Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 2-month-old child with infantile hypophosphatasia had hypercalcemia (3.49 mmol/L (14 mg/dl)), nephrocalcinosis, and diminished bone mineral content. Hypercalcemia was corrected with calcitonin. Hypercalciuria and bone demineralization abated with chlorothiazide. Hypercalcemia is hypothesized to be related to normal bone resorption in conjunction with impaired bone mineralization. Chlorothiazide may alleviate this impairment.
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PMID:Infantile hypophosphatasia: treatment options to control hypercalcemia, hypercalciuria, and chronic bone demineralization. 915 96

Calcitriol has been widely used in the management of osteoporosis, but its efficiency is a matter of controversy. It is not known whether combinations of calcitriol and antiresorptive agents such as etidronate and calcitonin are superior to calcitriol alone in the treatment of postmenopausal osteoporosis. To make this determination, 30 Turkish women with postmenopausal osteoporosis between 45 and 68 years of age were randomized to receive either intermittent cyclical etidronate (400 mg/day, for 14 days) followed by 60 days of cyclical calcitriol therapy 0.25 microg twice daily (group 1; n = 10), or calcitriol 0.25 microg twice daily (group 2; n = 10), or calcitriol 0.25 microg/day in combination with 100 IU intranasal salmon calcitonin taken every other day (group 3; n = 10) through a 1-year period. Bone mineral density (BMD) of lumbar spine (L2 to L4) was determined for each patient by dual-photon absorptiometry (153Gd) at baseline, after 6 months, and at the end of the study. There was no significant difference among groups with respect to mean spinal BMD at baseline, after 6, and after 12 months. No significant spinal BMD changes occurred in any group from baseline, after 6 months, and after 12 months. Four patients in groups 1 and 2 and five patients in group 3 developed hypercalcemia at least once during therapy. Hypercalciuria occurred at least once in 9, 10, and 7 patients in groups 1, 2, and 3, respectively. One patient in group 2 developed a renal stone at the end of the study. Mean urine hydroxyproline levels did not change significantly in any group with respect to baseline. The data suggest that one-year treatment with calcitriol, given either alone or in combination with antiresorptive agents, does not improve spinal BMD in Turkish women with postmenopausal osteoporosis, and is associated with a high rate of adverse events.
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PMID:Comparison of calcitriol treatment with etidronate-calcitriol and calcitonin-calcitriol combinations in Turkish women with postmenopausal osteoporosis: a prospective study. 919 11

Previous work in younger males with recurrent idiopathic calcium urolithiasis (RCU) demonstrated inappropriately high postprandial phosphaturia, hyperinsulinemia and insulin resistance, but normal glycemia. To investigate further whether these abnormalities occur also in RCU patients with a mean age corresponding to the life period with peak formation of calcium-containing stones, two trials were carried out in 155 males of comparable age and body mass index. All participants underwent a standardized laboratory examination, including collection of urine and blood before and following a test meal rich in carbohydrate and calcium but low in phosphorus. In trial 1, comprising control subjects (n = 12, mean age 42 years) and RCU patients (n = 24, mean age 41 years), phosphate (Pi) excretion and fractional Pi excretion in postprandial urine of controls did not change compared with the values in fasting urine, but were significantly increased in RCU, despite the fact that there was almost equal suppression of serum parathyroid hormone (PTH) and increase in serum calcitonin. Postprandially, RCU patients were hyperinsulinemic but still normoglycemic versus controls. In trial 2, carried out in unclassified (in terms of calciuria) RCU patients (n = 119, mean age 40 years) only, the post-load Pi-uria was similar in magnitude to Pi-uria of RCU patients in trial 1; increased postprandial Pi-uria was a phenomenon also of normocalciuria but was slightly more pronounced in hypercalciuria, while changes in calcium phosphate (brushite) and calcium oxalate supersaturation of urine were unrelated to calciuria. In RCU patients, but not controls, there was a tendency toward higher urinary glucose in post-load as compared with fasting urine. When urinary Pi and fractional Pi excretion in trial 2 were considered as dependent variables in multivariate regression analysis, they appeared unrelated to age, but positively associated with postprandial glycemia as the best predictor, followed by insulinemia, insulin resistance, to a lesser degree fasting serum PTH and the metabolic activity of stone disease, negatively associated with blood total lipids and very low density lipoprotein (VLDL) cholesterol. It was concluded that RCU males (1) show low Pi-uria during fasting but impaired renal Pi conservation in response to a mixed meal, a situation carrying the risk of Pi deficiency over the long term; (2) represent a population developing hyperPi-uria despite suppressed PTH; (3) exhibit insulin resistance but are still able to maintain normoglycemia at the expense of hyperinsulinemia. It is suggested that calcium-containing renal stones are related to impaired Pi and glucose translocation across cell membranes, and that the role of lipids in this setting deserves further investigation.
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PMID:Urinary phosphate excretion in the pathophysiology of idiopathic recurrent calcium urolithiasis: hormonal interactions and lipid metabolism. 944 52

