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)

Clinical observations of bone pain, abnormal gait, and unusual fractures during remission of leukemia led us to assess mineral status in a cohort of 16 children with acute lymphoblastic leukemia treated with intensive chemotherapy. During maintenance and 6 months after the completion of therapy, blood and urine were analyzed for calcium and magnesium and blood for osteocalcin, vitamin D, and parathyroid hormone. Bone mineral content and bone width of the distal one third of the radius of the nondominant arm was measured by single-photon absorptiometry. During therapy, mild ionic hypocalcemia (less than 1.19 mmol/L) and hypomagnesemia (less than 0.77 mmol/L) were demonstrated in 9 and 8 of 16 children, respectively; hypercalciuria (8/16) and hypomagnesiuria (12/16) were also observed. Plasma osteocalcin values correlated with plasma magnesium levels (r = 0.54; p less than 0.05). Oral magnesium supplements normalized plasma magnesium, calcium, and osteocalcin levels, all of which were normal at the postchemotherapy study. Plasma 1,25-dihydroxyvitamin D levels were nondetectable (less than 8 ng/ml) in 12 of 13 patients receiving therapy and in 7 of 14 patients not receiving therapy; alkaline phosphatase activity increased significantly after therapy (179 +/- 86 to 340 +/- 101 units/L), and parathyroid hormone levels were normal in both studies. Bone mineral content/bone width ratio was less than 1 SD below the mean for age- and sex-related population standards in 70% of patients. These data indicate that alterations in magnesium, calcium, and vitamin D metabolism in children treated for acute lymphoblastic leukemia may be instrumental in inducing or sustaining altered bone turnover during chemotherapy.
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PMID:Mineral homeostasis and bone mass in children treated for acute lymphoblastic leukemia. 278 92

A 14-year-old Turkish boy had severe rickets that had been clinically evident since he was 2 years of age. When he was 5 years of age, he had normal serum calcium and phosphorus levels and increased alkaline phosphatase activity. Treatment with modest dosages of vitamin D (5000 U/d for 3 weeks) resulted in hypercalcemia. At 10 years of age, high-dose vitamin D (40,000 U/d) plus phosphorus (1.1 g/d) therapy for 20 days resulted in symptomatic nephrolithiasis. When, 14 years of age, he had normocalcemia, hypophosphatemia, increased alkaline phosphatase activity, and normal circulating parathyroid hormone concentration. Levels of 25-hydroxyvitamin D were normal but those of 1,25-dihydroxyvitamin D were markedly increased. Rickets and osteopenia were evident on radiographs, and osteomalacia was present on trabecular bone obtained at biopsy. Balance study results showed increased intestinal absorption of calcium and phosphorus, hypercalciuria, and increased urinary phosphorus excretion. This patient manifests an unusual form of hypophosphatemic rickets in which hypercalciuria is a cardinal feature. In contrast with most varieties of hypophosphatemia, this disorder is characterized by appropriately increased production of 1,25-dihydroxyvitamin D in response to hypophosphatemia. It is recommended that urinary calcium excretion be assessed in all patients with hypophosphatemic rickets so that appropriate therapy will be instituted.
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PMID:Hypercalciuric hypophosphatemic rickets, mineral balance, bone histomorphometry, and therapeutic implications of hypercalciuria. 278 97

The treatment of premature infants with the diuretic furosemide appears to be a contributory factor in the development of metabolic bone disease presumably because of furosemide-induced hypercalciuria. In this study, we measured calcium and phosphorus balance in furosemide-treated very low birth weight infants (VLBW) infants with bronchopulmonary dysplasia (BPD) who were fed a specialized premature formula containing increased amounts of calcium and phosphorus. Furosemide-treated infants received 166 +/- 37 mg/kg/day and retained 80 +/- 34 mg/kg/day of calcium, and 87 +/- 19 mg/kg/day and retained 52 +/- 14 mg/kg/day of phosphorus. The amounts retained were approximately 65% of the calcium and 72% of the phosphorus requirements for in utero mineral accretion. Compared to a group of similarly fed VLBW infants without BPD and not treated with the diuretic, the furosemide-treated infants excreted a larger percent of the calcium intake in the urine but had similar total urinary calcium and phosphorus losses (mg/kg/day) and serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) levels. From the latter two findings, we suggest that the extra mineral content of the formula may have promoted bone mineralization and prevented the occurrence of secondary hyperparathyroidism.
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PMID:Effect of high calcium and phosphorus intake on mineral retention in very low birth weight infants chronically treated with furosemide. 280 41

