Department of Obstetrics, Gynecology, and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, and Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
Address for correspondence: Robert L. Barbieri, Department of Obstetrics, Gynecology, and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115. Voice: 617-732-4265; fax: 617-277-1440.
rbarbieri{at}partners.org
Two major methodological problems that impact clinical research
in endometriosis are the absence of a low-cost, highly reliable
method for diagnosing endometriosis and the possibility that
endometriosis is actually multiple different diseases that we
have not yet been able to differentiate. Animal models of endometriosis
clearly demonstrate that advanced endometriosis causes reduced
fertility. In humans, endometriosis and infertility are commonly
associated. However, few data from high-quality clinical trials
demonstrate that endometriosis causes infertility in humans.
Future research should focus on the implications of the observation
that, in ovarian endometriosis cysts, the epithelium is monoclonal.
This observation suggests that nonrandom somatic mutations cause
ovarian endometriosis cysts. If somatic mutations cause ovarian
endometriosis cysts, it is likely that a small number of genes
can be identified that play a central role in pathogenesis of
this disease.
