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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of postprandial-like plasma insulin levels on intestinal calcium absorption (CaA) was studied in 9 healthy men. On separate occasions, they received either an i.v. infusion of 40 mU/m2 minute synthetic human insulin as well as a variable glucose infusion in order to clamp the plasma glucose at the baseline level (= glucose clamp), or insulin- and glucose-free vehicle infusions (= vehicle). During these infusions, an oral load containing 326 mg Ca in the form of Ca chloride was administered and CaA was determined thereafter with a 47Ca/85Sr double tracer method. During glucose clamp, mean plasma insulin was 172 +/- (1 SEM) 10 as compared to 6 +/- 1 microU/ml during vehicle infusions. During the clamp, 3-hour cumulative CaA rose significantly by 14% as compared to vehicle (39.2 +/- 2.5 vs. 34.4 +/- 2%, P less than 0.02). AT the same time, serum potassium and phosphorus dropped significantly, whereas serum parathyroid hormone (PTH) and 1,25(OH)2D levels were unchanged as compared to vehicle. The urinary excretions of potassium, sodium, and inorganic phosphorus, as well as the urinary specific activity of 47Ca, dropped significantly during glucose clamp, whereas the urinary excretion of cAMP was unchanged as compared to vehicle. The results suggest that, under the conditions of euglycemic hyperinsulinemic clamp, insulin stimulates CaA of healthy humans in a PTH- and 1,25(OH)2D-independent manner. Insulin may thus possibly be regarded as a factor participating in the regulation of CaA in humans.
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PMID:Intestinal calcium absorption during hyperinsulinemic euglycemic glucose clamp in healthy humans. 210 52

Bleeding complications in uraemia are not uncommon. The pathogenesis of haemorrhage in uraemia is still a matter of controversy and the pattern of bleeding suggests a defect of primary haemostasis. Platelet aggregation and biochemistry, including calcium levels, have been studied; however, the results are controversial. We have examined platelet aggregation, platelet-free calcium and calmodulin in platelet-rich plasma because of the significant role of calcium and calmodulin in regulating platelet and other cells' functions. Platelet aggregation in uraemic subjects was similar to that of controls. Platelet basal free cytosolic calcium and platelet calcium in response to 10 microM Ca++ ionophore A23187 in eight subjects with uraemia were 117 +/- 33 nM and 2025 +/- 398 nM (mean +/- SEM) respectively. By contrast in seven matched healthy controls basal calcium and ionophore-stimulated calcium values were 47 +/- 14 nM and 1354 +/- 414 nM, significantly less than in the patients with uraemia (P less than 0.05). The sensitivity of uraemic platelets to A23187 was similar to that of controls. Calmodulin activity in platelet-rich plasma of 12 subjects with uraemia showed no significant difference from that of controls [1.86 +/- 0.29 micrograms/ml (mean +/- SEM) and 2.0 +/- 0.37 micrograms/ml (mean +/- SEM) respectively]. We conclude that despite elevation of platelet calcium in uraemia, which may be due to a plasma factor such as parathyroid hormone, platelet aggregation is normal and bleeding in uraemia is more likely to be due to other factors, including the effect of reduced haematocrit on platelet endothelial interaction. Disturbances in platelet calcium cannot explain the bleeding manifestations in uraemia but warrant further investigation in order to identify the pathogenic mechanisms responsible.
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PMID:Elevated platelet-free calcium in uraemia. 211 Apr 66

