Paper Presentations: AUGS Abstracts: 2005 26th Annual Scientific Meeting of The American Urogynecologic Society
Results from the Women's Health Initiative (WHI) study indicated that smoking was protective for pelvic organ prolapse. In recent studies, however, expression of human macrophage elastase was increased significantly in vaginal muscularis from women with pelvic organ prolapse, and presence of this enzyme in the vaginal wall was highly correlated with smoking. In the WHI study, prolapse was assessed only by visual examination without speculum or POPQ examination. Therefore, we sought to use a large database of standardized POPQ examinations to determine the relationship between tobacco smoking and pelvic organ prolapse.
Multiple logistic models were used to investigate the relationships between smoking status (currently or not currently), age, race, vaginal parity, BMI, and prolapse using data from the Pelvic Organ Support Study (POSST, a multi-center, cross-sectional, observational study of women presenting to outpatient gynecologic clinics for annual exams). Prolapse was defined as ≥stage 2 by POPQ examination. The statistical model was tested using the Hosmer-Lemeshow goodness of fit statistic.
Complete data from 906 women were analyzed. Mean age of the population was 42.7 years, and 43% were White, 29% Hispanic, 25% Black, and 3% other. The distribution of prolapse (as defined by POPQ staging) was 25% stage 0, 38% stage 1, 35% stage 2, and 2% stage 3. Fifteen percent of women were current smokers (n=133) and 85% (773) nonsmokers. Multivariate logistic regression revealed that smoking was an independent, noninteractive risk factor for pelvic organ prolapse [odds ratio 2.37 (1.52, 3.72)]. For comparison, the adjusted risk ratio for vaginal parity was 3.55 (2.34, 5.38). In nulliparous smokers, the prevalence of prolapse was increased significantly relative to nulliparous nonsmokers (28% vs. 12%, adjusted OR 1.95 (1.11, 3.42), P=0.008). In nonsmokers, the prevalence of prolapse increased to 27% with one vaginal delivery [adjusted OR 1.34 (1.20, 1.51), P<0.0001]. Thus, the risk of prolapse conferred by smoking in nulliparous women is greater than that conferred by one vaginal delivery in nonsmokers. Prevalence of prolapse was 58–60% in both smokers and nonsmokers with 3 vaginal deliveries.
In contrast to the WHI study, analysis of data from the POSST study (in which the POPQ was used to evaluate prolapse) revealed that tobacco smoking is an independent risk factor for pelvic organ prolapse. These results are consistent with laboratory investigations suggesting that smoking-induced activation of vaginal macrophage elastase may be involved in the pathogenesis of prolapse in women who smoke. Our results suggest that tobacco exposure is a modifiable risk factor for the prevention of pelvic organ prolapse.