Acute effects of an oral calcium load on markers of bone metabolism during endurance cycling exercise in male athletes.

Although sport and physical activity are generally considered as positive factors for bone metabolism some endurance trainings such as running and bicycling have few or no beneficial or even deleterious effects on bone mineral density. The present study was designed to investigate the acute effect of an intensive endurance cycling exercise on biochemical bone markers. Furthermore, the effect of the oral intake of 1 g calcium load, by drinking high-calcium mineral water, just prior to and during the exercise was checked. Twelve well-trained elite male triathletes aged 23-37 years were explored. The serum concentrations of calcium, phosphate, PTH, bone alkaline phosphatase (BALP) and C-terminal cross-linking telopeptide of type 1 collagen (CTX) were measured before, during and after a 60 min 80% VO2max cycle ergometer exercise. Since cycling exercise was accompanied by a reduction in plasma volume the total amount of biochemical bone markers was calculated. When the exercise was performed without calcium load both serum concentrations and total amount of CTX began to increase progressively 30 min after the start of the exercise and were still significantly elevated, by 45-50%, 2h after the end of the exercise. Ingestion of high-calcium mineral water completely suppressed the CTX response. By contrast serum concentrations and total amount of BALP fluctuated and showed no significant difference with or without calcium load. The present study demonstrates that the burst of osteoclastic activity acutely induced by an endurance cycling exercise can be suppressed by the previous intake of a calcium load afforded by drinking high-calcium mineral water.

Wintertime vitamin D deficiency in male adolescents: effect on parathyroid function and response to vitamin D3 supplements.

The first part of this study consisted of an 18 month follow-up of the vitamin D status and parathyroid function in a group of 54 French male adolescents, aged from 13 to 16 years old and all pupils of a jockey training school. During the 18 month period four samplings were made, one every 6 months. The first was during September of the first year, the second and third during March and October of the second year, and the last in March of the third year. Therefore we had two main periods: summer and winter. The summer 25-hydroxyvitamin D (25(OH)D) concentrations were higher (71.6 +/- 19.9 and 52.4 +/- 16.5 nmol/l) than the winter ones (20.4 +/- 6.9 and 21.4 +/- 6.1 nmol/l). Conversely, the winter intact parathyroid hormone (iPTH) serum levels (4.18 +/- 1.18 and 4.11 +/- 1.35 pmol/l) were higher than the summer ones (2.44 +/- 0.82 and 2.71 +/- 0.71 pmol/l). At the two winter time points the 25(OH)D concentrations were lower than 25 nmol/l (10 ng/ml) in 72% (2nd year) and 68% (3rd year) of the adolescents. In the second part of the study we tried a vitamin D3 supplementation procedure designed to maintain the 25(OH)D and iPTH postsummer serum levels throughout the winter. Pairs of male adolescents matched for height, weight and Tanner pubertal stage were randomly assigned to either vitamin D3 supplementation (2.5 mg, i.e., 100,000 IU) administered orally at three specific periods (end of September, November and January) or no vitamin D3 treatment (control subjects). Blood was collected just before the first intake of vitamin D3 and 2 months after the last intake (March). The control subjects had blood drawn at the same time points. In the vitamin D3-treated subjects, the concentrations of 25 (OH)D (55.3 +/- 11.5 nmol/l) and of iPTH (3.09 +/- 1.16 pmol/l) in March and September (53.8 +/- 12.3 nmol/l and 2.75 +/- 1.26 pmol/l) were not significantly different. In the control subjects, March 25(OH)D levels (21.0 +/- nmol/l were low, with values below 25 nmol/l in 78% of subjects, and iPTH concentrations (3.97 +/- 1.08 pmol/l) were significantly (p<0.001) higher than in September (2.91 +/- 0.81 pmol/l). The constant vitamin D wintertime deficiency and wintertime rise in iPTH in adolescent French males throughout puberty has been demonstrated. In adolescents with low dairy calcium intakes, the vitamin D3 treatment was sufficient to maintain 25(OH)D concentrations at their summer levels throughout winter and to prevent an excessive wintertime rise in iPTH levels.

Mineral water as a source of dietary calcium: acute effects on parathyroid function and bone resorption in young men.

