Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0020437 (
hypercalcemia
)
10,293
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Seven patients with osteoporosis of ageing were treated with synthetic 1alpha-hydroxycholecalciferol (1alpha-H.C.C.) for 3-4 months. The compound was given at a daily oral dose of 2 mug together with an oral supplement of 1 g of calcium. Clinically there was a striking improvement in the patients' physical fitness. Increased bone formation and mineralisation were seen on iliac-crest bone biopsy, and this was supported by an increased osteoblastic activity demonstrated by histochemical measurement of alkaline-phosphatase activity. Bone histology furthermore showed a reduced bone resorption, which was supported by a reduced urinary excretion of total hydroxyproline. Photon absorptiometry of the forearm accorded with the histological findings, showing a significant increase in the bone mineral content. Serum-calcium rose in all patients, one developing a severe transitory
hypercalcaemia
. The urinary excretion of calcium and magnesium increased significantly. The serum concentrations of
25-hydroxycholecalciferol
and parathyroid hormone were not significantly affected by the treatment. It is concluded that 1alpha-H.C.C. is an effective tool in the treatment of senile osteoporosis.
...
PMID:Treatment of osteoporosis of ageing with 1alpha-hydroxycholecalciferol. 5 56
A 36-year-old man with sarcoidosis had four episodes of
hypercalcaemia
in seven years, all of them during the summer months. Measurement over three years showed that
hypercalcaemia
was associated with small seasonal increases in serum-
25-hydroxycholecalciferol
within the normal range. These changes could be mimicked by the administration of 3000 units of vitamin D3 daily. Serum 1, 25-dihydroxycholecalciferol concentrations ranged between 26--62 pg/ml when serum calcium was normal, but were strikingly high, up to 137 pg/ml, when the patient was hypercalcaemic. These studies show for the first time that
hypercalcaemia
in sarcoidosis is associated with abnormally high circulating concentrations of 1, 25-dihydroxycholecalciferol, probably as a result of overproduction of this, the hormonal form of vitamin D.
...
PMID:1, 25-dihydroxycholecalciferol in the pathogenesis of the hypercalcaemia of sarcoidosis. 8 69
The long-term effects of the vitamin D metabolite,
25-hydroxycholecalciferol
(25-HCC), were evaluated in 2 children with hypophosphatemic vitamin D-resistant rickets. Serial total balance studies demonstrated an apparent lack of correlation between the effects of the vitamin on intestinal absorption of calcium and phosphorus and both the onset of healing in 1 of the 2 patients treated with 5,000 to 7,500 u of the metabolite and the absence of demonstrable radiologic improvement in another patient in whom the final dosage was 20,000 u. per day. At first, the metabolite induced a positive calcium balance in both patients resulting largely from a reduction in intestinal calcium excretion. Despite a continued positive calcium balance, 1 of the 2 patients did not demonstrate further healing, while in the other patient healing was noted even when total calcium balance was negative. Serum phosphate levels did not return to normal in either patient, nor was phosphate excretion altered by 25-HCC. Serum alkaline phosphatase remained elevated in both. Serum immunoassayable parathyroid hormone levels were consistently normal to high-normal in the 2 patients throughout more than 24 months of observation. No instances of
hypercalcemia
and only occasional hypercalciuric episodes were noted.
...
PMID:Long-term therapy of viramin D-resistant richets with 25-hydroxycholecalciferol. 16 13
The influence of 5,6-trans-
25-hydroxycholecalciferol
on renal osteopathy was investigated in a total of 132 patients in 26 dialysis centres. Various doses were used, the average being 4000-6000 IU/day. In 32 patients a daily dose of 6000-9000 IU was used. The average individual duration of treatment was 276 days with a maximum of 910 days. Histologically there was an improvement in the renal osteopathy in 55.9% of evaluable cases (n = 34) and in 25.3% there was no deterioration. Radiographically these results were found in 21% and in 70.5% of evaluable cases (n = 105). Serum calcium increased in 46.6% of cases (n = 131), remained the same in 32.8% and decreased in 20.6%. The changes in alkaline phosphatase were similar : it dropped in 42.1% of patients, remained the same in 28.1% and rose in 29.8%. Immunoreactive parathormone which was invariably raised at the beginning of treatment (n = 36), fell in 25.0%, remained the same in 44.4% and rose further in 30.6%. The clinical symptoms of renal osteopathy which had been present in 57 patients improved in 51.0%, remained the same in 46.0% and deteriorated in 3.0%. Signs of intolerance and side effects were rare. Severe
hypercalcaemia
did not occur.
