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

We report on a 5-year, prospective, double-blind trial of 1,25 dihydroxycholecalciferol (calcitriol) versus placebo in 76 hemodialysis patients without biochemical or radiological evidence of bone disease. Calcitriol, 1 microgram daily, regularly induced hypercalcemia. Doses of 0.25 microgram daily or less proved satisfactory in most patients. During calcitriol treatment, plasma calcium concentration was significantly higher and serum parathyroid hormone concentration significantly lower than on placebo. There was no difference in the rates of development or of progression of vascular calcification in the two groups. Significantly more patients on placebo (17 vs. 6, p less than 0.05) developed a sustained elevation of plasma alkaline phosphatase concentration. Calcitriol appeared to protect against the development of histological evidence of osteitis fibrosa but not of osteomalacia, but accumulation of aluminum in bone occurred during the study. We conclude that calcitriol delays and may prevent the development of osteitis fibrosa in patients receiving regular hemodialysis and may reasonably be prescribed routinely in hemodialysis patients without biochemical or radiological abnormality, unless there is a substantial prospect of early renal transplantation.
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PMID:Controlled trial of calcitriol in hemodialysis patients. 353 32

Mineral metabolism and bone histomorphometric status were evaluated in 31 hyperthyroid patients (HT) without clinical or radiological bone disease, both before and after treatment of hyperthyroidism. Blood and urine biochemical data were compared with those obtained in sex and age-matched controls. Iliac bone biopsies were available from 12 untreated HT and from 6 of them after treatment for analysis of trabecular bone. Mean plasma calcium was increased in HT but true hypercalcemia was seen in only one case and mean plasma immunoreactive parathormone (iPTH) was normal. Urine calcium excretion was markedly increased, especially in the fasting state. Biochemical parameters decreased after treatment, except for serum alkaline phosphatase and iPTH that, respectively, remained high and increased. Untreated state was characterized by an hyperremodelling state with enhanced activities of bone formation and bone resorption. Bone mineralization was normal. The mineral and bone changes were related to serum thyroid hormone levels. After treatment, the extent of formation surfaces still increased. The fact that, even though calcium metabolism abnormalities were corrected, active resorption surfaces did not change, suggests that trabecular osteoclastic resorption is not an important cause of mobilization of bone calcium to extracellular fluids in HT.
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PMID:Effect of thyrotoxicosis and its treatment on mineral and bone metabolism. 357 53

A unique case of familial hyperparathyroidism associated with carcinoma of the colon is presented. Two brothers presented initially with colonic carcinoma and years later both were found to have primary hyperparathyroidism on the basis of parathyroid hyperplasia. This raises the issue of associated malignancies in patients with hyperparathyroidism, especially if they are found to be familial. One member of the family developed severe, recurrent hypercalcemia with bone disease, and thus the need for continued follow-up is emphasized.
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PMID:Familial hyperparathyroidism in association with colonic carcinoma. 359 82

Of the 90 cases of primary hyperparathyroidism surgically treated in our department over the last decade (1975-1985), ten cases had a mediastinal parathyroidal adenoma. In only two of these patients was a median sternotomy required for excision of the mediastinal adenoma. Three of the ten patients underwent the initial operation in other institutions, having undergone a previous neck exploration. There were seven males and three females, ages ranging from 41-68 years. Six patients had nephrolithiasis, four had both renal stones and bone disease and two had peptic ulcer disease. One of them was operated on as an emergency because of hyperparathyroidism crisis with calcium levels of 15/16 mg%. Four patients were asymptomatic and had hypercalcemia detected by SMA screening. The calcium level ranged from 11.5-16.2 mg%. The phosphorus ranged from 1.6-2.8 mg% with a mean of 2.0 mg%. All ten patients had plasma PTH determination by radioimmunoassay, the values ranged from 1.5-3 times normal. In seven of the ten cases, the mediastinal parathyroid adenoma was localized within the thymus, the other three were adjacent to the great vessels, two to the aortic arch and one to the pulmonary artery-size ranging from 1.2-5.4 cm. Preoperative localization techniques: venous sampling in four cases; technetium scanning in three cases. No preoperative localization techniques were used in the other three cases. There was no mortality nor other significant postoperative complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism due to mediastinal parathyroid adenoma. 361 May 35