BACKGROUND: Calcium is a major component of mineralized tissues and is required for normal growth and maintenance of bone. Epidemiologic studies showed that a large percentage of the population fails to meet the currently recommended guidelines for optimal calcium intake. OBJECTIVE: The present study was designed to determine whether high-calcium mineral water is an efficient additional source of dietary calcium. DESIGN: Twelve healthy young men (mean +/- SD age: 21.1 +/- 1.2 y) ingested in a randomized order either 0.5 L of a mineral water containing 344 mg Ca/L or 0.5 L of a mineral water with a very low concentration of calcium (<10 mg/L) as a control. Blood samples were drawn before and 1, 2, 3, and 4 h after intake of the water. Urine was collected for 2 h before and every 2 h for 4 h after ingestion of the water. Serum concentrations of intact parathyroid hormone (iPTH) and serum concentrations and urinary excretion of a recently developed biochemical marker of bone resorption, type 1 collagen cross-linked C-telopeptide (CTx), were measured. RESULTS: Serum iPTH was significantly (P < 0.002) lower after ingestion of high-calcium water than after ingestion of the control. There was a significant (P = 0.01) progressive decrease in urinary CTx after ingestion of the high-calcium water, whereas after ingestion of low-calcium water the changes were modest and not significant. The fall in serum CTx concentrations was 34.7% 3 h after ingestion of high-calcium water, compared with 17.6% with the control. The decreases in serum CTx concentrations were significantly (P < 0.05) lower 1, 2, 3, and 4 h after ingestion of high-calcium water than after ingestion of the control. CONCLUSION: The present study showed that one oral intake of water containing a very moderate dose of calcium (172 mg) acutely inhibited iPTH secretion and bone resorption.

Acute effects of oral calcium load on parathyroid function and on bone resorption in young men.

AIM: The aim of the present study was to check whether a calcium oral load was able to inhibit bone resorption as assessed by urinary excretion of a new bone marker, type 1 collagen cross-linked C-telopeptide (CrossLaps(TM)), in healthy young male adults. METHODS: Twenty healthy young male adults (age 22 +/- 2 years) were studied. In one series of assays, an oral calcium load of 1 g of elemental calcium as calcium citrate dissolved in 200 ml of low-calcium water was ingested, while in another series of assays the subjects ingested 200 ml of water alone. Blood samples were collected before and 1, 2, 3 and 4 h after the intake of calcium. Urine was collected at 2-hour intervals, i.e. before and for 4 h after the intake of calcium. Serum ionized calcium, phosphate and intact parathormone (iPTH) were measured at each time point. Urinary calcium, phosphate, creatinine and CrossLaps (as a ratio to creatinine) were measured in each urine sample. RESULTS: Calcium intake was associated with very significant (ANOVA, p < 0.001) increases in serum ionized calcium and decreases in PTH. After calcium intake, measurements of urinary CrossLaps showed a progressive statistically significant (ANOVA, p < 0.001) decrease (-20% at 2 h and -55% at 4 h), whereas after ingestion of water, the changes were modest and not statistically significant. CONCLUSIONS: The present results show that bone resorption as assessed by urinary excretion of CrossLaps can be significantly suppressed by the ingestion of a 1-gram calcium load and attest that calcium supplementation has an acute effect on bone metabolism.

Vitamin D status during puberty in French healthy male adolescents.

The vitamin D status was determined on one to four occasions either after summer (September-October) or after winter (March-April) in 175 male adolescents (13-17 years), resulting in 394 measurements of serum 25-hydroxyvitamin D (25(OH)D) and intact parathyroid hormone (iPTH). The subjects lived in a rural area to the north of Paris (49 degrees N). After summer the 25(OH)D concentration was 58.5 +/- 18.0 nmol/l (mean +/- SD), while after winter it had fallen to 20.6 +/-6.0 nmol/l (p = 0.0001). Meanwhile the iPTH concentration was 2.76 +/- 0.97 pmol/l (mean +/- SD) after summer and increased to 4.20 +/- 1.21 pmol/l after winter (p = 0. 0001). All the results were pooled and a nonlinear population model with random parameters was used to describe the relationship between serum iPTH and 25(OH)D. When the concentration of 25(OH)D was higher than 83 nmol/l, an iPTH mean 'plateau' level at 2.48 pmol/l was reached. When 25(OH)D concentrations fell below 83 nmol/l, the increase in iPTH concentration accelerates, and when the mean 25(OH)D concentration was equal to or lower than 10 nmol/l the mean iPTH level (4.97 pmol/l) was twice as high as the 'plateau' value.

[Vitamin D status in the adolescent: seasonal variations and effects of winter supplementation with vitamin D3]. / Statut vitaminique D de l'adolescent: variations saisonnières et effets d'une supplémentation hivernale par la vitamine D3.

