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)

Experiments were performed to investigate the effects of polychlorinated biphenyl (PCB) on calcium metabolism, femur morphometry, and nephrotoxicity. Male Fischer 344 rats were dosed daily intragastrically (ig) for 5, 10 or 15 weeks with 0, 0.1, 1, 10 or 25 mg PCB/kg body weight. After 5, 10 and 15 weeks, liver weight and liver-to-body weight ratio were increased at the 2 higher dose levels. Overt toxicity was observed at the highest dose level after 10 and 15 weeks as evidenced by significantly smaller body weight. Urinary alkaline phosphatase and lactate dehydrogenase activities were elevated at 5, 10 and 15 weeks of PCB exposure and the kidney-to-body weight ratios were elevated at the 10 and 25 mg/kg dose levels after 10 and 15 weeks of exposure indicating nephrotoxicity. Hypercalcemia was present at the highest dose level after 5 and 10 weeks of exposure but serum calcium concentration was normal at 15 weeks. Serum triglycerides were significantly elevated after 5 weeks of exposure but were significantly decreased after 10 and 15 weeks of PCB exposure. Serum cholesterol was significantly elevated at the 2 higher dose levels at all 3 periods. Femur density was increased at the 10 mg/kg dose level after 5 weeks, at all dose levels after 10 weeks and at all dose levels which did not demonstrate overt toxicity after 15 weeks of PCB exposure. Cross-sectional, medullary and cortical areas of the midpoint of the femur were significantly decreased at the higher dose levels after 10 and 15 weeks of exposure. The percent medullary area though was significantly decreased after 10 and 15 weeks of PCB exposure indicating that not only was there a decrease in medullary size but a decrease relative to the cortical bone area. These changes in bone morphometry resulted in a significantly weaker bone after 15 weeks of exposure at the highest dose level. These results demonstrate that PCB exposure effects calcium metabolism and bone morphometry and is nephrotoxic.
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PMID:Polychlorinated biphenyl (Aroclor 1254) induced changes in femur morphometry calcium metabolism and nephrotoxicity. 250 9

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Altogether 184 patients with bone, renal or mixed hyperparathyroidism (HPT) presenting primarily were examined for blood levels of parathyroid hormone and indirect indicators of parathyroid function. None of the indices (calcium concentration, phosphorus level, serum activity of acid and alkaline phosphatase, oxyproline excretion with urine, etc.) was changed. The commonest biochemical signs of primary HPT were hypercalcemia, hypersecretion of parathyroid hormone, hyperoxyprolinuria. Biochemical indices deviations occurred more often and were more profound in bone primary HPT and parathyroid adenomas.
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PMID:[Clinico-biochemical parallels in diverse forms of primary hyperparathyroidism]. 258 52

In order to obtain a useful screening index for primary hyperparathyroidism (PHPT), seven patients with PHPT and fifty-one patients with nonparathyroid hypercalcemia (NPHC) were studied retrospectively. Serum calcium, inorganic phosphate (IP), alkaline phosphatase, albumin (Alb), chloride (Cl), total protein, urea nitrogen and creatinine (Cre) were analyzed at the same time. Discriminant analysis using a stepwise variable select method was applied to these patients. A discriminant function (F 1) was derived from three laboratory tests; F 1 = -0.660 x [IP] + 0.142 x [Cl] + 0.564 x [Alb] - 14.4 (PHPT: F 1 greater than 0.641). F 1 had sensitivity of 100% and specificity of 72.5% (14 false positives) in diagnosing PHPT. Next, another discriminant function (F 2) was derived from PHPT and the false positive patients; F 2 = -2.61 x [IP] + 0.286 x [Cl] - 4.24 x [Cre] - 19.3 (PHPT: F 2 greater than 0.412). When F 2 was applied to positive patients by F 1, final sensitivity was 100% and specificity was 98%. This screening method was tested prospectively in fifty-six consecutive samples of hypercalcemia (PHPT 4, NPHC 52), resulting in sensitivity of 100% and specificity of 98%. It was proved that our screening method using two step discriminant functions was very useful to diagnose PHPT.
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PMID:[A screening index for primary hyperparathyroidism using discriminant functions]. 260 57

