F ROM observations beginning in 1942,l we can state that androgen will not cure “external” endometriosis, exerts relatively little regressive effect upon hard infiltrates or fused masses as compared to cystic endometriomas, and, apart from the menopausal period, has but temporary action. Also, it may induce arrhenomimetic symptoms, which are always objectionable, possibly serious and permanent,* but, except from heavy prolonged dosage, are not inevitable and may be mild. Notwithstanding the above, aside from relation to endometriosis, androgen has both negative and positive values. Unlike estrogen, it is neither experimentally3 nor clinically fibromatogenic or carcinomatogenic,3al 4 but rather antigenie in these respects, particularly versus inception of mammary cancer.5 It has positive value in spasmodic dysmenorrhea and mastalgia, less value in premenstrual tension6 and “functional uterine bleeding,‘” although not comparable to estrogen*’ 8 for the latter condition. Androgen also exhibits a “tonic” effect approaching euphoria notably at the menopause, when other favorable action may be prominent.a* lo In relation to endometriosis, androgen has also both negative and positive values. Unlike estrogen, it will not reactivate the disease after the menopause,llT I2 and, according to two of our cases, will not cause regression of cystic ovaries associated with peri-oophoritis and excessive bleeding. Although androgen has been used for acute pelvic inflammatory disease to suppress menstruation, we have not seen regression of inflammatory residues, and therefore suggest the last two negative observations as diagnostic possibilities. The positive values of androgen, particularly in rapid reduction of pain, tenderness, and swelling of grossly cystic ovarian endometriomas, will be described in 19 brief case reports under diagnostic, therapeutic, preoperative, and postoperative headings, not including a larger number of early nodular cul-de-sac endometriosis with minor symptoms. Contrary to original intention, only inconclusive haphazard endometrial biopsies and vaginal smears were obtained and no hormonal assays13v I4 so that nothing new can be presented as to etiology of the disease or biologic action of androgen. However, the rapidity of effect suggests a direct antagonism of androgen versus estrogen, in addition to known reduction of urinary gonado. tropic hormone excretion, as indicated in two previous reports.‘1 I5 We have had no experience with the sterol desoxycorticosterone acetate, and no conclusive effect with progestin, each of which should theoretically
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