Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An adult patient presenting in summertime with sarcoidosis and demonstrating raised levels of serum calcium and 1,25-dihydroxycholecalciferol was observed to have a serum immuno-reactive parathyroid hormone concentration in the mid-normal range. Renal function was normal. Corticosteroid administration quickly depressed serum calcium and 1,25-dihydroxycholecalciferol into the normal range; serum parathyroid hormone also fell to low levels. It was concluded that corticosteroid suppression, when incorporating measurements of serum calcium and 1,25-dihydroxycholecalciferol concentrations, can distinguish between sarcoidosis-related hypercalcaemia and primary hyperparathyroidism. The significance of the changes in parathyroid hormone concentration is obscure.
 ...
PMID:Incomplete suppression of parathyroid hormone activity in sarcoidosis presenting with hypercalcaemia. 663 58

We have examined the effects of vitamin D3 metabolites on plasma calcium, plasma calcitonin (CT) and thyroidal CT contents in Rats before and after weaning. A daily injection of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3; approximately 25 pmoles/Rat/day during 4 days] induced a marked rise in plasma calcium (16.1 +/- 0.2 vs. 11.3 +/- 0.3 mg/dl in controls) and a great decrease in thyroidal CT content (-70% of control values) in 13-day-old suckling baby Rats, while no change occurred in response to 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) administration. A negative correlation between plasma calcium level and thyroidal CT stores was found in suckling and in weaning Rats treated with different doses of 1,25-(OH)2D3. The significant difference between the slopes of the two regression lines demonstrated a greater mobilization of the CT stores in weaning than in suckling Rats in response to a given hypercalcemia. Our results could suggest that 24,25-(OH)2D3 at the dose used, does not regulate CT secretion while 1,25-(OH)2D3 has probably an indirect effect on CT release, but in vitro experiments will be performed to confirm this hypothesis.
 ...
PMID:[Effect of 1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol on thyroid calcitonin content in the suckling or weanling rat]. 681 66

The influence of injections of calcitonin on the hypercalcaemia and hyperhophosphataemia induced by 1 alpha-hydroxycholecalciferol (1alpha-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was studied in growing lambs and lactating cows respectively. In lambs, the hypercalcaemic and hyperphosphataemic effect of 0.1 microgram 1 alpha-OHD3/kg body weight (i.v.) was completely inhibited by 20 units calcitonin/kg body weight, injected subcutaneously in four equal doses at intervals of 12 h, the first injection of calcitonin occurring immediately after injection of 1 alpha-OHD3. Moreover, the same dose of calcitonin partly inhibited the hypercalcaemia and hyperphosphataemia observed after injection of 0.25 microgram 1 alpha-OHD3/kg body weight. In lactating cows, four injections of calcitonin (5 u./kg body weight each, at intervals of 12 h) prevented the rise of plasma calcium and phosphate levels occurring after injection of 1,25-(OH)2D3 (0.01 microgram/kg body weight). The results indicated that high plasma calcitonin levels can inhibit the hypercalcaemic and hyperphosphataemic effects of 1,25-(OH)2D3 in ruminants. Thus, hypocalcaemia might occur in parturient cows in spite of raised concentrations of 1,25-(OH)2D3 in plasma.
 ...
PMID:Inhibition by calcitonin of hypercalcaemia induced by 1,25-dihydroxycholecalciferol. 689 56

Eleven patients with the Mendelian phenotype of x-linked hypophosphatemia (XLH) were treated with calcitriol [1,25-(OH)2D3] and phosphate. Ten patients had received prior treatment with ergocalciferol and phosphate. Five subjects were prepubertal and six were postpubertal. Response to calcitriol was measured under nonfasting and overnight fasting protocols. Bone biopsies were obtained before and after treatment. Calcitriol (mean dose, 30 ng/kg. day) 1) raised serum phosphorus uniformly in prepubertal patients but in only two of six postpubertal subjects; 2) did not change the theoretical renal phosphate threshold in the total patient group and thus had no effect on the primary transport defect in XLH; 3) improved trabecular bone mineralization in the total patient group, as determined by bone histomorphometry. The beneficial effect on extracellular phosphorus homeostasis was attributed to improved intestinal absorption of phosphorus; improvement in bone mineralization may reflect an additional effect of 1,25-(OH)2D3 on bone itself in XLH. Mild transient hypercalcemia occurred during 0.6% of 3545 treatment days and was readily controlled by adjusting the dosage of 1,25-(OH)2D3.
 ...
PMID:X-linked hypophosphatemia: effect of calcitriol on renal handling of phosphate, serum phosphate, and bone mineralization. 689 92