Osteitis fibrosa, a frequent complication of chronic renal failure, is characterized by increased rates of bone formation and bone resorption due to increased secretion of parathyroid hormone (PTH). Effective treatment with oral calcitriol is often impossible in patients with osteitis fibrosa, because low doses may cause hypercalcemia. Because short-term infusions of intravenous calcitriol are capable of suppressing the secretion of parathyroid hormone in patients with uremia without causing hypercalcemia, we evaluated the effectiveness of long-term intermittent calcitriol infusions (1.0 to 2.5 micrograms three times weekly, during dialysis) in treating severe osteitis fibrosa in 12 consecutive patients on hemodialysis whose disease was refractory to conventional therapy. After a mean (+/- SE) treatment period of 11.5 +/- 1.4 months, the mean bone-formation rate declined from 1642 +/- 277 to 676 +/- 106 microns 2 per square millimeter per day (P less than 0.01) in the 11 patients who successfully completed the study. Similar reductions occurred in the osteoblastic osteoid (18 +/- 3 to 9 +/- 2 percent; P less than 0.01) and the degree of marrow fibrosis (6.2 +/- 1.7 to 3.5 +/- 1.3 percent; P = 0.01). Concomitant serum biochemical changes included increased calcium levels (2.55 +/- 0.03 to 2.67 +/- 0.05 mmol per liter; P less than 0.01), decreased alkaline phosphatase levels (489 +/- 77 to 184 +/- 32 U per liter; P less than 0.001), and decreased levels of PTH (amino-terminal, 172 +/- 34 to 69 +/- 16 ng per liter in five patients, P less than 0.03; and carboxy-terminal, 1468 +/- 467 to 1083 +/- 402 ml-eq per liter in six patients, P not significant). Although the majority of the patients had transient episodes of asymptomatic hypercalcemia, this complication could be quickly reversed by temporarily halting treatment or decreasing the dose of calcitriol. We conclude that long-term intermittent infusions of intravenous calcitriol are effective in ameliorating osteitis fibrosa in patients on dialysis. Patients whose osteitis fibrosa is refractory to oral calcitriol and who are candidates for parathyroidectomy should be considered first for intravenous calcitriol therapy.
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PMID:Intravenous calcitriol in the treatment of refractory osteitis fibrosa of chronic renal failure. 274 71

Measured levels of serum calcium, phosphate, alkaline phosphatase, and urinary hydroxyproline were measured and calcium-phosphate product was calculated in 20 hyperthyroid patients and 20 normal controls. Eleven of the patients took propranolol 160 mg per day for 28 days. We found that the serum level of calcium was higher than that of normal controls. The incidence of hypercalcaemia in hyperthyroid patients was 10%. The serum level of phosphate and the calcium-phosphate product increased (P less than 0.01). Elevation of alkaline phosphatase and bone alkaline phosphatase were also observed (P less than 0.01). The urinary hydroxyproline was also elevated (P less than 0.01). After treatment with propranolol serum calcium and triiodothyronine decreased (P less than 0.05). It is suggested that the major mechanism of hypercalcaemia and hyperphosphatemia in hyperthyroidism was increase of bone absorption stimulated by triiodothyronine. Propranolol decreased the serum level of calcium through decreasing triiodothyronine level and through beta-receptor blocking effect as well as its direct effect on bone.
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PMID:[Hypercalcemia and hyperphosphatemia in thyrotoxoicosis and the therapeutic effect of propranolol]. 263 74

The author examined a group of 143 patients with osteomalacia of different origin before treatment and after adequate treatment with vitamin D, using laboratory tests, assessment of body weight and muscular strength (grip of the dominant hand). After treatment there was a significant rise of calcaemia, phosphataemia and calciuria and a drop of alkaline phosphatase activity. The body weight increased within the first month of treatment on average by 1.27 kg, during the second month by another 1.15 kg. The patients gained a total of 2.42 kg. The muscular strength increased during the first month on average by 3.23 kg and during the second month by another 2.16 kg, i.e. a total of 5.39 kg. From these results it may be concluded that vitamin D may have a certain anabolic effect if used in pharmacological does either due to an increased nutrient absorption from the gut because of hypertrophy of the intestinal wall or indirectly via hypercalcaemia which increases the hydrochloric acid secretion in the stomach as well as pepsin secretion, and promotes activation of trypsin and lipase in the duodenum and moreover causes retardation of the intestinal transit. The increased muscular strength in due to a rise of calcaemia, improved muscle contraction and probably also due to the mentioned nutritional factors. There may be also the factor of an improved lifestyle due to the immunomodulating action of vitamin D and disappearance of bone pain.
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PMID:[Anabolic effects of vitamin D in patients with osteomalacia]. 263 59

