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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serum concentration of parathormone is usually normal in hypophosphatasia, a rare disease with a defect of bone mineralisation and low serum alkaline phosphatase activity. Nevertheless there are three cases in the literature presenting a hyperparathyroidism with or without hypercalcemia. No anomaly of parathyroid was found at autopsy. The authors describe the first cases of hypophosphatasia with low serum concentration of parathormone and raise the possibility of a trouble in the calcium-parathormone feed-back. They also emphasize the interest of the urinary pyrophosphate excretion. Its increase seem to be the most constant and the most specific biological disorder.
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PMID:[Inorganic pyrophosphates and parathormone in hypophosphatasia. Study of a family]. 300 10

The diagnosis of primary hyperparathyroidism (PHP) depends increasingly on laboratory tests, since the majority of patients are elderly people without typical symptoms. A mean plasma calcium level close to the upper normal limit serves to diagnose hypercalcemia. To rule out malignant disease, the most common cause of hypercalcemia, measurement of plasma PTH is the most appropriate test. Determination of blood phosphorus, chloride, and alkaline phosphatase, and of urinary calcium and phosphorus, contribute to the investigation of the metabolic effects of the given disease but are not very useful for causal diagnosis. Urinary and nephrogenous cyclic AMP reflect PTH secretion but can be elevated in paraneoplastic hypercalcemia. Diagnosis of subtle forms of PHP by dynamic tests is largely of scientific interest, since they do not necessarily need treatment. The diagnosis of hypoparathyroidism is primarily clinical. PTH measurements rarely distinguish normal from low values. In severe hypocalcemia of non-parathyroid origin, plasma PTH is elevated (except in hypomagnesemia). In borderline cases, measurement of urinary cyclic AMP or of plasma PTH after attempted stimulation by EDTA infusion is helpful, especially in distinguishing between subtle hypoparathyroidism and tetany induced by hyperventilation.
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PMID:[Diagnostic tests in parathyroid diseases]. 300 36

Parathyroid hormone (PTH) is strongly concerned with the pathogenesis of urinary stones. PTH is mainly regulated by the serum calcium concentration and not by other hormones, as is usually the case. We studied whether PTH is also regulated by adrenocorticotrophic hormone (ACTH) or not. ACTH (0.25 mg) was injected intravenously to 17 patients with primary hyperparathyroidism PHP, 7 patients with urolithiasis, 7 patients with malignant hypercalcemia, and 6 control subjects. Serum calcium was significantly increased in only PHP. The serum calcium increase rate showed a significant positive correlation with serum alkaline phosphatase, and a negative correlation with the preinjected serum calcium. PTH was slightly increased in all four groups. Serum cortisol and ACTH concentrations were not significantly different among the groups. PTH concentration in a culture medium of parathyroid tissues increased after ACTH addition. Serum calcium was significantly increased after ACTH injection in an adrenalectomized rat, and decreased in a parathyroidectomized rat. From our data and those of others, it appears that ACTH acts on the adrenal glands to decrease the serum calcium concentration, and might act directly on the parathyroid gland or bones to increase it.
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PMID:[Studies on the endocrinological metabolism of the parathyroid. II. Influence of ACTH on parathyroid function and calcium metabolism]. 300 38

We present the results obtained using a 1-84 human parathyroid hormone (PTH) assay in patients with abnormal calcium metabolism. A normal range was established in a series of healthy volunteers. Patients with surgically proven hyperparathyroidism (HPT) showed increased PTH levels which were separate from the normal range. Patients with probable hyperparathyroidism and milder hypercalcaemia showed a raised median PTH level but the range overlapped with normal. Patients with hypercalcaemia of malignancy showed reduced PTH levels and these patients were readily differentiated from those with probable and proven HPT by the use of the assay. In patients with chronic renal failure PTH values ranged from normal to high, the PTH concentration was found to be correlated with plasma alkaline phosphatase, but not with plasma creatinine.
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PMID:The use of an intact molecule parathyroid hormone assay in disorders of calcium metabolism. 306 5

