Episodic changes of serum procollagen type I carboxy-terminal propeptide levels in fertile and postmenopausal women.

The aim of the present study was to optimize the use of serum procollagen type I carboxy-terminal propeptide (PICP) as a possible marker of postmenopausal-376lted changes of bone metabolism. Postmenopausal (n = 20) and healthy fertile young (n = 4) women were studied after informed consent. The postmenopausal women were subdivided in 4 groups: (1) nontreated; (2) treated with estrogen-progestogen replacement therapy; (3) treated with calcitonin, or (4) with kidney or liver diseases. Blood samples were collected at 15-min time intervals for 4, 6 or 8 h. Serum concentration of PICP was measured by radioimmunoassay, in duplicate at two different dilutions. In postmenopausal women mean +/- SEM serum PICP levels were slightly but nonsignificantly higher than in fertile women. Serum PICP levels in estrogen-progestogen or calcitonin-treated women were significantly lower than in non-treated postmenopausal women. Episodic changes of circulating PICP level were observed in fertile and postmenopausal women. The pulses of serum PICP levels did not show significant differences among the groups of women studied. The present study showed that the measurement of serum PICP levels is a useful marker for investigating the changes of bone metabolism. In particular, low PICP levels in postmenopausal women under steroid hormone or calcitonin treatment in part reflect the changes of bone turnover. The pulses of serum PICP levels during a time interval suggest that collagen metabolism in women undergoes a rapid turnover.

Hormonal treatments modulate pulsatile plasma growth hormone, gonadotrophin and osteocalcin levels in postmenopausal women.

Oestrogen plays a role in modulating growth hormone (GH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and osteocalcin secretion in women. Indeed, the postmenopausal period is characterized by changes in plasma GH, LH, FSH and osteocalcin levels. The aim of the present study was to investigate the changes in the secretory patterns of these hormones in postmenopausal women under different therapeutic regimens. A total of 20 subjects took part in the study. They were subdivided into four groups comprising 5 untreated postmenopausal women (time since menopause 1-5 years), 5 postmenopausal women receiving steroid hormone replacement therapy, 5 postmenopausal women receiving salmon calcitonin and 5 fertile women with regular menstrual cycles. Blood samples were collected every 15 min for 4 h and hormone levels were measured by radioimmunoassay. Plasma GH levels fell in the postmenopausal women, but were restored under oestrogen-progestogen treatment. The pulsatile patterns of plasma LH and FSH did not show significant differences in the treated and untreated women. Plasma osteocalcin levels showed episodic fluctuations and mean levels decreased under steroid hormone or calcitonin treatment. No significant correlation was observed between plasma GH and osteocalcin or gonadotrophin levels or body mass index.

Reduced spinal bone density in young women with amenorrhoea.

To assess the influence of diminished oestrogen production on bone density, we studied 23 amenorrhoeic women and 20 controls (age range 16-29 years) divided into four groups: group 1: 6 patients with idopathic hypogonadotrophic hypogonadism with primary amenorrhoea (IHH); group 2: 5 patients with delayed puberty owing to thalassaemia major (TM); group 3: 12 patients with secondary hypothalamic amenorrhoea (HA); group 4: 20 women with normal menses (controls). Secondary sexual characteristics had developed in all except the women with TM. Groups 1 and 2 had never menstruated and group 3 had been amenorrhoeic for 6 months to 3 years. The control group was studied during the follicular phase of the cycle. None of the patients were taking oestrogens at the time of observation. Plasma concentrations were determined for 17 beta-oestradiol (E2), deidroepiandrosterone sulphate (DHEA-S), cortisol (F), prolactin (PRL), thyroid hormones (T3 and T4), and gonadotrophins (LH and FSH). Spinal bone mineral density (BMD g/cm2) was assessed by dual photon absorbiometry. BMD (mean +/- 1SD) was reduced in the patients (group 2: 0.920 +/- 0.95; group 1: 0.980 +/- 0.94; and group 3: 1.037 +/- 0.75) as compared with the controls (1.290 +/- 0.95) (P less than 0.01). In the three groups of patients, plasma E2 levels were lower than 50 pg/ml and were positively correlated with the BMD. As expected, plasma gonadotrophin levels were highly and significantly reduced (P less than 0.01) in the patients, compared with that of the controls. These results suggest that reduced spinal BMD in hypogonadic women may be related to the lack of oestrogenic influence on bone metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)