In a chance observation, a 74-year-old woman was found to have hypercalcaemia (3.0 mmol/l) and multiple skeletal osteolyses. A diagnosis of multiple myeloma was made after the demonstration of paraproteins in serum (IgG-kappa) and a 10% proportion of plasma cells in a pelvic crest biopsy. Oral chemotherapy with melphalan and prednisone failed to alter the calcium level. Simultaneous increase in alkaline phosphatase and reduction in serum phosphate concentration led to further tests: determination of peripheral venous parathormone concentration, ultrasound examination of the neck, thallium-technetium subtraction scintigraphy and selective venous parathormone measurements. The results demonstrated the coexistence of primary hyperparathyroidism. The calcium level became normal after surgical removal of a parathyroid adenoma.
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PMID:[Hypercalcemia in coexistent parathyroid adenoma and multiple myeloma. Problems of differential diagnosis]. 266 81

Concomitance of hyperthyroidism and hyperparathyroidism is rare and only forty-nine well documented cases could be found in the literature. In the present study, only forty-three patients with adequate available clinical and laboratory data are reported. Hypercalcemia was found in all the patients and five of them (12%) had acute hyperparathyroidism. Two patients were also pregnant and had pancreatitis. Hypercalcuria was found in 73% and hypophosphatemia in 55% of the patients. Eleven patients (26%) had renal concretions. Skeletal roentgenograms showed abnormalities in 63% of the patients. Elevated serum level of alkaline phosphatase was present in 64% of the patients. However, there seemed to be no correlation with the severity of the skeletal lesions. Thyrotoxicosis commenced before that of Hyperparathyroidism in twenty-three patients (53%) whereas in the remaining twenty patients it was impossible to determine which disease began first. The etiologies of hyperparathyroidism as well as the differential diagnosis of parathyroid-related and nonparathyroid-related hypercalcemia are discussed. Microscopically, 74% of the patients had a single adenoma; 16% had hyperplasia of one to three parathyroid glands. One patient had an adenoma in combination with hyperplasia of one parathyroid gland, one had an adenoma and three hyperplastic glands, one had adenomas of two parathyroid glands in combination with hyperplasia of one parathyroid gland, and the other one had carcinoma of a parathyroid gland.2+ Finally, if a thyrotoxic patient still has hypercalcemia when becoming euthyroid after antithyroid therapy, coexisting hyperthyroidism should be considered and an operation should be performed as surgical treatment cured both diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism and coexisting hyperthyroidism--review of the literature. 267 Jan 39

Aluminium-containing phosphate binders were replaced by a calcium and magnesium carbonate-containing antacid in 20 patients on long-term haemodialysis, over a three-month period in all of them, for 12 months in ten. After two months the serum aluminium level fell (mean +/- SD) from 3.0 +/- 1.6 to 1.4 +/- 0.5 mumol/l (P less than 0.001). After three months the serum phosphate level had fallen from 1.8 +/- 0.4 to 1.5 +/- 0.4 mumol/l (P less than 0.05), while during the same period parathormone (PTH-NH2) fell from 1.4 +/- 1.4 to 0.8 +/- 0.7 ng/ml (P less than 0.05). Serum total calcium concentration rose after two months from 2.2 +/- 0.2 to 2.4 +/- 0.2 mmol/l (P less than 0.001). In a third of patients the uraemic acidosis was corrected, standard bicarbonate rising from 18 +/- 2 to 21 +/- 3 mmol/l (P less than 0.05). Serum pH, potassium, sodium, magnesium and alkaline phosphatase did not change significantly. Hypercalcaemia was an expected disadvantage: repeated symptom-free episodes of hypercalcaemia occurred in six of 20 patients during the first three months and in a further two up to 12 months. These episodes were successfully controlled by a reduction of CaCO3/MgCO3 dosage and readministration of Al(OH)3. Extraosseous calcifications were not observed.
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PMID:[Replacement of aluminum-containing phosphate binders by calcium and magnesium carbonates in long-term hemodialysis]. 270 34


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