The endometrium of infertility. A review.
Almost all functional disturbances involved in sterility result in morphological changes in the endometrium. Since hormone levels fluctuate depending upon various biorhythms, the histological examination of the endometrial biopsy is the most reliable parameter for evaluating the cause of infertility. A major subdivision can be made into anovulatory and ovulatory infertility. The anovulatory cycle is most frequently caused by a polycystic ovary syndrome, less frequently by gonadal dysgenesis, receptor or enzyme deficiencies, ovarian neoplasms, autoimmune reactions, or the luteinized unruptured follicle syndrome. Histologically the endometrium, depending upon the amount of estrogen secreted and reacting, is atrophic, resting, deficiently or irregularly proliferated or hyperplastic at the end of a menstrual cycle. A limited and deficient luteinization within a non-ovulating insufficient follicle may also result in abortive secretion which must be differentiated from deficient secretion following ovulation. In ovulatory infertility an absolute or relative progesterone deficiency results in a deficient secretory phase with delayed maturation of glands and stroma. The delay in maturation may be dissociated in the presence of an insufficient corpus luteum with absolute progesterone deficiency or coordinated when progesterone secretion is normal but counteracted by too much estrogen, as from a preceding persistent follicle. Since in these instances ovulation is delayed, the coordinated delay in maturation of the endometrium is only apparent. A truly delayed coordinated maturation may occur when the progesterone cannot fully act because of a preceding deficient proliferation. In addition, cyclic asynchrony with shortened or prolonged menstrual cycles may cause infertility by altering the endometrium so the blastocyst cannot implant. Rare non-functional endometrial changes as causes of infertility may be tuberculous endometritis, polyps or true neoplasms.
D000858:Anovulation / Q000209:etiology / Q000473:pathology; D001284:Atrophy; D001683:Biological Clocks; D004717:Endometrium / Q000473:pathology* / Q000503:physiopathology; D004967:Estrogens / Q000378:metabolism; D005260:Female; D006801:Humans; D006965:Hyperplasia; D007247:Infertility, Female / Q000209:etiology / Q000473:pathology*; D008597:Menstrual Cycle; D010060:Ovulation; D011374:Progesterone / Q000378:metabolism
D004967:Estrogens; D011374:Progesterone