We have studied calcium regulation in 11 consecutive patients undergoing radical surgery for upper aerodigestive tract malignancy. Eight patients received postoperative parenteral nutrition including calcium (19 mmol/day) and tri-iodothyronine (30 micrograms/day) supplementation. Three patients received enteral nutrition with calcium (70 mmol/day), 1.25 dihydroxycholecalciferol (1 microgram) and thyroxine (150 micrograms/day) via a nasogastric tube. Mean (SEM) corrected calcium fell from 2.42 (0.013) to 2.03 (0.036) mmol/l after 24 h (P less than 0.01). Replacement therapy generally maintained the serum calcium above 2.0 mmol/l. However, values were associated with only one episode of tetany. Phosphate increased from 1.10 (0.05) to 1.79 (0.11) mmol/l, 7-9 days postoperatively (P less than 0.001). Tubular calcium reabsorption fell and urinary calcium excretion rose, consistent with loss of parathyroid hormone (PTH) action on the distal nephron. However, the renal leak of calcium can be considerably reduced by concomitant salt depletion. This enhances proximal tubular sodium and calcium reabsorption thereby limiting calcium delivery to the distal nephron. This offsets the consequences of the loss of PTH which normally regulates distal calcium reabsorption.
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PMID:Maintenance of serum calcium after total thyroparathyroidectomy. 212 83

Synthetic human parathyroid hormone (1-34) (hPTH(1-34] infusion test has been utilized in the differential diagnosis of hypoparathyroidism by examining the incremental response of urinary phosphate and cyclic adenosine monophosphate (AMP). The response of plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) in parathyroid hormone (PTH) infusion test was studied as a new criterion for the differential diagnosis of idiopathic hypoparathyroidism (IHP) and pseudohypoparathyroidism (PHP). Fourteen patients with IHP, 4 patients with PHP, and five control subjects were studied. All subjects received an intravenous infusion of 30 micrograms hPTH(1-34) over 5 minutes. The basal levels of plasma 1,25(OH)2D in patients with IHP and PHP were significantly lower than those in control subjects, but there was no significant difference between the levels in patients with IHP and in patients with PHP. The plasma levels of 1,25(OH)2D increased after the infusion of hPTH(1-34) and reached a peak 6 to 24 hours afterward. The 1,25(OH)2D increase at 24 hours afterward the infusion (delta 1,25(OH)2D) in control subjects and in patients with IHP were 18.1 +/- 3.91 (mean +/- SEM) and 24.1 +/- 2.80 pg/ml, respectively. There was no significant increase in patients with PHP (delta 1,25(OH)2D = 4.9 +/- 1.97 pg/ml). From these results, the measurement of delta 1,25(OH)2D in hPTH(1-34) infusion test is useful as a criterion for the differential diagnosis of hypoparathyroidism.
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PMID:Response of plasma 1,25-dihydroxyvitamin D in the human PTH(1-34) infusion test: an improved index for the diagnosis of idiopathic hypoparathyroidism and pseudohypoparathyroidism. 215 33

1. To determine the relationships between parathyroid hormone activity and long-term sodium fluoride therapy in osteoporosis, cytochemical bioassays (for biologically active parathyroid hormone) were performed in 22 osteoporotic control patients and in 18 patients after 15 +/- 10 months of treatment (60 mg of sodium fluoride daily). Ten patients were studied longitudinally by repeated metabolic balances and were therefore common to both groups. All patients were receiving mineral supplements. 2. Cross-sectional data showed a fourfold mean increase in biologically active parathyroid hormone on fluoride treatment (P less than 0.005) together with a 51% increase in serum alkaline phosphatase (P less than 0.005). Longitudinal data showed, in addition, a significant increase in the calcium balance of 2.4 +/- 1.2 (SEM) mmol daily (P less than 0.05) and the development of a positive phosphorus balance (P less than 0.02). 3. Fluoride-treated patients were then analysed in two groups according to the level of biologically active parathyroid hormone. Thirty-two per cent of values were above the upper limit of normal (18 pg/ml). The mean serum alkaline phosphatase level in this group showed no elevation above that of the control patients, the overall rise being accounted for entirely by patients with normal levels of biologically active parathyroid hormone. High levels of biologically active parathyroid hormone were also associated with relative hypophosphataemia (P less than 0.01), relative hypercalciuria (P less than 0.05) and an increased urine/faecal calcium ratio (P less than 0.025). 4. Results show that long-term fluoride and calcium therapy increase biologically active parathyroid hormone in osteoporosis and that excessive parathyroid hormone activity may account for certain features of the refractory state.
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PMID:Fluoride therapy and parathyroid hormone activity in osteoporosis. 216 71