High doses of calcitriol were used prospectively for 11 to 29 months to raise serum calcium levels in an effort to control renal osteodystrophy in 16 children undergoing CAPD. Serum Ca, P, iPTH and alkaline phosphatase were measured monthly; hand radiographs were obtained every six months, and a semiquantitative score of bone abnormalities was evaluated by two independent observers. During the study, serum Ca increased from 9.9 +/- 0.9 to 11.0 +/- 0.6 mg/dl (P less than 0.001); serum iPTH decreased by 113 +/- 131 microliter Eq/ml (P less than 0.005); serum P was unchanged; and serum alkaline phosphatase fell by 33 +/- 46% (P less than 0.02), 530 +/- 397 to 204 +/- 551 IU/liter. The radiographic score fell from 4.8 +/- 4.6 to 0.9 +/- 1.2 (P less than 0.005). The average and maximal doses of calcitriol were 0.61 +/- 0.37 and 0.95 +/- 0.56 microgram/day or 28 +/- 18 and 46 +/- 28 ng/kg body wt/day, respectively. Transient and asymptomatic hypercalcemia occurred in nine patients and two patients had reversible conjunctivitis in association with the hypercalcemia. Thus, "high dose" calcitriol prevented or controlled progression of hyperparathyroid bone disease in most pediatric CAPD patients. The failure to suppress PTH or reverse secondary hyperparathyroidism until the serum Ca rose to 10.5 to 11.0 mg/dl could reflect an increase in the "set point" for PTH suppression by serum calcium in many uremic children.
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PMID:"High-dose" calcitriol for control of renal osteodystrophy in children on CAPD. 362 2

45 bone biopsies from patients with chronic uremia were reviewed to define which noninvasive investigations were of value in predicting the histological diagnosis and to quantify the spectrum of uremic bone disease at a center that has consistently used an aluminum-free dialysis bath. 17 biopsies were taken postmortem. 15 patients received conservative treatment, the rest were on maintenance dialysis. 13 patients had symptomatic bone disease. Virtually all patients with a uremia duration greater than 3 years had uremic osteodystrophy. All patients with clinical bone disease, hypercalcemia or raised alkaline phosphatase activity had osteodystrophy, but the specific histology was not indicated. Greatly raised parathyroid levels suggested secondary hyperparathyroidism, but the test was only 100% specific when 20 times normal. Total aluminum consumption was highly indicative of bone aluminum concentration (p less than 0.0001) and aluminum-related osteomalacia (5 cases), suggesting that a considerable proportion of uremic bone disease is iatrogenic. Serum aluminum was of some use in the diagnosis of aluminum-related osteomalacia, but was not wholly reliable. Bone mineral content (BMC) using both forearm measurements and total body bone mineral levels (TBBM) were assessed in 32 patients and were found to be reduced in 12, with a preponderance of secondary hyperparathyroidism. BMC and TBBM were negatively correlated to resorbing surfaces and bone formation rate, suggesting that secondary hyperparathyroidism is the uremic bone disease that represents the greatest threat to bone mass. It is concluded that while noninvasive investigations give considerable information, reliable diagnosis requires the use of histological methods.
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PMID:Noninvasive diagnosis of uremic osteodystrophy: uses and limitations. 363 Nov 50

The relation between circulating 1,25-dihydroxyvitamin D (1,25(OH)2D) levels and intestinal calcium absorption--as determined by an oral calcium load test--was studied in 16 patients with hypercalcaemia of malignancy (HM) and 16 with hypercalcaemic primary parathyroidism (HPT). In the HPT group serum calcium rose significantly after the oral calcium load and the increment correlated significantly with 1,25(OH)2D levels. While 1,25(OH)2D levels were raised to within the hyperparathyroid range in a number of HM patients, there was no correlation between change in serum calcium and 1,25(OH)2D level in the HM group and serum calcium did not rise significantly after the oral calcium load. HM patients with detectable or raised 1,25(OH)2D levels typically had few, or no, bone metastases in association with squamous lung cancers. A high proportion of these patients exhibited other aspects of hyperparathyroid-like activity such as increased renal tubular calcium reabsorption, depressed renal tubular phosphate reabsorption and elevated urinary cyclic AMP excretion. Conversely, HM patients with undetectable 1,25(OH)2D levels typically had extensive metastatic bone disease in association with breast carcinoma and were less likely to exhibit other hyperparathyroid-like features. It is postulated that in the former, the 'inappropriately' detectable or raised 1,25(OH)2D levels may have been due to enhanced renal 1 alpha-hydroxylase activity stimulated by the parathyroid hormone (PTH)-like effect of a non-PTH ectopic humoral mediator. In the latter the suppressed 1,25(OH)2D levels would be the predicted result of a non-humorally mediated hypercalcaemia. It is currently unclear why intestinal calcium absorption was depressed in all HM patients when 1,25(OH)2D levels were normal or raised in some cases. It is possible, however, that in HM there is 'end organ' resistance to the effects of 1,25(OH)2D due to a generalized malabsorptive process.
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PMID:Comparison of intestinal calcium absorption and circulating 1,25-dihydroxyvitamin D levels in malignancy-associated hypercalcaemia and primary hyperparathyroidism. 365 75

