ABSTRACT
Gross cystic breast disease (GCBD) is common in women, especially in the age range between 35 and the menopausal years. The present study examined the possible role of progesterone (Pg) in the chorionic gonadotropin (hCG) concentration in GCBD. The breast cyst fluids (BCFs) were drawn by fine needle aspiration between the sixth and the eighth day of the menstrual cycle and twenty days later. On the day of the first aspiration the patient began to take 100 mg of natural micronized Pg orally until the second aspiration. At both times blood samples were also taken. Determinations were done of both BCFs and blood sample using two fully automated chemiluminiscent enzyme immunometric assays. Pg has been demonstrated to induce a significant increment in hCG + free ss-hCG (median, range): 0.27 ng/ml, 0.12-6.24 vs. 1.92 ng/ml, 0.12-423.5; free ss-hCG: 0.11 ng/ml, 0.02-2.40 vs. 0.91 ng/ml, 0.02-58.40 in the BCFs, with no change in the circulating concentrations of the hormone. None of the sera studied presented levels of hCG + free ss-hCG or free ss-hCG above 0.5 ng/ml or 0.1 ng/ml, respectively. The occurrence of hCG or a derivative polypeptide in BCFs, when they are present in high concentrations suggests that this glycoprotein could be synthesized in situ and possibly involved in the pathogenesis of GCBD by the degree of differentiation of breast epithelial cells induced by the hormone.
Subject(s)
Chorionic Gonadotropin/metabolism , Cyst Fluid/drug effects , Cyst Fluid/metabolism , Fibrocystic Breast Disease/drug therapy , Fibrocystic Breast Disease/metabolism , Progesterone/administration & dosage , Administration, Oral , Adult , Chorionic Gonadotropin/blood , Chorionic Gonadotropin, beta Subunit, Human/blood , Chorionic Gonadotropin, beta Subunit, Human/metabolism , Epithelium/metabolism , Female , Fibrocystic Breast Disease/etiology , HumansABSTRACT
Cytosol progesterone (PgR) and estradiol (E2R) receptors were quantified simultaneously in "normal" and tumoral endometrium samples, located symmetrically on the longitudinal axis of the uterine cavity. With this experimental model two different groups of patients were detected. In the first group (7 of 10 women), the endometrial carcinoma had a greater cytosolic concentration of PgR than the corresponding "normal" endometrium, both kinds of tissue being affected by the same circulating hormonal "environment," peculiar to each patient. The opposite occurs in the other group (3 of 10 women), since the "normal" endometrium was found to be "richer" in receptors than the tumoral endometrium. It is suggested that this difference in the capacity of the tumor for synthesizing PgR and even E2R as compared to the "normal" endometrium may be a marker which improves selection of patients who will be more likely to respond favorably to endocrine therapy.