Vitamin D deficiency is associated with a generalized aminoaciduria which has been shown to be independent of parathyroid hormone (PTH) and urinary cyclic AMP excretion. To further characterize the mechanism underlying the tubulopathy, weanling rats were placed on one of the following diets for 5 weeks: (1) control [0.7% phosphorus (P), 5.5 micrograms % vitamin D]; (2) D-P- (0.1% P, 0 vitamin D); (3) D+P- (0.1% P, 5.5 micrograms % vitamin D); (4) D-P+ (0.3% P, 0 vitamin D); (5) D-P++ (0.7% P, 0 vitamin D). All diets contained 1.2% calcium (Ca). A group of rats raised on D-P++ for 4 weeks were fed D-P- for 7 days after which they received 500 pmol of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3; SUPP] or an equal volume of the vehicle (ETH). The above diets resulted in partial vitamin D depletion in that 1,25(OH)2D levels were 50.25-79 pg/ml in the presence of very low 25(OH)D concentrations. Augmentation in the urinary excretion of 6 out of 8 amino acids measured was observed in P depletion irrespective of vitamin D status. For the most part, acute supplementation with 1,25(OH)2D3 did not ameliorate the tubulopathy. Plasma PTH and Ca concentrations remained normal in all diets, except D+P-, where plasma Ca was 15.88 +/- 0.54 mg/dl. P depletion was associated with hypercalciuria, hypophosphatemia, avid reabsorption of P and growth retardation, irrespective of vitamin D status. Using taurine as a representative of the amino affected, there was a strong correlation between urinary taurine on the one hand and dietary P content (r = 0.613), plasma P (r = 0.399) and 1,25(OH)2D levels (r = -0.576) on the other. The present study suggests that the aminoaciduria of vitamin D deficiency is not related to elevated levels of PTH. A similar defect may be produced by P depletion, suggesting the possibility of a common pathway for the effect.
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PMID:Effect of vitamin D deficiency on amino acid excretion in the phosphate-depleted rat. 281 86

We report 2 cases of hypercalcaemia and hypercalciuria, with detectable levels of parathyroid hormone, which appeared to be precipitated by enteric fever. Extensive investigation of one case, including ultrasound, isotope scanning, angiography, computed tomographic scanning and surgical exploration, failed to detect a parathyroid adenoma. In both cases biochemical and hormonal abnormalities resolved several months after recovery of enteric fever. The mechanism of the proposed association is unexplained but it should be considered in any patient with hypercalcaemia and detectable parathyroid hormone levels, who is suffering from or has recently recovered from enteric fever. If such a patient is well, a period of several month's observation is recommended. We believe these two cases to be the first such reports of hypercalcaemia in association with enteric fever.
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PMID:Hypercalcaemia in association with enteric fever. 281 40

To evaluate the cause of hypercalciuria, we carried out the oral calcium tolerance test before and after parathyroidectomy in a patient with primary hyperparathyroidism who had recurrent and multiple nephrolithiasis. Preoperative laboratory examination showed hypercalcemia, hypophosphetamia, hypercalciuria, decrease in % tubular reabsorption of phosphorus and strikingly elevated urinary cyclic AMP excretion. The oral calcium tolerance test indicated a significantly greater increase in serum calcium (delta serum calcium: 1.4 mg/dl vs 0.8 mg/dl) and a significantly greater suppression of urinary cyclic AMP excretion (delta U-cyclic AMP:-3.56 moles/gCre vs-1.17 moles/gCre) before parathyroidectomy than after. These results showed that hypercalciuria in this case was induced not only by the significant increase in the filtrated load of calcium but by the reduction in the resorption of calcium in the distal tubule caused by the significantly suppressed parathyroid hormone effect.
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PMID:[A case report: primary hyperparathyroidism--comparison before and after parathyroidectomy by oral calcium tolerance test]. 283 26

116 normocalcemic and 8 primary hyperparathyroid (PHPT) patients with calcium (Ca) nephrolithiasis and 10 normal controls underwent 1 g of oral Ca tolerance test following 4 days of Ca restricted diet (400 mg/day). On the basis of urinary Ca/creatinine (Cr) ratio obtained by the test, the 116 patients with normocalcemic nephrolithiasis were divided into 3 groups (normocalciuric nephrolithiasis; NN, absorptive hypercalciuria; AH, renal hypercalciuria; RH) according to our criteria which were slightly modified from Pak et al. Changes in urinary Ca/Cr ratio, and those in serum Ca and phosphorus (P), tubular maximum reabsorption of phosphate/glomerular filtration rate (TmPO4/GFR), nephrogenous adenosine 3',5'-monophosphate (NcAMP) and plasma immunoreactive parathyroid hormone (iPTH) were determined. As a result, the 116 patients were divided into 82NN, 13AH and 21RH. In general, a rise in serum Ca and fall in NcAMP were seen first, followed by rises in urinary Ca/Cr ratio, serum P and TmPO4/GFR although the changes were small. The group PHPT showed abnormality in the changes of TmPO4/GFR, NcAMP and plasma iPTH. The former one decreased constantly during the test and the latter two did not fall to within the normal range, suggesting parathyroid autonomy or abnormal suppressibility. Regarding the normal controls, all the changes were smallest among the 5 groups and clear parathyroid suppression was not observed while it was seen in the groups NN, AH and RH. In conclusion, oral Ca tolerance test is useful not only to separate NN, AH and RH, but also for the diagnosis of PHPT by demonstrating parathyroid autonomy or abnormal suppressibility assessed by NcAMP and/or TmPO4/GFR.
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PMID:Biochemical changes before and during oral calcium tolerance test in calcium stone formers. 284 10

