Women in the menopausal transition lose trabecular bone at a rapid rate despite intermittently high and usually normal estrogen levels. This is the only prospective study to date that documents trabecular bone changes in women through the entire perimenopause, which may last up to 10 years.
Based on the results of a French cohort of postmenopausal women, it has been claimed that micronized progesterone does not enhance breast cancer risk. The impact of reproductive factors on breast cancer risk and a high prevalence of occult breast carcinomas at the time of menopause suggest an involvement of endogenous progesterone in the development of breast cancer. High mammographic density in the luteal phase and during treatment with estrogen/progestogen combinations reflect a change in the composition of mammary stroma and an increased water accumulation in the extracellular matrix which is caused by hygroscopic hyaluronan-proteoglycan aggregates. Proteoglycans are also involved in the regulation of proliferation, migration, and differentiation of epithelial cells and angiogenesis, and may influence malignant transformation of breast cells and progression of tumors. Reports on a lack of effect of estrogen/progesterone therapy on breast cancer risk may be rooted in a selective prescription to overweight women and/or to the very low progesterone serum levels after oral administration owing to a strong inactivation rate. The contradictory results concerning the proliferative effect of progesterone may be associated with a different local metabolism in normal compared to malignant breast tissue. Similar to other progestogens, hormone replacement therapy with progesterone seems to promote the development of breast cancer, provided that the progesterone serum levels have reached the threshold for endometrial protection.
The findings of this survey demonstrate the preponderant differences in awareness of benefits and risks in HT users. To a large extent, users are satisfied with their HT and willing to pursue its use for longer periods of time.
Seminal and endocrinological investigations were done on 50 fertile men whose wives became pregnant spontaneously (Group I), on 100 men from our fertility clinic whose wives conceived after treatment of the couple (Group II) and in 100 infertile men whose wives failed to become pregnant even after 5-year treatment of the couple (Group III). Patients with azoospermia were excluded. While there were no significant differences in the mean sperm density and total sperm count of the men from all three groups, mean sperm motility and sperm morphology were significantly better (p less than 0.001) in both Group I and Group II men than in the infertile Group III men. The mean serum LH and FSH concentrations were significantly lower in Group I than in the two other groups. However, there were no differences between Groups II and III. The mean serum concentrations of prolactin, testosterone, and estradiol were similar in all three groups. Based on semen and hormone data, stepwise multiple discriminant analysis could allocate 80% of the Group I men correctly, whereas only 50% of Groups II and III could be correctly classified. Although overall differences in sperm motility and morphology as well as in serum gonadotrophin concentrations were noted, no specific seminal or hormonal variable could be identified as being of value in predicting the fertility of an individual man.
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