BACKGROUND: Recently, 25 hydroxyvitamin D (25 OHD) blood concentrations measured in adolescents during or at the end of winter were found very low. A concomitant stimulation of parathyroid function was observed. The aim of the present study was to test the biological effects of a treatment with vitamin D3 during winter. POPULATIONS AND METHODS: The effects of vitamin D3 supplementation (100,000 IU, twice, at the end of November and of January) were assessed in 24 male Caucasian adolescents (mean age +/- SD: 14 y 6 m +/- 9 m). They were pupils in a lad-jockeys training center located in the countryside near Chantilly (49 degrees northern latitude). Blood concentrations of 25 OHD, calcium and intact parathormone (PTH) were measured three times: before each oral intake of vitamin D3 and 2 months after the last intake (March). A group of 32 male adolescents (mean age +/- SD: 14 y 9 m +/- 6 m), pupils in the same center, receiving no vitamin D and sampled in November and in March, served as controls. RESULTS: In March, mean concentrations of 25 OHD (8.36 +/- 2.73 micrograms/L) were very low in vitamin D-not supplemented adolescents since 34% had levels less than 6 micrograms/L. In March, PTH concentrations (40.5 +/- 12.2 ng/L) were significantly (P = 0.0001) higher than in November (28.8 +/- 9.9 ng/L). In boys receiving vitamin D3 25 OHD serum concentrations measured in January (17.5 +/- 3.2 micrograms/L) and in March (18.7 +/- 4.0 micrograms/L) remained at a level not very different from that measured in November (16.6 +/- 3.8 micrograms/L). During the same period, calcium and PTH concentrations (32.2 +/- 11.7 ng/L in November; 32.4 +/- 14.3 in January and 32.9 +/- 13.5 ng/L in March) remained at their basal level as well. CONCLUSIONS: The observation that, after winter, a relatively large number of adolescents presented low concentrations of 25 OHD suggests that, during winter, usual dietary intakes and/or vitamin D stores are not sufficient to provide for their needs. Administration of two oral doses of 100,000 IU of vitamin D3 could maintain the vitamin D status at its initial level. The efficiency of such a prophylactic treatment is also assessed by its effect on parathyroid function.

Blunted 5-HT1A-receptor agonist-induced corticotropin and cortisol responses after long-term ipsapirone and fluoxetine administration to healthy subjects.

OBJECTIVES: To assess whether acute 5-hydroxytryptamine-1A (5-HT1A)-receptor-mediated corticotropin, cortisol, and temperature responses are maintained after 3 weeks of treatment with controlled-release (CR) ipsapirone and fluoxetine compared with placebo and whether changes are reversible after cessation of treatment. METHODS: This was a randomized parallel-group study. Ten healthy subjects received ipsapirone CR or fluoxetine, and eight received placebo in a double-blind manner. An ipsapirone challenge test with 20 mg ipsapirone immediate-release formulation (IR) was performed before treatment (day 0) and after 20 days of treatment with placebo, 80 mg/day ipsapirone CR, or 20 mg/day fluoxetine (day 21). From day 22 to day 34 all subjects received placebo in a simple-blind manner. A third ipsapirone challenge test was performed on day 35. RESULTS: Before treatment, resting plasma corticotropin and cortisol concentrations and increases in plasma corticotropin and cortisol concentrations after challenge with 20 mg ipsapirone IR were similar for the three groups. After 20 days of treatment, plasma corticotropin and cortisol concentrations were similar before challenge, but ipsapirone IR-induced increases in plasma corticotropin and cortisol concentrations were significantly lower in both the ipsapirone CR group (corticotropin, 6.5 +/- 2 pg/ml; cortisol, 1.5 +/- 0.7 micrograms/dl) and fluoxetine group (corticotropin 4.4 +/- 2 pg/ml; cortisol 1.5 +/- 0.7 micrograms/dl) compared with placebo (corticotropin, 34 +/- 14 pg/ml; cortisol, 5.8 +/- 2 micrograms/dl, mean +/- SEM). After 2 weeks of placebo administration, plasma corticotropin and cortisol responses to ipsapirone IR again became identical in all three groups. Plasma ipsapirone concentrations were similar in all groups during each challenge. The hypothermic response to ipsapirone IR showed no difference before treatment, at the end of the treatment period, or 2 weeks after cessation of treatment. Long-term administration of antidepressants to the healthy subjects did not lead to any serious adverse effects. CONCLUSIONS: Long-term administration of fluoxetine and ipsapirone did not influence resting plasma corticotropin and cortisol concentrations in the morning. Stimulation of corticotropin and cortisol release by a selective 5-HT1A-agonist is reduced with long-term administration of these serotoninergic antidepressants. This subsensitivity of postsynaptic 5-HT1A-receptors is reversible.