This study was undertaken to determine the success of surgical treatment of advanced secondary (renal) hyperparathyroidism. From 1978 to 1985, total parathyroidectomy and autotransplantation (TPA) were performed for secondary hyperparathyroidism in 23 patients who had had dialysis for a mean of 6.5 years preoperatively. Indications for surgery included hypercalcemia, bone pain and pathologic fractures, metastatic calcification, and pruritus. Four glands were found and removed in all patients; 100-150 mg of diced tissue were autotransplanted to one forearm. Two patients died of myocardial infarction in the first postoperative week. Bone pain, present in 19 of 23 patients, was relieved almost immediately postoperatively and relief was sustained to death (of unrelated causes) or most recent follow-up in 13 patients. All fractures healed. All patients had markedly elevated serum parathormone (PTH) preoperatively and 14 of 23 were hypercalcemic. The group mean values of serum calcium, alkaline phosphatase, and PTH all fell to and remained in a normal range by 1 year postoperatively in that subset of patients who did not suffer recurrence. Six patients were reoperated on after 12 to 37 months with partial graft excision for recurrent bone pain and hypercalcemia. Bone pain in two of these patients was due to aluminum-associated bone disease and the diagnosis of recurrent secondary hyperparathyroidism was erroneous. The actual recurrence rate was thus 19 per cent. Consistent technical success, with no late hypocalcemia, was achieved and most patients were restored to medical manageability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A community hospital experience with total parathyroidectomy and autotransplantation for renal hyperparathyroidism. 368 58

To evaluate the effects of calcitriol (1,25-dihydroxyvitamin D3) therapy for the bone disease induced by long-term treatment with anticonvulsants, we reviewed the medical records of 330 institutionalized oligophrenic children and young adults under 26 years of age to identify the 144 children who required anticonvulsant therapy. Of this latter group, 52 children were found to have serum alkaline phosphatase levels elevated more than 2 SDs above normal and were enrolled into this prospective three-year study. To achieve rapid resolution of the bone disease, we elected to use calcitriol at 0.25 to 0.75 micrograms/d. After 1195 patient-months of treatment, our data suggest that the dystrophic process was reversed in 42.3% of the cases, as judged by decreases in serum alkaline phosphatase levels at six months, 65.4% of cases at 12 months, and 83.3% of cases at 13 to 18 months. By 30 months of follow-up, all patients showed significant lowering of serum alkaline phosphatase levels. The improvements were slow and gradual. Twenty-six patients in the treatment series of 52 patients initially showed signs of rickets or osteomalacia on roentgenograms of the wrists. Of these 26 patients, 12 (46%) showed improvement on roentgenograms within 24 months of the beginning of treatment. With reference to complications, hypercalcemia (calcium level, greater than 11 mg/dL [2.74 mmol/L]) was encountered at the rate of one episode per 44 patient-months of treatment. Our results strongly suggest that calcitriol is effective in healing anticonvulsant-related osteomalacia among children and youths, with a low incidence of complications.
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PMID:Bone disease induced by anticonvulsant therapy and treatment with calcitriol (1,25-dihydroxyvitamin D3). 375 5

Over a 3 years period, PTH, 25 OHD, calcium and phosphate levels were measured in all patients admitted to a department of Internal Medicine with abnormal phospho-calcic metabolism or bone disease. The diagnostic value of iPTH was analysed, especially in cases of hyper- and hypocalcaemia. In hypercalcaemia, the iPTH did not differentiate between the two main differential diagnoses: hyperparathyroidism and cancer. In patients with a negative calcium balance, the iPTH level is often raised and many help towards diagnosis. However, it should first of all orientate the clinician towards the detection of renal failure which is a common cause of this condition.
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PMID:[Clinical value of assays of parathyroid hormone and 25-hydroxyvitamin D in internal medicine]. 376 84


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