Clinical effects of EHDP on relief of bone pain, changes in bone lesions on X-ray and 99mTc-MDP scintigram and performance status were investigated in 19 patients with bone metastasis from urogenital cancers (4 renal cell cancers, 1 renal pelvic cancer, 4 bladder cancers and 10 prostatic cancers). EHDP was effective in relieving bone pain in prostatic cancer patients with osteoblastic lesions. Bone lesions on X-ray and 99mTc-MDP scintigram were slightly improved in prostatic cancer patients with osteoblastic lesions. Administration of EHDP did not improve the performance status. Changes in laboratory data such as serum alkaline phosphatase, serum calcium and urinary total hydroxy-proline following EHDP administration indicated inhibition of osteolytic activity with no effect on bone formation in the early period of treatment (in 4 weeks) and development of both osteolytic activity and bone formation in the later period (from 8 to 12 weeks). No marked side effects were observed. EHDP seems to be effective in relieving bone pain in prostatic cancer patients with osteoblastic bone metastasis. Moreover, some diphosphonate groups including EHDP are expected to be useful to the patients with malignant hypercalcemia.
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PMID:[Effects of etidronate disodium (EHDP) on urogenital malignancies with bone metastasis: a multicentered collaborative evaluation]. 313 34

The efficacy and safety of calcium carbonate as a phosphate binder was evaluated in 20 patients on chronic hemodialysis who had previously received aluminum hydroxide. During the control period the patients were on aluminum hydroxide and calcitriol therapy and had plasma phosphorus levels less than 6 mg/dL (4.95 +/- 0.8 mg/dL). Aluminum hydroxide was then discontinued and no phosphate binder was prescribed for 1 month. Every patient developed hyperphosphatemia so that calcium carbonate treatment was begun and calcitriol dose was adjusted in relation to plasma calcium changes. After 24 months of calcium carbonate therapy, plasma phosphorus was 4.85 +/- 0.7 mg/dL, using a daily dose of calcium carbonate of 2.57 +/- 1.3 g (range, 1 to 6 g). The daily dose per patient of calcitriol was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia. At the end of the study plasma calcium, magnesium, bicarbonate, alkaline phosphatase, and parathyroid hormone values were unchanged in comparison with the control period, whereas a significant reduction in plasma aluminum and plasma aluminum increase induced by deferoxamine infusion was observed. The frequency of hypercalcemic and hyperphosphatemic episodes during the last 12 months of calcium carbonate therapy (6.2% and 16.6%, respectively) was not different from that observed during the 12 months on aluminum hydroxide therapy preceding the control period (4.5% and 14.7%, respectively). It was concluded that calcium carbonate is effective in the control of hyperphosphatemia and secondary hyperparathyroidism in patients on chronic hemodialysis and that the incidence of hypercalcemia is low when the daily dosage is less than 6 g.
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PMID:Efficacy and safety of long-term treatment with calcium carbonate as a phosphate binder. 314 60

Serum osteocalcin (BGP) is an osteoblast product that probably reflects the rate of bone formation. It is a potential marker of skeletal metastases and, to investigate this, BGP was measured by radioimmunoassay in the serum of normal subjects and patients with breast or prostate cancer. Significantly higher levels were found in patients with metastatic bone disease in comparison to both normal subjects (P less than 0.001) and patients with non-metastatic cancer (P less than 0.05 for breast cancer and less than 0.001 for prostate cancer). The range of values was wide. Levels were higher in sclerotic than lytic bone metastases (P less than 0.01) and lower in patients with hypercalcaemia (P less than 0.001). Serial measurements of BGP were made in 53 patients with skeletal metastases from breast cancer receiving systemic therapy. At 1 month BGP rose by greater than 0.5 ng/ml in 15/16 responding patients compared with 7/23 patients with progressive disease (P less than 0.01). Responding patients also showed a rise in the bone isoenzyme of alkaline phosphatase and a paradoxical deterioration in the bone scan appearance, both reflecting a flare in osteoblast activity. The early increase in responding patients was followed by a gradual decrease over subsequent months as the osteoblast reaction induced by systemic therapy subsided. We conclude that BGP measurements reflect a wide variability of bone formation rates in metastatic bone disease. Bone formation was usually increased, particularly when metastases were sclerotic in appearance, but in patients with hypercalcaemia the low BGP levels suggest uncoupling of bone resorption and formation. Serial measurements of BGP may be useful in monitoring response to treatment.
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PMID:Osteocalcin: a potential marker of metastatic bone disease and response to treatment. 326 63