Bone assessment in patients with ileal pouch-anal anastomosis for inflammatory bowel disease.

BACKGROUND: Patients with ulcerative colitis are at risk of low bone mineral density (BMD). Proctocolectomy with ileal pouch-anal anastomosis (IPAA) for ulcerative colitis diminishes the risk of bone disease. The aims of this study were to assess the mechanism of low BMD and to measure bone density changes after IPAA. METHODS: Twenty patients with IPAA for ulcerative colitis, of mean(s.d.) age 38(9) (range 21-58) years, had measurements of lumbar spine and femoral neck BMD by dual energy X-ray absorptiometry, a mean(s.d.) 28(23) (range 3-84) months after proctocolectomy. Serum levels of calcium, phosphate, parathyroid hormone, osteocalcin and 25-hydroxy vitamin D were determined. Fifteen patients were followed for 28(12) (range 8-50) months. RESULTS: At baseline, six patients had spine BMD more than two standard deviations below the normal value, and three had vertebral crush fractures. Mean vitamin D values were normal and no patient had osteomalacia. BMD increased with time elapsed since IPAA (spine: r = 0.71, P = 0.005). During follow-up, mean(s.d.) changes in bone density were +2.3(3.8) and +2.1(5.6) per cent per year at the spine and femoral neck respectively. CONCLUSION: These results suggest that in patients with IPAA for ulcerative colitis, low BMD is not associated with vitamin D malabsorption and may be reversible after surgery.

Acute PTH response to oral calcium load and seasonal variation of vitamin D status in healthy young adult subjects.

OBJECTIVE: The aim of the present study was to check the relationship between seasonal variations of vitamin D status and parathyroid function explored both in basal conditions and after oral calcium load. DESIGN: The calcium and parathyroid hormone response to the intake of calcium load was studied at two different seasons, before winter (November) and after winter (March-April), corresponding to different vitamin D status. SUBJECTS: Eighteen healthy young male adults (age: 25 +/- 3 y) were studied. All were medical students who were selected as having no disorders known to affect calcium metabolism. INTERVENTION: At each period an oral calcium load (1 g of elemental calcium as calcium carbonate) was administered. Blood samples were collected before and 1 h, 2 h, 3 h and 4 h after the intake of calcium. Serum ionized calcium (Ca2+) and intact parathormone (PTH1-84) were measured at each time point and 25-hydroxyvitamin D (25(OH)D) was measured before each calcium test. RESULTS: After winter, basal 25(OH)D concentrations were decreased (from 16.4 +/- 6.6 to 11.5 +/- 4.4 micrograms/l) and basal PTH concentrations were increased (from 24.1 +/- 6.5 to 31.7 +/- 9.1 pg/ ml), and the difference between pre- and post-winter basal concentrations were statistically significant for both variables (P < 0.001). A statistically significant negative correlation between PTH and 25(OH)D was obtained both before (r = -0.63; P = 0.005) and after (r = -0.64; P = 0.004) winter. The maximum decrement in PTH (delta PTHmax) was not different before (13.92 +/- 4.58 pg/ml) and after (14.14 +/- 7.79 pg/ml) winter, but as a consequence of post-winter higher basal levels of PTH, at all time points after oral calcium load, concentrations of PTH after winter were significantly higher than before. CONCLUSIONS: The present results show that PTH concentrations are physiologically linked to 25(OH)D concentrations, and emphasize the need of taking into account the vitamin D status of each subject to predict the effect of an oral calcium load on absolute concentrations of PTH.

Vitamin D-dependent seasonal variation of PTH in growing male adolescents.

