Epidemiology of uterine leiomyomas. With an etiologic hypothesis.

OBJECTIVE

The few previous epidemiologic studies of uterine myomas have relied on clinical evaluation to select controls, but we previously showed that myomas may be present in more than 75% of such uteri.

STUDY DESIGN

We therefore attempted to evaluate risk factors using age-matched controls whose uteri were serially sectioned to exclude the presence of myomas.

RESULTS

The small study size precluded a meaningful evaluation of most parameters but tended to confirm the negative association of myomas with cigarette smoking (P = .07).

CONCLUSION

Using monoclonal smooth muscle proliferation in human atherosclerotic plaques as a model, we suggest that excessive injury to and repair of the endometrial lining of the uterus may promote monoclonal expansion of smooth muscle cell populations in the uterine wall (i.e., myomas). This theory is largely compatible with the estrogen hypothesis, but fundamental principles of tumorigenesis and previous epidemiologic data on myomas suggest that nutritional factors should be scrutinized as possible initiators (DNA-damaging substances) in the pathogenesis of uterine myomas.