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

Plasma immunoreactive parathyroid hormone (iPTH), 1,25(OH)2D3, calcium and phosphate and urinary creatinine, calcium and phosphate were measured before and following unilateral nephrectomy in six kidney donors. Unexpectedly, plasma calcium rose, from 2.27 +/- 0.02 mmol/l (mean +/- SEM) to 2.41 +/- 0.03 mmol/l on day 7 and to 2.37 +/- 0.02 mmol/l on day 30 (P less than 0.02). A parallel rise in iPTH occurred, from 0.61 +/- 0.16 ng/ml initially, to 1.83 +/- 0.54 ng/ml on day 7 (P less than 0.05) and to 1.18 +/- 0.18 on day 30 (P less than 0.01). The ratio of maximal tubular reabsorption of phosphate to GFR (TmP/GFR) fell by day 2 (P less than 0.01), remaining reduced on day 30 (P less than 0.05). The significance of elevated iPTH in renal insufficiency was further assessed by determining the time course of the disappearance of iPTH after parathyroidectomy in three haemodialysis subjects. Fifty per cent baseline iPTH level occurred after an average of 104.7 min, suggesting that the assay did not predominantly recognize C-terminal PTH fragments. By day 2, plasma 1,25(OH)2D3 had fallen from 34.3 +/- 4.5 pg/ml to 22.8 +/- 3.8 pg/ml (P less than 0.001), but by day 4 had regained its pre-nephrectomy value. Our results suggest that hypocalcaemia may not be the sole stimulus to parathyroid hormone secretion. It is speculated that reduction in circulating 1,25(OH)2D3 may be involved.
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PMID:Acute responses of parathyroid hormone and 1,25 dihydroxyvitamin D3 to unilateral nephrectomy in healthy donors. 311 Jun 74

Severe, prolonged hypocalcemia in observed in some, but not all, hemodialysis patients after parathyroidectomy performed because of uncontrolled hyperparathyroidism. The aim of the present study was to investigate whether calcitriol and calcium supplementation in the immediate period after parathyroidectomy (days 1-14) was of more help in the control of plasma calcium than calcium supplementation alone. Fourteen hemodialysis patients were enrolled in a prospective, randomized, double-blind and placebo-controlled study. From the day after parathyroidectomy, 7 patients received calcitriol and the remaining 7 a placebo using incremental doses adjusted to the degree of hypocalcemia (up to 4 micrograms/day for calcitriol). Plasma calcium, phosphorus, alkaline phosphatase and immunoreactive parathyroid hormone levels before parathyroidectomy were comparable in both patients groups, as was the lowest plasma calcium achieved after parathyroidectomy. The decrease in plasma calcium after parathyroidectomy was related to plasma alkaline phosphatase and to the number of osteoclasts and osteoblasts on bone biopsy surface before parathyroidectomy. The mean decrement of plasma calcium (days 3-9) as compared to that before parathyroidectomy was less pronounced in calcitriol-treated than in placebo-treated patients (0.25 +/- 0.06 versus 0.45 +/- 0.05 mM, mean +/- SEM, p less than 0.025). Treatment with placebo was interrupted before day 14 because of persistent severe hypocalcemia in 4 of 7 patients, whereas calcitriol treatment was continued in all 7 patients up to 14 days. Patients on calcitriol treatment required less mean calcium supplements (days 1-9) than patients receiving placebo (37.4 +/- 3.2 versus 49.4 +/- 3.7 g, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of calcitriol in the control of plasma calcium after parathyroidectomy. A placebo-controlled, double-blind study in chronic hemodialysis patients. 329 16