Twenty-eight young male adolescents (age from 13 years 6 months to 15 years 9 months) from a horseback-riding school were studied. They were studied at the end of summer (September of 1993) and, six months later, at the end of winter (March of 1994). At each timepoint their height and weight were measured and their pubertal status determined. Blood was collected and 25-hydroxyvitamin D [25(OH)D], intact parathyroid hormone (PTH1-84), and 1,25-dihydroxy-vitamin D [1,25(OH)2D] were measured. After winter, weight and height had increased by a mean of 2.9 +/- 1.3 kg and of 3.3 +/- 1.2 cm, respectively. 25(OH)D concentrations which were 29.96 +/- 7.46 micrograms/L in September had significantly (p = 0.0001) fallen by a mean of 23.31 +/- 6.6 micrograms/L in March (6.61 +/- 2.04 micrograms/L). March and September concentrations of 25(OH)D were significantly correlated (r = 0.536, p = 0.0039). March values were negatively correlated with the pubertal status (r = 0.41; p = 0.03). In the meantime, PTH had significantly (p = 0.0001) increased by a mean of 8.59 +/- 8.53 ng/L (22.8 +/- 7.44 ng/L in September vs. 30.33 +/- 8.05 ng/L in March). A statistically significant correlation between PTH and 25(OH)D concentrations (r = 0.493; p = 0.0001) was obtained. Serum 1,25(OH)2D concentrations measured in September (37.7 +/- 12.94 ng/L) and in March (38.2 +/- 7.8 ng/L) were not different. March values were positively correlated with pubertal status (r = 0.49; p = 0.008). Modulation of PTH secretion by vitamin D appears to be a physiological mechanism occurring during adolescence. In spite of a marked depletion of vitamin D stores after winter, PTH values remained within normal range. Nevertheless, we cannot exclude that a more prolonged vitamin D deficiency could adversely affect bone metabolism during this critical period of life characterized by an increased need of vitamin D.

Bone loss in patients with inflammatory bowel disease: a prospective study.

To assess the rate of bone loss in patients with inflammatory bowel disease, we prospectively studied 35 patients (17 women) aged 36 +/- 13 (range 17-60) years, 14 of whom had Crohn's disease and 21 with ulcerative colitis (including 12 with ileoanal anastomosis). Bone mineral density was measured by dual-energy X-ray absorptiometry at the lumbar spine and femoral neck. The follow-up was 19 +/- 8 months. During this period, 14 patients received oral steroids. Lumbar bone density changes expressed as a percentage per year were -3.1 +/- 4.9%, -6.4 +/- 7.5% and +2.0 +/- 4.0% in Crohn's disease and ulcerative colitis without and with ileoanal anastomosis respectively (p = 0.007). The same pattern was observed at the femoral neck. Mean annual lumbar bone density changes were -6.2 +/- 7.0% and +0.9 +/- 3.9% in patients with and without steroids during follow-up (p = 0.002). We conclude that patients with inflammatory bowel disease are at risk of lumbar and femoral bone loss. However, bone loss is not observed in patients with ileoanal anastomosis.

Beta-adrenoceptor agonists do not stimulate daytime melatonin secretion in healthy subjects. A double blind placebo controlled study.

Noradrenergic stimulation of pineal beta-adrenoceptors results in melatonin secretion. To investigate beta-adrenoceptor mediated plasma melatonin responses in humans, ritodrine, salbutamol (beta 2-adrenoceptor agonists) and dobutamine (beta 1-adrenoceptor agonist) were infused from 0900 to 1200 h to 8 healthy subjects (four men and four women) in a double blind, crossover, placebo controlled study. Ritodrine and salbutamol significantly increased plasma cyclic AMP and decreased serum potassium concentrations indicating the presence of beta 2-adrenoceptor stimulation. Dobutamine substantially increased systolic blood pressure corresponding to its beta 1-adrenoceptor agonist propriety. However, neither beta 2- nor beta 1-adrenoceptor stimulation modified plasma melatonin concentration. These results show that beta-adrenoceptor agonists do not increase daytime plasma melatonin concentration.

Metabolic bone assessment in patients with inflammatory bowel disease.

BACKGROUND/AIMS: Patients with inflammatory bowel disease are at risk for osteopenia. To study the metabolic bone status of these patients, a cross-sectional study was conducted. METHODS: Eighty-four patients (49 women, 35 men) with inflammatory bowel disease, 34 of whom had Crohn's disease and 50 ulcerative colitis (including 18 with prior coloproctectomy and ileoanal anastomosis), underwent clinical, dietary, and spine radiological assessments. Bone metabolism was assessed by measuring serum levels of calcium, phosphate, parathyroid hormone (1-84), 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and osteocalcin. Lumbar and femoral neck bone mineral densities were measured by dual energy X-ray absorptiometry. RESULTS: Serum osteocalcin level was decreased in 29 patients (34%), 12 of whom had never undergone steroid therapy. The other biochemical markers of bone metabolism were in the normal range. Thirty-six patients (43%) had osteopenia, and 6 patients (7%) had vertebral crush fractures. Osteopenia was observed in 27 patients (52%) and 9 patients (28%) with and without corticosteroid therapy, respectively. No patient had clinical or biological signs of osteomalacia. Analysis of bone density (lumbar Z score) by a multiple regression analysis showed a statistically significant correlation with age, cumulative corticosteroid doses, sedimentation rate, and osteocalcin level (R2 = 0.76; P = 0.05). CONCLUSIONS: The results suggest that bone turnover in inflammatory bowel disease is characterized by low bone formation in the presence of normal levels of calcium-regulating hormones.