...
PMID:[Treatment of renal osteopathy with 5,6-trans-25-hydroxycholecalciferol (author's transl)]. 52 Jan 65
The effects of streptozotocin-induced diabetes on the vitamin D metabolism of pregnant rats were investigated in mothers and their fetuses, 11 and 14 days after streptozotocin (SZ) injection, i.e., on days 18 and 21 of gestation. In the mothers' plasma, the levels of
25-hydroxycholecalciferol
(25OHD) and 1,25-dihydroxycholecalciferol (1,25(OH)2 D) were not different from control levels on day 18, but on day 21, 25OHD had increased, 1,25 (OH)2 D had diminished, and significant
hypercalcemia
was noted (10.1 +/- 0.27 mg/dl vs. 9.47 +/- 0.19 mg/dl, mean +/- SD). In hyperglycemic fetuses from the diabetic mothers, plasma insulin levels were reduced at day 18 but enhanced at day 21. 25OHD levels were not different from those of the controls at day 18, but were lower at day 21 (2.12 +/- 0.70 ng/g BW, n = 13, vs. 3.75 +/- 1.40 ng/g BW n = 29 controls, means +/- SD). Fetal body levels of 1,25 (OH)2 D were lower than that in the controls at day 18 (16.6 +/- 2.9 pg/g BW, n = 9 x 2, vs. 28.7 +/- 6.3 pg/g BW, n = 7 x 2, mean +/- SD P less than 0.001), but identical to control levels on day 21. The role of fetal or placental enzymes in the regulation of vitamin D metabolism in fetuses is discussed.
...
PMID:Effects of experimental diabetes on the vitamin D metabolism of pregnant rats and their fetuses. 296 93
Plasma concentrations of vitamin D3 (cholecalciferol) metabolites have been studied in rainbow trout (Salmo gairdneri) adapted to varying environmental calcium concentrations in both fresh water and artificial seawater, and in natural seawater. In vivo, intraarterial injection of tritiated
25-hydroxycholecalciferol
was followed by its transformation to a number of metabolites including compounds that cochromatographed on high performance liquid chromatography (HPLC) with 1,25-dihydroxycholecalciferol and 25,26-dihydroxycholecalciferol.
Hypercalcaemia
and increased environmental calcium were associated with a greater transformation to the compound cochromatographing with 25,26-dihydroxycholecalciferol, while hypocalcaemia and reduced environmental calcium concentrations induced more conversion to the 1,25-dihydroxycholecalciferol-like compound. In vitro, both metabolites were produced by liver but not by kidney preparations, and the difference in conversion ratios observed in vivo associated with changes in plasma calcium were also seen in vitro. It is concluded that the metabolism of
25-hydroxycholecalciferol
in the trout can be influenced by calcium status, but at present the physiological importance of this metabolism and the mechanisms and site(s) of action of the metabolites are unknown.
...
PMID:Metabolism of 25-hydroxycholecalciferol in a teleost fish, the rainbow trout (Salmo gairdneri). 355 76
A 42-year-old woman, with a previously resected jejunal leiomyoblastoma, was first seen with liver metastases 31/2 years after the tumor resection. Intractable malignant
hypercalcemia
appeared eight months later, together with renal insufficiency. No osteolytic lesions were detected. Levels of parathyroid hormone, cyclic adenosine monophosphate, and 1,25-dihydroxycholecalciferol (1,25[OH]2D) were not useful in distinguishing between the hypercalcemia of malignancy and concurrent hyperparathyroidism. Despite renal insufficiency,
hypercalcemia
, and subtotal parathyroidectomy, the 1,25(OH)2D levels remained elevated, consistent with the speculation that a tumor product stimulated 1-alpha-hydroxylation of
25-hydroxycholecalciferol
. Phenytoin and phenobarbital (enzyme induction therapy), in combination with phosphorus and glucocorticoids, appeared to be useful in controlling the
hypercalcemia
.
