Abstract
The progestogenic component of combination oral contraceptives (OCs) intervenes in the negative feedback on pituitary luteinizing hormone secretion thereby inhibiting ovulation. Further combined OCs inhibit early growth and differentiation of glandular epithelium of the endometrium. During the 1st several cycles of the beginning of combined OC therapy secretory vacuoles appear in endometrial glands earlier than they do in untreated women. Histologists observe pronounced shedding of the endometrium more often in OCs of >5mg of progestogen with 10- nortestosterone derivatives than the low dose OCs. Therefore histologic characteristics of the endometrial glands and stroma may be at different stages of maturity that do not coincide to the actual day of the cycle on which a biopsy is taken. Prolonged sequential OC therapies promotes irregular proliferative or deficient secretory endometrium which often induces simple hyperplasia and/or adenomatous hyperplasia. Sequential OCs were removed from the US and Canada markets due to studies associating them with adenocarcinoma of the endometrium. Continuous low dose progestogen OC therapy causes endometrial atrophy to occur earlier in women who take them tan does other combined OC therapies. This may occur because of the induced suppression of pituitary gonadotropin secretion. Combined OCs cause 2 changes in the endometrium that inhibit the implantation of the blastocyst. They include atypical proliferative changes of blood vessels and the absence of normal spiral arteriolar development. Progestational and combination OCs foster microglandular hyperplasia of the cervix but low doses of these OCs apparently do not stimulate the growth of leiomyomas.
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