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In 45 women with Colles' fracture, two types of complementary medical treatment (calcitonin with calcium [SCT+Ca] and calcium alone [Ca]) were compared with placebo. Consecutive patients were assigned randomly to one of the three study groups at the time of inclusion in the study: 15 women (68.6 +/- 5.7 years) were given 100 IU/day I.M. of SCT plus 1200 mg of elemental Ca for 10 successive days each month; 15 women (71.7 +/- 6.1 years) were given only 1200 mg of elemental Ca for 10 days each month; and 15 women (66.9 +/- 7. 9 years) were treated with placebo. Biochemical and radiogrammetric studies were made at baseline and after 1 year of treatment. In the SCT+Ca group tartrate-resistant acid phosphatase decreased (Wilcoxon test, P = 0.014) and the metacarpal index and the cortical and total area (CA/TA) ratio increased (both P = 0.001). In the group treated with Ca alone, no changes were observed. In the placebo group, the metacarpal index and CA/TA decreased (P = 0.015 and P = 0.007, respectively). Ca alone, at the dosage used here, inhibited bone loss after Colles' fracture. The addition of SCT to Ca administration not only impeded bone loss but significantly increased cortical bone mass.

Objective: To evaluate three different therapeutic regimens for the prevention of osteoporosis in natural and surgical postmenopausal women who had been found to have rapid bone loss in analytical studies., Methods: A total of 104 naturally or surgically postmenopausal women were studied, and subsequently followed-up during 1 year for avoidance of the influence of seasonal variation on bone mass, a factor overlooked in several studies. They were randomized into four groups of 26 patients each: the untreated control group (mean age 50 +/- 5 years); the hormonal replacement treatment (HRT) group (mean age 48 +/- 6 years), which was treated for 24 days each month with transdermal 17 beta-estradiol, 50 mg/day, together with medroxiprogesterone, 10 mg during 12 days; the calcium group (mean age 50 +/- 4 years), which was treated with elemental calcium, 1 g/day; and the calcitonin group (mean age 50 +/- 5 years), which was treated for 10 days each month with eel calcitonin, 40 IU/day and with elemental calcium, 500 mg/day. Full-body bone densitometry, for measuring total body bone mineral content (TBBMC), was carried out in all the women at baseline and 1 year. TBBMC was corrected for body weight by dividing its value by body weight (TBBMC/W)., Results: After 1 year TBBMC/W was lower in every group: -2.14% (P < 0.001) in the control group; -0.14% (P = NS) in the HRT group (P < 0.05 vs. controls); -0.18% (P = NS) in the calcium group (P < 0.05 vs. controls); and -0.06% (P = NS) in the calcitonin group (P < 0.01 vs. controls; P < 0.05 vs. calcium and HRT)., Conclusions: These findings show that all three treatments are effective in the prevention of postmenopausal loss of bone mass.

The effect of thiazides on total body bone mineral content and axial (trunk) and peripheral (arms) bone mass was evaluated. First, dual-energy X-ray absorptiometry was used to study bone mass in 24 patients with idiopathic hypercalciuria and in 22 healthy subjects. Next, the patients were randomized into a group of 14 patients treated with chlorthalidone (50 mg/day) and a group of 10 untreated patients who served as controls; in these two groups biochemical and bone mass studies were repeated 1 year later. Compared with healthy controls, patients with idiopathic hypercalciuria had less bone mass in total body (p < 0.02), arms (p < 0.001), and trunk (p < 0.05). After 1 year, the group of patients treated with thiazides manifested an increase of bone mass in total body (p < 0.0045), arms, and trunk (p < 0.0001) and a decrease in 24-hour calciuria, urinary calcium/creatinine ratio, and serum tartrate resistant acid phosphatase concentration; the untreated group of patients lost bone mass in all three sites. Under baseline conditions, the groups of treated and untreated patients exhibited a negative linear regression between total body bone mass and both urinary calcium/creatinine (r2 = 0.234; p < 0.001) and serum tartrate resistant acid phosphatase concentration (r2 = 0.399; p < 0.0001). Our results confirm the favorable effect of thiazides on bone mass and provide evidence of enhanced bone remodeling in idiopathic hypercalciuria.

This report was motivated by the finding that calciotropic hormones, except parathormone (PTH), do not show any response to 1a(OH)D3 therapy in psoriatic patients. These showed high basal whole PTH levels (127 +/- 38 pg/ml) which declined to 45 +/- 15 pg/ml after treatment (p less than 0.001) but did not correlate to calcemia values. Basal calcemia and calciuria were normal and rose with treatment (p less than 0.001 for both). Basal calcitonin and 25(OH)D3 were normal and did not change with treatment nor correlate to changes in calcemia. Due to the effect of 1-hydroxyvitamin D and calcemia on calcitonin and 25(OH)D, the lack of changes in the latter suggests a calciotropic hormone imbalance in psoriasis, which may be an etiologic factor in this entity.