In the present study Farnolith (a granular powder consisting of different dietary fibres) was given to normals (n = 6), patients suffering from absorptive hypercalciuria type I (n = 6) and to one patient suffering from renal hypercalciuria. Farnolith binds calcium and reduces the calcium absorption from the intestine. In normals the urine- and serum parameters of calcium metabolism (total- and ionised calcium, parathyroid hormone and vitamin-D-metabolites) remained unchanged. In patients suffering from absorptive hypercalciuria type I a significant reduction of hypercalciuria was found; oxalic acid excretion had decreased as well. Lowered parathyroid hormone values returned to normal, vitamin-D-metabolites remained unaffected. In one patient suffering from renal hypercalciuria parathyroid hormone and 1,25-dihydroxy-vitamin D values increased, calcium excretion had not decreased, though. Our investigation shows that Farnolith is suitable for the treatment of absorptive hypercalciuria. Calcium homoeostasis is returned to normal by Farnolith, at the same time it does not produce secondary hyperoxaluria (as e.g. sodium cellulose phosphate). Patients with primary renal calcium loss should not be treated by Farnolith.
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PMID:Calcium metabolism in normal and in hypercalciuric patients on Farnolith, a dietary fibre preparation. 285 67

To clarify the mechanism of development of hypercalcemia in adult T-cell leukemia/lymphoma (ATLL), ten patients with a serum creatinine level less than 177 mumol/L (2 mg/dL) were examined. Although hypercalcemia was seen in only four (40%) of these patients, four of six normocalcemic patients showed hypercalciuria (greater than 5 mmol/d [greater than 200 mg/24 h]). All hypercalcemic patients exhibited high nephrogenous cyclic adenosine monophosphate (NcAMP) levels in the face of low-normal immunoreactive parathyroid hormone and reduced serum 1,25-dihydroxyvitamin D [1,25(OH)2D] concentration. Half of the hypercalciuric patients with normocalcemia also showed high NcAMP and reduced serum 1,25(OH)2D levels. Furthermore, the changes in NcAMP and serum 1,25(OH)2D concentration closely paralleled the development of hypercalcemia and hypercalciuria in two patients. These results are reminiscent of the syndrome of humoral hypercalcemia of malignancy and suggest that derangements in calcium metabolism develop by a similar mechanism in patients with ATLL. The present data also indicate the importance of the measurement of urinary calcium excretion for early detection and prevention of fatal hypercalcemia in patients with ATLL.
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PMID:Clinical evaluation of calcium metabolism in adult T-cell leukemia/lymphoma. 289 17

Fifteen patients with lymphoma and hypercalcemia (greater than or equal to 11.0 mg/dL) were identified by screening the serum chemistry profile obtained from patients upon admission to the Los Angeles County/USC Medical Center. Seven of the 15 (47%) possessed a frankly elevated serum concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2-D]. An additional patient with severe hypercalcemia (16.2 mg/dL) had a serum 1,25-(OH)2-D concentration in the midnormal range, not a suppressed value. To examine the potential existence of hypercalciuria in absence of overt hypercalcemia, prospective screening of 23 normocalcemic patients with lymphoma was undertaken. Four of the 23 patients (17%) had increased fractional urinary calcium excretion rates (0.35 +/- 0.3 mg calcium/100 mL glomerular filtrate [GF], mean +/- SE; normal, less than 0.16 mg/100 mL GF); two of the hypercalciuric patients had a frankly elevated serum 1,25-(OH)2-D concentration. Of the 19 hypercalcemic/hypercalciuric lymphoma patients identified, none had an elevated serum immunoreactive parathyroid hormone concentration. Fourteen of the 19 hypercalcemic/hypercalciuric patients (74%) suffered from B-cell neoplasms, three had Hodgkin's lymphoma, and two had adult T-cell leukemia/lymphoma. All hypercalcemic/hypercalciuric patients had widespread disease (stage III or IV). Six patients, four with hypercalcemia and two with hypercalciuria, had acquired immunodeficiency syndrome (AIDS). These data suggest that the deregulated synthesis of a 1,25-(OH)2-D-like metabolite is a common cause of hypercalcemia and hypercalciuria in patients with lymphoma including patients with AIDS-associated tumors.
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PMID:Vitamin D metabolite-mediated hypercalcemia and hypercalciuria patients with AIDS- and non-AIDS-associated lymphoma. 291 Mar 61


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