Calcium citrate was evaluated as a dietary phosphate binder in 81 patients with end-stage renal disease. These patients were grouped as follows: Group 1, 43 patients who were treated with calcium citrate; and Group 2 (the control group), 38 patients who were treated with aluminum-containing compounds. Blood chemistries were measured monthly and medications adjusted to maintain the following levels: serum calcium, greater than 9 mg/dl; serum phosphorus, less than 5.5 mg/dl; and total CO2 content, greater than 22 mmol/liter. At the end of the treatment period, the following serum values were obtained in Groups 1 and 2, respectively: calcium, 9.6 +/- 1.2 mg/dl (mean +/- SD) versus 8.9 +/- 0.8 mg/dl (P less than 0.001); phosphorus 5.5 +/- 1.9 mg/dl versus 7.0 +/- 2.3 mg/dl (P less than 0.005); and calcium-phosphate product, 52 +/- 18 versus 61 +/- 21 (P less than 0.05). Differences in alkaline phosphatase, total CO2 content, and C-terminal parathyroid hormone (C-PTH) values were not statistically significant between the two groups. Fifteen patients in Group 1 were then switched to aluminum-containing compounds and chemistries were compared one month later. During calcium citrate therapy, serum calcium was significantly higher, while C-PTH and serum alkaline phosphatase were significantly reduced. No difference was noted in serum phosphorous and total CO2 content. A questionnaire completed by 17 patients in Group 1 documented excellent patient tolerance to calcium citrate. Hypercalcemia (greater than 10.5 mg/dl) was the only significant complication, but only one patient became symptomatic. We conclude that, as a phosphate binder, calcium citrate is at least as effective as aluminum-containing compounds.
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PMID:Calcium citrate, a nonaluminum-containing phosphate-binding agent for treatment of CRF. 328 Aug 55

In a study of 35 children with benign transient hyperphosphatasemia, I found a marked seasonal clustering of cases after the summer months. Furthermore, plasma 25-hydroxyvitamin D concentrations were almost twice those of controls matched for age and time of year. Many children had evidence of weight loss and one had idiopathic hypercalcemia of infancy. Activities both of liver and bone isoenzymes of alkaline phosphatase (EC 3.1.3.1) in plasma were increased. The liver and (to a lesser extent) bone isoenzymes had enhanced electrophoretic mobility, and both showed increased binding to wheat-germ lectin by affinity electrophoresis. For the liver (and probably also the bone) isoenzyme, these changes were due to an increased content of sialic acid. A possible etiology for the condition is proposed involving (a) increased synthesis of alkaline phosphatase, mediated by vitamin D metabolites, and (b) decreased hepatic clearance caused by the high sialic acid content and exacerbated in some cases by the effects of some drugs on the liver.
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PMID:What is the cause of benign transient hyperphosphatasemia? A study of 35 cases. 334 6

Administration of the antifungal drug ketoconazole reduces serum 1,25-dihydroxyvitamin D (1,25-D) levels in normal subjects. To determine whether a similar effect occurs in hypercalcemic patients, ketoconazole (200 mg every 8 h for 7 days) was given to nine patients with confirmed primary hyperparathyroidism, three patients with probable primary hyperparathyroidism who were awaiting surgery, and three patients with mild hypercalcemia of uncertain etiology who were being followed. Ketoconazole administration led to a significant reduction in mean serum 1,25-D levels in the hypercalcemic patients [basal, 64 +/- 7 (+/- SEM) pg/mL (154 +/- 17 pmol/L) vs. 36 +/- 5 pg/mL (86 +/- 12 pmol/L) after ketoconazole; P less than 0.001]. Serum total calcium fell slightly but significantly [basal, 11.05 +/- 0.17 mg/dL (2.76 +/- 0.04 mmol/L) vs. 10.77 +/- 0.16 (2.69 +/- 0.04 mmol/L) after ketoconazole; P less than 0.02], but the falls in total serum calcium and serum 1,25-D after ketoconazole treatment were not correlated with one another. Ketoconazole administration did not alter serum ionized calcium, 25-hydroxyvitamin D, phosphate, alkaline phosphatase, or PTH concentrations or urinary cAMP excretion. The responses to ketoconazole were similar in all three patient subgroups. We conclude that short term administration of ketoconazole to hypercalcemic patients causes a substantial fall in serum 1,25-D and a small fall in total serum calcium. These effects render ketoconazole a potentially useful agent for investigation of the importance of 1,25-D in patients with hypercalcemic disorders and for their treatment.
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PMID:Ketoconazole-induced reduction in serum 1,25-dihydroxyvitamin D and total serum calcium in hypercalcemic patients. 336 Sep 1


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