We studied the effects of estrogen on daylong circulating levels of calcium, inorganic phosphorus, parathyroid hormone (PTH), and 1,25-(OH)2D3 (calcitriol) in a group of 10 postmenopausal women (68.5 +/- 1.4 years, mean +/- SEM). The study was conducted under strict dietary control, with mean calcium and phosphorus intakes of 845 and 970 mg. After treatment with conjugated equine estrogens, 1.25 mg/day, for 1 month, significant decreases in fasting (0800 h) serum levels were observed for calcium (9.09 +/- 0.08 versus 9.46 +/- 0.10 mg/dl, p less than 0.01) and phosphorus (3.38 +/- 0.10 versus 3.73 +/- 0.08 mg/dl, p less than 0.01). On the 0800 h fasting specimen, midmolecule PTH concentrations were higher (44.0 +/- 7.9 versus 34 +/- 8.2 pg/ml, p less than 0.05), but intact PTH was unchanged (28.6 +/- 2.7 versus 29.1 +/- 1.7 pg/ml) and a rise in circulating calcitriol (39.8 +/- 4.3 versus 31.6 +/- 2.1 pg/ml) was marginally significant (p = 0.07). When data represented multiple samples averaged over 7 and 15 h, significant estrogen-related reductions in serum calcium and phosphorus concentrations were observed. In addition, estrogen was associated with a significant rise in the daylong (15 h) level of calcitriol (39.4 +/- 4 versus 30.5 +/- 2.4 pg/ml, p less than 0.01). Daylong mid- and intact PTH concentrations were unchanged on estrogen compared to baseline values. No significant correlations were observed between changes in fasting calcitriol level and changes in fasting concentrations of calcium, phosphorus, or PTH. Further, the rise in daylong calcitriol concentration did not correlate significantly with changes in fasting or integrated values of calcium or PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of estrogen on daylong circulating calcium, phosphorus, 1,25-dihydroxyvitamin D, and parathyroid hormone in postmenopausal women. 217 58

Mild hypercalcaemia associated with primary hyperparathyroidism has been increasingly recognized with the use of automated biochemical screening. Management is often difficult as symptoms are often absent or non-specific. Accordingly, we employed the hypocalcaemic effect of the diphosphonate APD to assess the effect of an acute fall in plasma calcium on indices of general well being, blood pressure, and vasoactive hormones in patients with mild primary hyperparathyroidism. Ten patients were studied in a randomized single blind, placebo-controlled cross-over study, using 30 mg APD intravenously or control saline infusion, over 2 h. Metabolic measurements, formal tests of muscle strength and cognitive function, and a standardized questionnaire were assessed 7 days after infusions. Albumin corrected plasma calcium was significantly lower (mean 2.49 +/- 0.04 SEM mmol/l) after APD when compared to control values (2.70 +/- 0.06 mmol/l, P less than 0.001). Twenty-four-hour urinary calcium, plasma magnesium and absolute monocyte count decreased significantly, whereas plasma parathyroid hormone increased after APD (P less than 0.05). There was no significant change in hypercalcaemic symptoms, muscle strength or cognitive function, and blood pressure, renin, aldosterone and atrial natriuretic peptide did not change. Side-effects, when they occurred, were mild. It is concluded that APD is a safe and effective means of lowering plasma calcium in mild primary hyperparathyroidism, but these acute reductions are associated with little or no improvement in clinical status in these patients.
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PMID:Aminopropylidine diphosphonate (APD) in mild primary hyperparathyroidism: effect on clinical status. 218 63

