin trial. Distinct variants (cystocele, rectocele, and uterovaginal) and severity (mild, moderate, or severe) of POP were recognized. A history of "fracture after age 55" was considered as the event of interest.
Moderate to severe POP was identified in 9% of 11,096 participants aged 60 years or older. Women with moderate to severe rectocele were significantly more likely to report fracture (odds ratio: 1.37, 95% CI: 1.06-1.77, P = 0.02) compared with those with absent to mild prolapse. Of the subset of participants who underwent bone mineral density assessment, those with moderate to severe prolapse demonstrated significantly lower whole-body bone mineral density (β = −0.03, SE 0.02); this difference was of borderline significance (P = 0.05) compared with that for participants with absent to mild POP. Multivariate logistic regression analysis confirmed an independent association between moderate to severe rectocele and fracture (odds ratio: 1.45, 95% CI: 1.08-1.95, P = 0.01).
We demonstrate a relationship between moderate to severe POP and low bone mineral density in postmenopausal women enrolled in the Women's Health Initiative Estrogen Plus Progestin trial. Our findings of an association between clinically significant (moderate to severe) POP, specifically rectocele, and a history of fracture suggest that suboptimal collagen status purported to associate with POP may also involve bone collagen and hence translate into skeletal compromise.
Baseline data from the Women's Health Initiative Estrogen Plus Progestin trial were analyzed to determine whether a higher lifetime prevalence of postmenopausal fractures in association with moderate to severe rectocele is a common underlying pathophysiology.
From the Departments of 1Obstetrics and Gynecology and Women's Health and 2Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY; 3Shady Grove Fertility Center, Annapolis, MD; and 4Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI.
Received February 27, 2007; revised and accepted May 14, 2007.
This work was presented as an abstract at the annual meeting of the Society for Gynecologic Investigation, March 2006.
Funding/support: The Women's Health Initiative program is funded by the National Heart, Lung, and Blood Institute, US Department of Health and Human Services. L.P. received funding support from NIH-5K12 RR17672.
Financial disclosure: None reported.
Address correspondence to: Lubna Pal, MBBS, MRCOG, MS, Assistant Professor, Obstetrics and Gynecology and Women's Health, Division of Reproductive Endocrinology and Infertility, Mazer 316, 1300 Morris Park Ave, Bronx, NY 10461. E-mail: firstname.lastname@example.org