Response to acute and chronic administration of calcitonin and calcium and of biphosphonates (EHDP) was evaluated in 14 patients with Paget's bone disease who were grouped on the basis of homogeneous disease activity, as appraised by bone involvement and alkaline phosphatase and hydroxyproline levels. At first, 100 MRC U of calcitonin followed 4 hours later by 500 mg of elemental calcium were given for 10 days; a significant (p less than 0.001; paired and unpaired Student t test) reduction in alkaline phosphatase (-25%) and hydroproline (-55%) was observed. Subsequently, 5 mg/kg/day of EHDP was given for 20 days. Both parameters increased to levels similar to basal values. These increases were significant (p less than 0.001 for the paired and unpaired Student test) compared with those obtained after calcitonin administration; alkaline phosphatase rose +27% and hydroxproline +135%. After this, patients were divided into 2 groups (A and B). Group A was treated with calcitonin and calcium, at the dosage indicated above, for 10 days a month during 6 months. Group B continued with the same protocol with the addition of EHDP for the 20 days during which calcitonin and calcium were not given. The results of 6 months of treatment showed that calcitonin was more active and suggested that EHDP diminishes hormonal effects. These results also demonstrate a short-term absence of EHDP activity.

It has been suggested that the intensity of hypocalcaemic response to the administration of calcitonin may reflect the degree of osteoclastic activity and thus the state of the parathyroid function. We have performed the calcitonin test in 14 healthy volunteers and in 17 patients with chronic renal failure undergoing haemodialysis. The test involved the intramuscular injection of 100 MRC units of synthetic salmon calcitonin, serum calcium being determined before and after 5 h of the injections of the hormone. In 7 of the patients, the test was repeated using intranasal administration by means of a spray of calcitonin. In renal patients, serum calcium fell from 9.73 +/- 0.76 to 7.88 +/- 1.01 mg/dl (1.85 +/- 0.67 mg/dl). In the control group, serum calcium fell from 9.51 +/- 0.56 to 8.89 +/- 0.34 mg/dl (0.62 +/- 0.35 mg/dl). The calcium fall in renal patients was significantly greater than in the control group (p less than 0.001). In patients there was a statistically significant correlation between the fall in serum calcium and the level of alkaline phosphatase, but no with the serum concentration of immunoreactive parathormone (C-Terminal). After intranasal calcitonin, serum calcium fell from 9.81 +/- 0.55 to 8.83 +/- 0.72 mg/dl (1.42 +/- 0.42 mg/dl), a reduction comparable to that obtained after the intramuscular injection of the hormone in the same patients (1.84 +/- 0.69 mg/dl). These results provide evidence of an increase in osteoclastic activity in chronic renal failure, perhaps reflecting parathyroid hyperfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Osteocalcin synthesis is dependent on the influence of the renal vitamin D metabolite, 1,25(OH)2D3. This metabolite is an etiological factor in some hypercalciurias, and osteocalcin may thus be a parameter for discovering them. In turn, parathormone, which stimulates 1,25(OH)2D3 synthesis, is also implicated in the hypercalciurias. Mean molecular parathormone, osteocalcin, 24-hour calciuria and the calcium/creatinine and hydroxyproline/creatinine ratios were determined in urine samples obtained after a 12-hour fast from 18 patients with absorptive hypercalciuria and 11 patients with renal hypercalciuria out of a total of 62 patients with renal lithiasis. No changes were observed in osteocalcin or parathormone, indicating that neither is valid for the diagnosis of hypercalciuria. Significant differences were only found in the Ca/Cr ratio (p less than 0.001), which was higher (0.31 +/- 0.07 vs. 0.13 +/- 0.04 mg/mg) in renal hypercalciuria than in absorptive hypercalciuria. No changes in osteocalcin have been reported in the hypercalciurias, but variations in parathormone have been reported, therefore requiring further study and thought to understand the processes involved.