The effects of the Ca antagonist, verapamil, on the behaviour of parathyroid hormone was studied in normal and uraemic male Wistar rats. Parathyroidectomy was by cautery. Acute uraemia was induced by bilateral nephrectomy, and moderate uraemia by s.c. injection of gentamicin (200 mg/kg). Ethylendiamine tetracetic acid (50 mg/kg X d) was injected subcutaneously. Parathyroid hormone was determined by radioimmunoassay. The degree of uraemia was determined from plasma urea levels. Renal failure resulted in a significant increase in plasma parathyroid hormone (mean +/- SEM, ng/l) (84 +/- 6, n = 10, in the control; 277 +/- 39, n = 7, in the moderate uraemics and 667 +/- 128, n = 6, in the acute uraemics). Injection of verapamil significantly increased plasma levels of parathyroid hormone, ranging from 21% in the controls to 62% in the moderate uraemia group. In the acute uraemics, parathyroid hormone levels were very high and verapamil did not cause any further elevation of the hormone in the blood. Parathyroidectomy significantly lowered plasma parathyroid hormone, and verapamil resulted in a mean increase of 29%. EDTA caused an increase of 64%, compared with the control group.
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PMID:Effect of verapamil on plasma parathyroid hormone. 357 10

Magnesium (Mg) deficiency is a possible etiologic factor contributing to neonatal hypocalcemia. In adults, parathyroid hormone (PTH) secretion is negatively feedback regulated by acute changes in serum Mg concentration, but paradoxically Mg deficiency may lead to functional hypoparathyroidism and hypocalcemia. We hypothesized that in neonates, Mg administration will cause changes in PTH secretion and serum Ca concentration that will be inversely related to serum Mg status. We also hypothesized that Mg administration will result in increased calcitonin (CT) secretion. Thirty-nine newborn infants with birth weights greater than 1500 g were studied on day 3 of life. Ten received placebo, and 29 intravenous magnesium sulfate (MgSO4), 6 mg elemental Mg/kg body weight, over 1 h. Serum Mg, Ca, PTH, and CT were measured at time 0 (baseline, preinfusion) and 1, 2, 6, 12, 24, and 48 h postinfusion. In both groups combined, baseline PTH correlated with baseline Mg (r = 0.72, p less than 0.005), and with baseline Ca (r = 0.68, p less than 0.005). In the control group there was no change in serum Mg, Ca, PTH, and CT during the study period. In magnesium sulfate-infused infants: 1) serum Mg concentration rose from 1.80 +/- 0.06 to 2.82 +/- 0.07 mg/dl (mean +/- SEM, p less than 0.001); 2) the change from baseline in serum PTH at 1, 6, and 12 h postinfusion correlated inversely with baseline Mg (p less than 0.05); 3) the change from baseline in serum Ca at 1, 2, and 24 h postinfusion correlated inversely with baseline Mg (p less than 0.005); 4) serum CT remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of magnesium in neonatal calcium homeostasis: effects of magnesium infusion on calciotropic hormones and calcium. 365 52

This study was designed to follow the evolution of serum 1,25(OH)2D after surgery for primary hyperparathyroidism. Ten patients were studied before and for up to 85 d after removal of a single parathyroid adenoma. Blood and 24 h urine were obtained at various time points, for the measurement of serum or urinary phosphate and calcium indices. Before surgery, serum calcium (2.91 +/- 0.06 mmol/l; mean +/- SEM), parathyroid hormone (354 +/- 47 pg/ml) and 1,25(OH)2D (61.2 +/- 7.8 pg/ml) were elevated while serum phosphate (1.01 +/- 0.07 mmol/l) tended to be low. Relative hypoparathyroidism was evident for up to 5 d after surgery with the lowest value for serum parathyroid hormone (41 +/- 16 pg/ml) on day 1, serum calcium (2.12 +/- 0.06 mmol/l) on day 3 and highest value for serum phosphate (1.41 +/- 0.13 mmol/l) on day 5. As expected, serum 1,25(OH)2D levels decreased to 35.9 +/- 4.2 pg/ml 24 h after surgery. Stabilization of serum and urinary parameters to normal values was seen between day 5 and day 27; the only exception was serum 1,25(OH)2D, which increased again at day 27 to 57.6 +/- 5.0 pg/ml, a value as high as that before surgery. It was still elevated at day 50 (58.3 +/- 4.3 pg/ml), but returned towards normal values in three out of four patients (44 +/- 3.9 pg/ml) by day 80. No variation in 25(OH)D or 24,25(OH)2D was seen throughout the study. 1,25(OH)2D values could be related to serum parathyroid hormone values before surgery (r = 0.659, P less than 0.05) but not after. The secondary increase in serum 1,25(OH)2D could not be related to variations in serum calcium, phosphate, parathyroid hormone or diet. Further studies will be required to explain this phenomenon.
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PMID:Late increase in serum 1,25-dihydroxyvitamin D one month after surgery for adenomatous hyperparathyroidism. 375 58