Age-related effect of a single oral dose of calcium on parathyroid function: relationship with vitamin D status.

The parathyroid response to the administration of a single oral dose of 0.5 g Cal was studied in 71 normal subjects of both sexes (34 males, 37 females) aged 20-88 y. Serum 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] were measured before the intake of calcium. Serum ionized calcium (Ca++) and intact parathormone (PTH1-84) were measured before and 1, 2, and 3 h after the intake of calcium. The Ca++ maximal response (delta Ca++max), which significantly decreased with age (P = 0.0001), was correlated with both 25(OH)D (r = 0.375, P < 0.01) and 1,25(OH)2D (r = 0.284, P < 0.02). The maximal PTH1-84 suppressive response expressed as a function of basal values (delta PTH%) decreased with age. Basal PTH1-84 values were significantly increased with age (P = 0.0002) and were negatively correlated with 25(OH)D concentrations (r = 0.414, P < 0.002) which were low in elderly people. These results suggest that correction of vitamin D deficiency should improve delta Ca++max, lower basal PTH1-84, and consequently make the oral intake of calcium more efficient to decrease PTH1-84 concentrations.

Biologic, histologic and densitometric effects of oral risedronate on bone in patients with multiple myeloma.

Recent studies have shown that treatment with bisphosphonates could be effective against the myelomatous skeletal deterioration. However, the mechanisms of action of these drugs in multiple myeloma (MM) have been poorly studied. In the present study, 11 patients with MM and bone lesions were treated orally with 30 mg/day of risedronate for 6 months, and monitored for 6 additional months. Mean serum calcium decreased from day 4, with a concomitant increase in circulating levels of PTH (1-84) and 1,25-(OH)2D. These parameters reached their nadir on day 7 and returned to baseline value during the treatment period. Markers of bone resorption, pyridinoline and deoxypyridinoline decreased from day 7; they were at 50% and 78% of their basal value at the end of treatment and follow-up periods, respectively. A significant reduction of estimates of bone formation (serum alkaline phosphatase and osteoclacin) appeared at month 3 and persisted for the remainder of the 9-month period. Histomorphometric analysis showed a significant reduction of activation frequency, number of osteoclasts and erosion depth. Bone turnover was high at baseline, and normal after treatment, without mineralisation defects. Mean wall thickness was not different before and after treatment. Spinal bone mineral density measured by dual energy X-ray absorptiometry increased (5.3%) at the end of treatment. We conclude that oral risedronate in multiple myeloma induces a noticeable and rapid inhibition of bone resorption.

Comparison of the suppressive effect of two doses (500 mg vs 1500 mg) of oral calcium on parathyroid hormone secretion and on urinary cyclic AMP.

The respective effects of the ingestion of two different doses of calcium (500 and 1500 mg) on serum ionized calcium, intact parathyroid hormone (PTH 1-84), and the urinary excretion of 3',5'-cyclic adenosine monophosphate (cyclic AMP) were evaluated in 15 young male adults. Ionized serum calcium and PTH 1-84 were measured before and 1 hour, 2 hours and 3 hours (P1, P2, and P3) after the oral intake of calcium. Cyclic AMP was measured in 2-hour urine samples collected before and during 4 hours after the ingestion of calcium. Similar increments in serum ionized calcium (delta Ca2+) were observed except at P3 where the delta Ca2+ was significantly (P < 0.02) higher after 1500 mg (0.088 mmol/liter) than after 500 mg of (0.062 mmol/liter). In the same way, the comparison of the PTH 1-84 concentrations showed no statistical difference except at P3 (P < 0.002). When expressed as a percentage of P0, the P1 and P2 PTH 1-84 values were more suppressed after 1500 mg than after 500 mg of calcium (P1: -69% vs -59%; P < 0.02; P2: -66% vs -50%; P < 0.02). However, the simultaneous cyclic AMP responses (-24% vs -19%) were not significantly different. The results show that the respective maximal effects on PTH secretion and on urinary cyclic AMP of two very different oral doses of calcium are only slightly different.