Nine patients with renal osteodystrophy were tested for 6.5 to 35 months with 1,25-dihydroxycholecalciferol (1,25-DHCC). A close biochemical follow-up was performed during the first 6 months of treatment, including biweekly determinations of serum calcium, phosphorus, magnesium, alkaline phosphatase and creatinine levels. A bone biopsy, radiologic investigations and determinations of plasma levels of immunoreactive parathyroid hormone (IPTH) and intestinal absorption of calcium 47 were performed before and after the 6 months. Although the five patients with osteitis fibrosa showed a significant improvement, the four with predominantly osteomalacic lesions showed no response to treatment. These four had a normal initial plasma iPTH level, higher serum calcium levels than the other five patients, extreme sensitivity to 1,25-DHCC, with frequent episodes of hypercalcemia, and only a slightly increased serum alkaline phosphatase level, which remained unchanged during treatment. All but one of the patients, irrespective of the histologic abnormality, showed a decrease in the uptake of radionuclide by bone after treatment. The renal function of one patient, a man with long-standing stable renal failure who had not undergone dialysis, deteriorated during treatment.
 ...
PMID:Treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol. 689 3

We describe a sporadic, vitamin-D-resistant osteomalacic syndrome in 19 patients undergoing hemodialysis. The syndrome was found in less than 1.5% of patients from referring dialysis centers. All 19 patients had multiple fractures, severe myopathy, and many developed spontaneous hypercalcemia. Severe osteomalacia without evidence of secondary hyperparathyroidism distinguished this syndrome from other forms of renal osteodystrophy. Bone aluminum, measured in six patients, was greatly elevated. Therapy with calcitriol (1 alpha, 25-dihydroxycholecalciferol) lad to clinical improvement in seven patients with reduced pain and myopathy, decreased serum alkaline phosphatase, or both, but no improvement in bone histology. Patients who did not respond clinically to calcitriol developed marked hypercalcemia. The cause of this severe osteomalacia, which occurs despite normal or slightly elevated levels of serum calcium and phosphorus and fails to mineralize with calcitriol, is unclear.
 ...
PMID:Vitamin-D-resistant osteomalacia in hemodialysis patients lacking secondary hyperparathyroidism. 689 20

We studied six oliguric patients with rhabdomyolysis-induced acute renal failure. On admission, all had marked hyperphosphatemia and hypocalcemia associated with low levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. During the early polyuric phase, moderate hypercalcemia was accompanied by marked elevations in plasma 1,25(OH)2D and persistent elevations in parathyroid hormone (both amino and carboxy terminals). During the late polyuric phase, the levels of serum calcium and 1,25(OH)2D reverted to normal. Thus, in rhabdomyolysis-induced acute renal failure, the hypocalcemia of the oliguric phase may be secondary to decreased synthesis of 1,25(OH)2D; severe hyperphosphatemia may also have a major role. The hypercalcemia of the polyuric phase may be partly due to increased synthesis of 1,25(OH)2D, resulting from the high parathyroid hormone levels and recovery of renal function.
 ...
PMID:The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. Interactions of parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. 689 30

Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
 ...
PMID:Long-term therapy of uremic osteodystrophy in adults with calcitriol. 689 93

The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.
 ...
PMID:Prostaglandin-dependent polyuria in hypercalcemia. 689 50

To study the developmental controls for both intestinal and placental calcium-binding protein (CaBP), we have altered mineral metabolism by feeding pregnant mice diets high in calcium and strontium. The effects of these dietary changes on CaBP content of maternal intestine and placenta and also on fetal mineral accumulation have been measured. Feeding high-calcium diets to pregnant mice decreased CaBP content in both maternal intestine and placenta (45 and 58%, respectively). Under these conditions of maternal hypercalcemia, fetal mineral accumulation was unchanged. In experiments with strontium-containing diets, CaBP content was reduced in both maternal intestine and placenta (66 and 67%, respectively), and fetal mineral accumulation was markedly reduced (70%). Administration of 1,25-dihydroxycholecalciferol [1,25(OH)2D] to the strontium-fed mice allowed the gestational rise in maternal intestinal CaBP to proceed to normal levels or above; however, the level of placental CaBP was not affected. Similarly, administration of 1,25(OH)2D to pregnant mice on a normal diet increased maternal intestinal CaBP, but had no effect upon placental CaBP. Thus, administration of 1,25(OH)2D to the mother, in amounts sufficient for a maternal intestinal response, was not a sufficient condition to increase placental production of CaBP.
 ...
PMID:Regulation of calcium-binding protein in mouse placenta and intestine. 689 17


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>