Prolonged immobilization or physical inactivity has been shown to produce increased bone resorption due to enhanced osteoclastic activity and diminished bone formation. These skeletal changes are a typical complication in tetraplegic patients, who are at risk of developing hypocalcemia. Hypercalciuria is the most characteristic symptom. However, some patients develop hypercalcemia, which is infrequent in these patients, and the hypercalcemia can become a life-threatening complication. Until now, it has been unclear why a small percentage of immobilized patients develop hypercalcemia. Here we present a case of symptomatic hypercalcemia (serum calcium: 3.5 mM/l) following immobilization due to a critical illness polyneuropathy. The diagnosis could be established after malignant hypercalcemia, primary hyperparathyroidism, and other causes of hypercalcemia were excluded. Treatment with intravenous saline, furosemide, and calcitonin was not effective in lowering serum calcium. Treatment with pamidronate (Aredia) was successful and reduced the serum calcium to normal values.
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PMID:[Immobilization hypercalcemia as a complication of polyneuropathy]. 1099 16

We report on a 29-year-old patient who received high doses of prednisone and cyclosporine for the treatment of Still disease. She consulted about dorsolumbar pain leading to physical disability. She presented multiple vertebral fractures, decreased lumbar bone mineral density in the rank of osteoporosis, high bone turnover, and associated hypercalciuria. Cyclosporine and corticoids induced severe changes in bone and mineral metabolism. All patients in treatment with these drugs should undergo radiology, bone densitometry and biochemical determinations of mineral metabolism at the beginning of therapy. Treatment with high doses of intravenous pamidronate (225 mg in 3 months), calcitonin (200/400 IU daily), tiazide (25 mg/daily), and kinesiotherapy mitigated the pain quickly and she recovered motility. We discuss this approach of treating osteoporosis with corticoids and immunosuppressors according to the present knowledge of bone biology.
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PMID:[Vertebral osteoporosis induced by corticoids and cyclosporine ina a patient with Still disease]. 1147 83

The population of thyroid C-cells of female rabbits with ovariectomy-induced osteoporosis was studied using immunohistochemical method with antibodies against calcitonin (CT) and morphometrically. The development of osteoporosis was confirmed using radiology and densitometry. 8 weeks after the operation, after the detection of hypercalcemia and hypercalciuria, some of the animals were given a correcting treatment with calcium-containing drug and vitamin D3 or with a combination of calcium drug with hormonal estrogen-containing drug. 4 weeks after the treatment was started, thyroid C-cells in animals that received the drugs, were significantly larger than in the cells of control and ovariectomized rabbits that received no treatment. Following 12 and 22 weeks, in the animals treated with hormonal drug, both calcium concentrations in blood and urine and C-cell dimensions were normalized. Large C-cells with an intensive reaction to CT were observed at weeks 12 and 22 (weeks 20 and 30 after the operation) in the thyroid gland of the animals that received no treatment and of the animals that received calcium with food. In the last case, the morphological changes of C-cells were more pronounced, despite the insignificant differences in blood calcium concentrations in both groups. These results permit to suggest that the intensity of CT synthesis by C-cells may be influenced by calcium concentrations not only in the blood, but also in the intestinal lumen.
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PMID:[C-cells of the thyroid gland in experimental osteoporosis]. 1289 84

