Serum PSA levels are not affected by the menstrual cycle or the menopause, but are increased in subjects with polycystic ovary syndrome.

BACKGROUND/AIMS: Prostatic specific antigen (PSA) is the most specific prostatic tumor marker in man. Recently, PSA has been detected in a variety of tissues and fluids in women, and its determination suggested as a marker of hyperandrogenism. However, precise information about the physiology of PSA in females is not available. The goal of this study was to assess serum concentrations of PSA in healthy pre-menopausal women (healthy pre-menopausal group), menopausal women (menopause group) and patients with polycystic ovary syndrome (PCOS group). METHODS: PSA, androgens, LH, FSH, 17-beta-estradiol (E2), progesterone (Pg) were assessed in 40 post-menopausal women, 35 fertile controls and 35 women with PCOS. RESULTS: No significant difference in PSA concentrations could be demonstrated in different phases of the menstrual cycle in healthy pre-menopausal group and between pre- and post-menopausal groups. No correlations could be demonstrated between serum PSA levels and the following parameters: age, body mass index (BMI), LH, FSH, E2, testosterone (T), DHEAS, and SHBG, both in pre- and post-menopausal women. Significantly higher PSA levels (median=14 pg/ml) were found in the PCOS group compared to both pre-menopausal (median=5 pg/ml) and menopausal (median= 5 pg/ml) groups (p< 0.05). CONCLUSIONS: only minor fluctuations of serum PSA concentrations are observed in healthy pre- and post-menopausal women, while serum level is higher in PCOS, and therefore PSA can be considered a suitable marker of female hyperandrogenism.

Beta-endorphin response to oral glucose tolerance test in obese and non-obese pre- and postmenopausal women.

Beta-endorphin (beta-EP) is a neuropeptide involved in several brain functions, regulating the reproductive axis and behavioral changes. Estrogens play a modulatory role on circulating levels of beta-EP in women. Previous clinical studies have demonstrated high plasma beta-EP levels in obese subjects and increased beta-EP release after an oral glucose tolerance test (OGTT) in normal or obese women. The aim of the present study was to evaluate plasma beta-endorphin levels in response to an OGTT in pre- and postmenopausal obese and non-obese women, in order to investigate if the decrease in gonadal steroid levels at menopause could modify in a different manner the control of beta-endorphin release in response to glucose administration. A group of 24 normal women (age range 45-55 years) were included in the study. The patients were subdivided in four groups of six subjects each: group A, premenopausal women with body mass index (BMI) < 25 (control); group B, premenopausal women with BMI > 25 (obese); group C, post-menopausal women with BMI < 25 (control); group D, postmenopausal women with BMI > 25 (obese). All women were studied between 8.30 and 9.00 am, after overnight fasting, and underwent an OGTT. In obese premenopausal women, basal plasma beta-EP levels were significantly higher than in non-obese women (p < 0.01). In postmenopausal women, regardless of body weight, low basal plasma beta-EP levels were found. A significant increase in plasma beta-EP levels, at 30 and 60 minutes after oral glucose ingestion, was shown in control premenopausal women. No significant modifications to OGTT were shown in plasma beta-EP levels in the other three groups of women. In conclusion, while in premenopausal women the response of plasma beta-EP levels to OGTT is maintained, in postmenopause there is a lack of response to OGTT. This suggests that beta-EP release is dependent upon gonadal steroids, while it is only in part influenced by body weight.

Endogenous digitalis-like factors (EDLF) in obese individuals: preliminary results.

We measured by RIA the serum and urinary digoxin-like immunoreactivity (EDLF) in 8 subjects with severe obesity and in 10 healthy, non-obese individuals (as a control group), to evidentiate whether circulating and urinary levels of EDLF are increased in obesity. For each individual, we measured the mean EDLF on two sera collected consecutively on two successive mornings, between 8-9 a.m. and the daily urinary EDLF excretion. Every subject collected his/her 24 hour urine in 5 different timed fractions. For each urine fraction, we measured the excretion of EDLF, electrolytes (Na and K), and creatinine. In obese people, the mean serum digoxin-like immunoreactivity (no. 8, 27.3 +/- 8.7 ng/L de) was significantly higher (unpaired t test, p = 0.0002) than in the controls (no. 10, 12.0 +/- 7.3 ng/L de), whereas control and obese subjects had superimposable 24 hour EDLF urinary excretion. Urinary excretion of EDLF significantly changed throughout the day in normals, but not in obese people. In a multiple stepwise regression analysis, urinary K+ and Na+ significantly (p less than 0.01) contributed to the regression with urinary EDLF (EDLF = 76.9 + 0.67 K+ - 0.24 Na+; R = 0.601, no. 40) in obese individuals. The in vivo kinetic and metabolic pathways of EDLF are conceivably different in obese and normal subjects. A difference in the production rate, binding to plasma proteins and/or removal mechanisms could explain the findings of higher circulating levels with normal EDLF urinary excretion in obese persons.(ABSTRACT TRUNCATED AT 250 WORDS)