A study of the uterine walls, ovaries, and endometria in a series of 100 patients having fibromyomas with a correlation between these findings and the clinical histories and symptoms, still gives us no definite basis upon which to make an absolute statement as to a single etiologic or stimulating factor in the production of fibromyomata uteri, adenomyosis externa or interna, and hyperplasia of the endometrium with resultant menorrhagia, dysmenorrhea, or sterility.Evidence in favor of Witherspoon's theory making hyperestrinism the single activator in the production of these pathologic and clinical entities, can be found in the observation of the rapid growth of fibromyomas during pregnancy and their puerperal and menopausal regression. Such facts follow very closely the estrin levels now well established, as does the discovery of hyperplasia of the endometrium associated with the presence of theca and granulosa cell tumors of the ovary in women who have passed the menopause.We have presented in our discussion factors that may tend to oppose this theory, at least in part. We must, therefore, feel with Witherspoon that hyperestrinism plays a part in the production of the changes herein studied and discussed, but we cannot be convinced that it is the sole agent because of the lack of consistency in the finding of other pathologic and symptomatologic entities in association with fibromyomas.The logical conclusion that can be derived from this study is that fibromyomata uteri, endometriosis, adenomyosis uteri, and hyperplasia of the endometrium with associated menorrhagia, dysmenorrhea, and sterility cannot be traced to a single etiologic agent but appear to be products of various and varying factors.
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