We report a newborn girl with a de novo terminal 4q deletion (q31.3 --> qter) and a characteristic phenotype of minor facial anomalies, cleft palate, congenital heart defect, abnormalities of hands and feet, and postnatal onset of growth deficiency. Laboratory studies showed excessive urinary calcium excretion on standard milk formula and on oral calcium load. Blood measurements of parathyroid hormone, calcitonin, bicarbonate, calcium, phosphorus, magnesium, sodium, chlorine, potassium, and urinary measurements of phosphorus, magnesium, sodium, chlorine, potassium were normal for age. At 2 months of life, ultrasonography showed kidney calcifications. Clinical and laboratory data support the diagnosis of absorptive hypercalciuria or abnormal regulation of calcium-sensing receptors in the renal tubules. The evidence of hypercalciuria and kidney calcifications associated with 4q terminal deletion strengthens the hypothesis that a putative gene for hypercalciuria is located on the terminal segment of chromosome 4q.
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PMID:Hypercalciuria and kidney calcifications in terminal 4q deletion syndrome: further evidence for a putative gene on 4q. 1505 84

Management with glucocorticoid, high iv fluid saline intake, furosemide and calcitonin may not result in a favorable reduction of hypercalcemia and may cause several side effects in infants with acute vitamin D intoxication. The bisphosphonate pamidronate, a specific inhibitor of bone resorption through osteoclast mediation was successfully used in a 6-month old infant with acute vitamin D intoxication managed in the Pediatric Emergency and Intensive Care Unit, after an ineffective trial of hydration, furosemide, calcitonin and prednisolone. After a double infusion of pamidronate on two consecutive days (1 mg/kg/day), an early and safe correction of hypercalcemia/hypercalciuria was supplied. Pamidronate therapy may be considered in patients with hypercalcemia secondary to acute vitamin D poisoning.
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PMID:Pamidronate treatment in acute vitamin D intoxication. 1550 94

We studied bone mineral metabolism changes complicated by acute gastroenteritis in a clinical acute metabolic acidosis milieu where we observed hypercalcemia, hypercalciuria, and elevated urinary hydroxyproline excretion. Serum magnesium and plasma osteocalcin, alkaline phosphatase, and IGF-1 levels were decreased. No significant changes in serum inorganic phosphate and plasma PTH, calcitonin, or 25-hydroxy vitamin D3 levels were detected. All abnormalities disappeared with the correction of acidosis. Observed hypercalcemia seems to be the result of increased calcium efflux from bone due to metabolic acidosis-induced catabolism of type 1 collagen and decreased osteoblastic activity. This study provides data regarding acute metabolic acidosis-induced changes in noninvasive parameters of bone modeling, assessed for the first time in humans.
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PMID:Bone mineral changes in acute metabolic acidosis due to acute gastroenteritis. 1559 94

The calcium-sensing receptor (CaSR) has been detected in human antral gastrin-secreting cells, where, upon calcium and/or amino acid allosteric activation, it stimulates gastrin secretion. Patients with absorptive hypercalciuria (AH) display an enhanced gastric acid output; therefore, we evaluated the secretion of gastrin in subjects with AH (30 subjects vs. 30 healthy female controls, all postmenopausal) after oral calcium administration (1 g calcium gluconate) and, on a separate occasion, after peptone loading test (protein hydrolyzed, 10 g). Gastrin and monomeric calcitonin responses were higher in AH after both oral calcium administration (P < 0.01) and peptone loading (P < 0.01). Because the activation of CaSR by oral calcium and peptones directly induces gastrin release, the higher gastrin responses to these stimuli suggest an increased sensitivity of gastrin-secreting cells CaSR in patients with AH. A similar alteration in thyroid C cells might explain the enhanced calcitonin responses to both calcium and peptones. If the same alterations should in addition be present in the distal tubule (where CaSR is expressed as well), then a possible explanation for amino acid-induced hypercalciuria in AH would have been identified.
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PMID:Increased gastrin and calcitonin secretion after oral calcium or peptones administration in patients with hypercalciuria: a clue to an alteration in calcium-sensing receptor activity. 1561 38


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