Twenty patients with malignant hypercalcemia were treated with aminohydroxypropylidene bisphosphonate (AHPrBP, previously APD) a potent inhibitor of osteoclast-mediated bone resorption. To assess the efficacy of oral vs intravenous therapy, the patients were divided into two groups: group A received AHPrBP intravenously (30 mg/day), and group B received the drug orally (1200 mg/day) for 6 days. In both groups all the patients responded to AHPrBP with a rapid decrease in plasma calcium concentration after a mean time lag of 1 day. Within 9 days plasma calcium concentration fell from 3.42 +/- 0.13 (mean +/- SEM) to 2.26 +/- 0.13 mmol/l in group A and from 3.28 +/- 0.12 to 2.24 +/- 0.09 mmol/l in group B. There was no significant difference in plasma Ca level between both groups on days 4, 6, and 9, and plasma Ca was within the normal range in all patients on day 9. On both treatment regimens urinary calcium excretion fell dramatically and similarly. Plasma phosphate concentration decreased significantly on AHPrBP in both groups of patients, reaching values slightly below the normal range from day 4 to day 9. TmP/GFR decreased progressively on AHPrBP. However, this decrement was significant at day 6 only. Plasma parathyroid hormone concentration rose significantly in both groups from day 4 to day 9. We conclude that at the doses used in the present study treatment of tumor-induced hypercalcemia with AHPrBP is equally effective whether given orally or intravenously.
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PMID:Oral versus intravenous AHPrBP (APD) in the treatment of hypercalcemia of malignancy. 376 3

Hypercalcemia has not previously been recognized as a complication of advanced chronic liver disease without hepatoma. During a five-year period, 16 patients evaluated in the liver transplantation program at the University of Pittsburgh developed hypercalcemia. All had advanced chronic liver disease with mean total bilirubin concentration of 29.5 +/- 4.6 mg/dL (50.1 +/- 78.2 mumol/L) (mean +/- SEM) and prothrombin time 16.8 +/- 0.8s. The highest serum calcium level was 17.2 mg/dL (4.3 mmol/L). The mean serum calcium level was 11.7 +/- 0.3 mg/dL (2.93 +/- 0.075 mmol/L) with an ionized calcium level of 5.41 +/- 0.35 mg/dL (1.35 +/- 0.088 mmol/L) and a phosphorus level of 4.2 +/- 0.4 mg/dL (1.4 +/- 0.1 nmol/L). Mild to moderate renal insufficiency was present in 14 (87%) patients; the mean serum creatinine level was 2.8 +/- 0.4 mg/dL (247 +/- 35 mumol/L). In five (38%) patients parathyroid hormone was completely suppressed and in an additional five (38%) patients, it was in a range most compatible with nonhyperparathyroid hypercalcemia. The 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D levels were normal or low in the 11 patients in whom determinations were made. Hypercalcemia that is not due to hyperparathyroidism or hypervitaminosis D is a potential complication of advanced chronic liver disease.
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PMID:Hypercalcemia. A complication of advanced chronic liver disease. 381 45