...
PMID:Leiomyoblastoma associated with intractable hypercalcemia and elevated 1,25-dihydroxycholecalciferol levels. Treatment by hepatic enzyme induction. 383 34
We report a case of
hypercalcemia
in a patient with leprosy. Aminoterminal parathyroid hormone and
25-hydroxy-cholecalciferol
concentrations were suppressed. Urinary hydroxyproline concentrations were elevated. There was no evidence of malignancy. The
hypercalcemia
resolved with corticosteroid therapy.
...
PMID:Hypercalcemia in leprosy. 401 81
Vitamin D intoxication was induced in chicks by treatment with large amounts of radioactive cholecalciferol (vitamin D3) either by s.c. injections or by stomach tube.
Hypercalcemia
and nephrocalcinosis were present, confirming toxicity. The distribution of cholecalciferol and its metabolites in the tissues of the intoxicated birds was compared with that in birds that were treated with physiological amounts of radioactive cholecalciferol. Treatment with pharmacological doses resulted in marked elevation of cholecalciferol and its metabolites in all tissues examined, including elevation of 1 alpha,25-dihydroxycholecalciferol in the intestine. The predominant form of cholecalciferol in these birds was found to be the unchanged vitamin, whereas in birds treated with physiological doses
25-hydroxycholecalciferol
was the predominant metabolite. The route of vitamin administration was found to be of importance only when pharmacological doses were given: generally, higher levels were noted when administered via s.c. injections than via stomach tube, except in the arteries. It is suggested that in vitamin D intoxication, the factor responsible for the pathological changes in soft tissues is cholecalciferol itself. High levels of 1 alpha,25-dihydroxycholecalciferol may be responsible for the
hypercalcemia
.
...
PMID:Metabolism of cholecalciferol in vitamin D intoxicated chicks. 628 28
The purpose of the present investigation was to study various aspects of renal bone disease in patients treated at a centre with a low general incidence of symptomatic renal osteodystrophy. In a study of signs of progressive secondary hyperparathyroidism (HPT) in a random sample of patients with chronic renal disease, symptomatic bone disease occurred only in transplanted patients with osteonecroses of major joints. Biochemical and radiographic signs of severe progressive HPT were comparatively infrequent.
Hypercalcaemia
was the major indication for parathyroid surgery. Normocalcaemic patients on haemodialysis (HD) investigated with dynamic bone histomorphometry showed normal mean bone formation rates. Serum PTH was a major determinant of bone remodelling activity. Histochemical evidence of bone aluminium accumulation was found in the majority, and the trabecular surface extent of aluminium was directly related to indices of defective mineralization. Long-term continuous ambulatory peritoneal dialysis (CAPD) was associated with normocalcaemia and acceptable control of hyperphosphataemia. Serum PTH remained high and radiographic evidence of progressive HPT developed in some patients. Histomorphometrical findings, including signs of aluminium accumulation, were similar to those in HD, indicating that CAPD has no specific effect on renal bone disease. Low serum
25-hydroxycholecalciferol
in CAPD could not be related to specific findings regarding histomorphometry. Chronic haemofiltration (HF) was associated with a high risk of calcium loss and hypocalcaemia. Despite decreasing serum calcium serum PTH decreased, and bone biopsy findings indicated decreased skeletal effects of PTH as a further cause of hypocalcaemia. Bone histomorphometry also showed the development of a progressive mineralization defect probably related to calcium deficiency, while trabecular bone aluminium decreased in all patients during HF.
...
PMID:Bone disease in renal failure. Clinical and histomorphometric studies. 639 22
1
2
3
Next >>