OBJECTIVE: We investigated the controversial effects of coffee and other nutrients on bone mass.METHODS: In a study of 93 healthy postmenopausal women (mean ± standard deviation: 57.3 ± 7.1 y old and 8.9 ± 7.5 y since menopause) selected on the basis of not having changed their eating habits since premenopause, not smoking, not exercising, not receiving hormone-replacement therapy, and having a weight in the range of 70% to 130% of their ideal weights, amplitude-dependent speed of sound (Ad-SOS) was determined by quantitative bone ultrasound, and a prospective 7-d diet survey evaluated the intake of caffeine and nutrients involved in calcium metabolism. Women were stratified according to their caffeine, calcium, and vitamin D intakes and ratios of calcium to phosphorus and to protein. Ad-SOS differed only with vitamin D intake and was greater in the group taking at leasst 400 IU/d (P < 0.0001).RESULTS: In simple and multiple regression analyses, the only significant variable that affected Ad-SOS and nutrient intake was vitamin D (P < 0.0001). Phalangeal bone Ad-SOS was influenced only by the intake of vitamin D, not of caffeine or other nutrients.CONCLUSIONS: This lack of effect of caffeine and protein may be related to good nutritional intake or the low levels of caffeine consumed. [ABSTRACT FROM AUTHOR]

Objective: Longitudinal changes in bone mass were evaluated with use of ultrasonography and bone remodeling markers in 40 normal pregnant women in relation to their calcium intake.Study Design: The study took place at the University of Alcalá Hospital in Madrid. Biochemical markers of bone remodeling and ultrasonographic bone propagation velocity in the proximal phalanxes of fingers 2 to 5 were measured in all three trimesters of pregnancy. Wilcoxon, unpaired and paired t tests, and analysis of variance were used.Results: Ultrasonographic bone propagation velocity (meters per second) was lower in the second and third trimesters of pregnancy (p < 0.0001) compared with the respective preceding trimesters and in the third trimester in the overall group of pregnant women. Tartrate-resistant acid phosphatase and alkaline phosphatase levels increased significantly (p < 0.0001) in parallel with the ultrasonographic bone propagation velocity decrease.Conclusions: Gestation was accompanied by a reduction in ultrasonographic bone propagation velocity that was greater in women with low calcium intake. [ABSTRACT FROM AUTHOR]

Seventy-two postmenopausal osteoporotic women having more than one nontraumatic vertebral crush fracture were studied. Thirty-six of them, aged 68.8 +/- 1.2 years (18 +/- 4 YSM-years since menopause), were treated with 100 IU/day of salmon calcitonin i.m. plus 500 mg of elemental calcium for 10 days each month. The remaining 36 patients, aged 69.6 +/- 1.4 years (19 +/- 3 YSM), were given only 500 mg of elemental calcium for 10 days each month. All patients underwent clinical and analytical evaluation every 3 months. Radiological evaluation, assessment of vertebral deformities, and metacarpal radiogrammetry were done every 6 months. Densitometric measurements of total and regional bone mass were made every 12 months. At 24 months, the calcitonin group showed a 60% reduction in the number of new fractures and the group receiving only calcium had a 45% increase (P < 0.001). The incidence of vertebral fractures was 0.07 per patient-year in the group treated with calcitonin and 0.45 per patient-year in the group treated with calcium (P < 0.001). At 2 years, the calcitonin group showed a 12% increase in cortical bone mass on metacarpal radiogrammetry, a 16% increase in the axial skeleton on trunk densitometry, a 3.5% increase in total body bone mineral content, a 30.7% increase in pelvic bone mineral content, and a 6.2% increase in arm bone mineral content (all P < 0.001). In the group treated with calcium alone there was a loss of bone mass in every region. These findings suggest that salmon calcitonin is effective in the treatment of osteoporosis and show that it acts on cortical and trabecular bone. [ABSTRACT FROM AUTHOR]

Seventy-two eugonadal women, mean age 39 +/- 4 years, with a z score for total body bone mineral content (BMC) of less than -1.5 (mean -1.80 +/- 0.12) were selected from a previous screening study of normal values of total body and regional BMC in women using dual-energy X-ray absorptiometry. The women were distributed into two groups: 36 women undergoing treatment with 1 g/day of elemental calcium in the form of calcium pidolate and 36 women not treated. One year later, total body BMC, regional BMC in arms, legs and trunk, 24-hour urinary calcium excretion (Ca 24 hour), fasting urinary calcium/creatinine ratio, and serum tartrate-resistant acid phosphatase concentration were measured in both groups. There was a significant increase in total body and regional BMC (P < 0.001) in the group taking calcium pidolate. The increase was greater in arms and legs (2.5%) than in trunk (1.7%), being 2.6% for total body BMC. The z score increased from -1.81 +/- 0.13 to -1.52 +/- 0.12 (16%, P < 0.001). The corporal index did not change, and total body BMC corrected for fat-free body mass increased by 6.7% (P < 0.001). These changes were accompanied by an increase in 24-hour urinary calcium excretion and a decrease in urinary calcium/creatinine ratio and serum tartrate-resistant acid phosphatase concentration (P < 0.05 for all). There was a correlation between cumulative calcium dose at the end of treatment and gain in total body BMC (r2 = 0.925, P < 0.001). The untreated group showed no changes.(ABSTRACT TRUNCATED AT 250 WORDS) [ABSTRACT FROM AUTHOR]