Cord clamping at birth leads to interruption of calcium (Ca) supply to the fetus. After birth, neonatal parathyroid hormone (PTH) secretion appears stimulated by hypocalcemia, with serum PTH increasing after birth and peaking at 24 hours of age. This rise in PTH presumably leads to bone resorption and Ca release. We theorize that bone formation may also be affected and that a serum marker of bone formation, serum osteocalcin (OC) concentrations, will decrease postnatally. OC is synthesized by osteoblasts and its serum concentrations are believed to reflect bone formation. We measured serum ionized Ca (iCa), PTH, and OC in cord blood and at 2 and 24 hours in 26 neonates born after uncomplicated pregnancies, labors, and deliveries. Serum iCa (mg/dl) decreased from 5.79 +/- 0.06 (cord, means +/- SEM) to 5.31 +/- 0.05 (2 hr), then to 4.89 +/- 0.05 (24 hr) (p less than 0.05). Serum PTH (microliter Eq/ml) increased from 35.9 +/- 4.3 (cord) to 41.7 +/- 4.0 (2 hr) (p = 0.1), and to 50.3 +/- 4.6 (24 hr) (p less than 0.01). Serum OC (ng/ml) decreased from 55.1 +/- 10.6 (cord), to 12.4 +/- 4.3 (2 hr) (p less than 0.01), then remained stable at 12.7 +/- 1.9 (24 hr). The change (cord minus 24 hr) in OC correlated inversely with the change in PTH over the first 24 hours of age (r = -0.42. p = 0.03). Therefore, there is a sudden decrease in an index of bone formation (i.e., serum OC) in the first 24 hours of life in which rising serum PTH may have had an impact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postnatal changes in serum osteocalcin and parathyroid hormone concentrations. 221 95

To determine if parathyroid hormone (PTH) is essential for lactation in rats, the parathyroid glands were removed surgically during the first week of lactation and the rats were given a diet containing a high calcium-phosphorus ratio to maintain a normal serum calcium concentration. Lactating rats were placed on diet containing 1.2% calcium (Ca) and 0.8, 0.6, or 0.4% phosphorus (P) on day 2 postpartum (PP) and were parathyroidectomized (PTX) at 4-6 days PP. At 10 days PP serum Ca was 10.5 +/- 0.2 mg/dl (mean +/- SEM) for PTX rats and 10.4 +/- 0.3 mg/dl in sham-operated lactating rats when the diet contained 0.6% P. When the diet P was 0.8%, the litters gained little or no weight and serum Ca fell to 6.9 +/- 0.6 mg/dl by day 10 PP in PTX rats compared with 10.2 +/- 0.2 mg/dl in sham rats. PTX rats fed the diet containing 1.2% Ca and 0.6% P maintained a normal serum Ca level until at least day 18 PP, but their serum P levels fell gradually from approximately 5 mg/dl at 10 days to 3 mg/dl at 18 days PP. In spite of this hypophosphatemia, the litters of PTX and sham rats had gained the same amount of weight by age 16 days, indicating equal milk production in the two groups. Milk Ca, P, and total solids were not significantly different between PTX and sham rats on day 11 PP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone is not required for normal milk composition or secretion or lactation-associated bone loss in normocalcemic rats. 230 81

Rheumatoid arthritis is associated with a generalised loss of bone mass. One of the factors that have been implicated in the pathogenesis of this bone loss is the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs). These drugs are known to increase gastrointestinal permeability and may thus influence the absorption of calcium; they may also influence glomerular filtration rate and the renal excretion of calcium; in addition, NSAIDs may inhibit osteoblast function as well as osteoclastic bone resorption. Calcium homeostasis was studied in eight healthy volunteers during eight days' treatment with 150 mg indomethacin daily. No changes in serum concentration of calcium, phosphorus, parathyroid hormone, 25-hydroxyvitamin D3, and 1,25-dihydroxyvitamin D3 were found. The creatinine clearance and the urinary excretion of phosphorus and sodium did not change, but a decrease in calcium excretion was noted (mean (SEM) calcium/creatinine excretion 0.52 (0.05) v 0.28 (0.06)). This decrease is probably due to renal retention of calcium. Whether this decrease of urinary calcium excretion has a positive or a negative effect on bone is presently unknown.
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PMID:Influence of indomethacin on extracellular calcium homeostasis. 231 15


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