This study asks whether arterial blood ionized calcium concentration (Ca++) can regulate the serum level of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] independently of serum phosphorus and parathyroid hormone (PTH). We infused either PTH (bovine 1-34, 10 U/kg body wt/h) or saline into awake and unrestrained rats for 24 h, through a chronic indwelling catheter. PTH raised total serum calcium and arterial blood ionized calcium, yet serum 1,25(OH)2D3 fell from 35 +/- 6 (mean +/- SEM, n = 10) with saline to 12 +/- 3 pg/ml (n = 11, P less than 0.005 vs. saline). To determine if the decrease in serum 1,25(OH)2D3 was due to the elevated Ca++, we infused PTH into other rats for 24 h, along with varying amounts of EGTA. Infusion of PTH + 0.67 micron/min EGTA reduced Ca++, and 1,25(OH)2D3 rose to 90 +/- 33 (P less than 0.02 vs. PTH alone). PTH + 1.00 micron/min EGTA lowered Ca++ more, and 1,25(OH)2D3 increased to 148 +/- 29 (P less than 0.01 vs. saline or PTH alone). PTH + 1.33 micron/min EGTA lowered Ca++ below values seen with saline or PTH alone, and 1,25(OH)2D3 rose to 267 +/- 46 (P less than 0.003 vs. all other groups). Thus, during PTH infusion lowering Ca++ with EGTA raised 1,25(OH)2D3 progressively. There were no differences in serum phosphorus concentration or in arterial blood pH in any group infused with PTH. The log of serum 1,25(OH)2D3 was correlated inversely with Ca++ in all four groups infused with PTH (r = -0.737, n = 31, P less than 0.001), and also when the saline group was included (r = -0.677, n = 41, P less than 0.001). The results of this study indicate that serum 1,25(OH)2D3 may be regulated by Ca++ independent of PTH and serum phosphorus levels in the rat. Since 1,25(OH)2D3 regulates gastrointestinal calcium absorption, there may be direct feedback control of 1,25(OH)2D3, by its regulated ion, Ca++.
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PMID:Evidence that blood ionized calcium can regulate serum 1,25(OH)2D3 independently of parathyroid hormone and phosphorus in the rat. 384 Apr 95

Five full-term infants with birth weights appropriate for gestational age presented with hypocalcemic tetany at 5 to 9 days of age. All infants had been fed Similac 20, a cow milk formula. Initial mean serum calcium (Ca), phosphorus (P), and magnesium (Mg) levels of the tetanic infants were 6.8, 9.5, and 1.6 mg/dL, respectively. The mean serum parathyroid hormone (PTH) level was elevated at 79 mu LEq/mL (adult normal values, less than or equal to 57 mu LEq/mL). Following restoration of normocalcemia with Ca supplements, feeding was reinstituted with Similac 20 in two infants and Similac PM 60/40 in three infants. Serum biochemical and hormonal values were compared with those of 18 exclusively breast-fed infants followed up from three weeks to six months and 14 Similac 20-fed full-term infants followed up from one week to six months. In tetanic infants, serum Ca concentrations became elevated (10.4 +/- 0.05 mg/dL; mean +/- SEM) by six weeks (vs 9.2 +/- 0.3 mg/dL in breast-fed infants) (P less than .001) and serum Mg concentrations (2.26 +/- 0.01 mg/dL) by four weeks (vs 1.92 +/- 0.07 mg/dL in breast-fed infants) (P less than .01). Mean serum P concentrations declined progressively. Mean serum PTH concentrations were elevated and ranged from 74 to 143 mu LEq/mL at two to 16 weeks (vs mean 28 to 35 mu LEq/mL in breast-fed infants (P less than .0001). In 14 formula-fed-nontetanic full-term infants, serum PTH concentrations were intermediate between formula-fed-tetanic and breast-fed infants, mean serum Ca concentrations ranged from 10.2 to 10.4 mg/dL, and mean serum P concentrations declined from 8.3 to 7.1 mg/dL. We speculate that acute hypocalcemic tetany in the study infants was induced by the relatively high P load in cow milk formulas (vs human milk); with the continued P load, secondary hyperparathyroidism continued, maintaining P, Ca, and Mg homeostasis.
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PMID:Late infantile tetany and secondary hyperparathyroidism in infants fed humanized cow milk formula. Longitudinal follow-up. 387 38

Cerebrospinal fluid (CSF) levels of immunoreactive parathyroid hormone (iPTH) and immunoreactive calcitonin (iCT) were measured by radioimmunoassay in 23 outpatient leukemic children on maintenance chemotherapy. These hormones were detectable in the CSF of all patients: iPTH 148 +/- 11 pg/ml (mean +/- SEM); iCT 14.3 +/- 0.8 pg/ml. iPTH and iCT were also measured in serum (iPTH 396 +/- 18 pg/ml; iCT 32.3 +/- 1.4 pg/ml). CSF values were significantly lower (p less than 0.001) than serum concentrations; no significant correlation between the two compartments was found. Our study indicates the presence of iPTH and iCT in the CSF of children.
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PMID:Immunoreactive parathyroid hormone and calcitonin in children's cerebrospinal fluid. 394 89


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