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)

We characterized the bone disease of transilial biopsy specimens from children with hereditary hypophosphatemic rickets with hypercalciuria (HHRH) and genetically related asymptomatic hypercalciuric subjects. All HHRH patients showed irregular mineralization fronts, markedly elevated osteoid surface and seam width, increased number of osteoid lamellae, and prolonged mineralization lag time. These findings are consistent with a mineralization defect and indicate unambiguously that the bone disease in HHRH is osteomalacia. The only abnormality seen in the asymptomatic hypercalciuric subjects was slightly extended osteoid surface. Parametric and nonparametric statistical analyses performed on a pooled sample of HHRH patients and asymptomatic hypercalciuric subjects revealed a very high inverse correlation and a tight linear relationship between serum phosphorus and osteoid parameters. Serum 1,25-dihydroxyvitamin D, which is low in other forms of hereditary hypophosphatemia and osteomalacia, is elevated in HHRH and correlated positively with osteoid parameters and the mineralization lag time. Serum alkaline phosphatase showed similar relationships. These results as well as the clinical, biochemical, and radiological remission of bone disease consequent to phosphate therapy strongly suggest that in HHRH 1) hypophosphatemia alone is sufficient to cause osteomalacia; and 2) the elevation of 1,25-dihydroxyvitamin D reflects the degree of the primary renal phosphate leak, but is not involved in the pathogenesis of the bone disease.
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PMID:Osteomalacia in hereditary hypophosphatemic rickets with hypercalciuria: a correlative clinical-histomorphometric study. 198 23

The classical manifestations of primary hyperparathyroidism (hypercalcemia, hypophosphatemia, hypercalciuria, increased blood alkaline phosphatase level, and bone changes of the type of generalized osteoporosis) were found in approximately half of patients in a group of 23 who were examined. When Recklinghausen's disease is suspected, the patients must be subjected to a purposeful examination. The intraoperative diagnosis of parathyroid adenoma is difficult. In distinction from thyroid tissue, a lymph node, and adipose tissue a parathyroid adenoma almost always has a vascular pedicle, which makes verification of the diagnosis easier.
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PMID:[Diagnosis and treatment of parathyroid adenomas]. 206 59

To investigate our impression that hypercalciuria is relatively common in children with osteogenesis imperfecta, we performed a retrospective study of data accumulated from our pediatric population with this skeletal disorder. Children with osteogenesis imperfecta (17 girls, 30 boys; mean (+/- SD) age 7.8 +/- 4.6 years; range 0.7 to 16.8 years) had undergone detailed inpatient evaluation of mineral homeostasis during periods of clinical stability and controlled dietary calcium intake. Hypercalciuria was found in 36% of the patients and averaged (+/- SEM) 6.1 +/- 0.3 mg/kg per 24 hours (0.15 +/- 0.01 mmol/kg per 24 hours) or 392 +/- 28 mg/gm of creatinine (1.10 +/- 0.07 mmol calcium/mmol creatinine) in the group with hypercalciuria. There were no statistically significant differences in age, gender, or dietary calcium intake (per kilogram of body weight) between the normocalciuric and hypercalciuric children. However, the group with hypercalciuria was shorter than the normocalciuric group and had a greater lifelong fracture rate. When patient height z scores were regressed against urinary calcium levels, a significant negative correlation was found in the group with hypercalciuria (r = -0.76; p less than 0.001). Although serum alkaline phosphatase activity was lower in the group with hypercalciuria, no difference was found between groups with regard to serum levels of calcium, phosphate, magnesium, creatinine, immunoreactive parathyroid hormone, or osteocalcin. The groups were also similar with respect to both their total body mineral density, as determined by dual-photon absorptiometry (n = 17), and their static indexes of bone formation and resorption, as assessed histomorphometrically with iliac crest specimens (n = 19). We conclude that hypercalciuria occurs frequently in children with osteogenesis imperfecta, and that its magnitude appears to reflect the severity of the skeletal disease.
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PMID:Hypercalciuria in children severely affected with osteogenesis imperfecta. 206 61

Because of the bone remodelling it induces, hyperthyroidism modifies the parameters of calcium-phosphorus metabolism. For a better determination of the mechanism involved, we studied 13 patients with Graves' disease compared with 13 controls. We measured the various parameters of calcium-phosphorus metabolism, notably the levels of parathormone, 25-hydroxycholecalciferol, 1-25 dihydroxycholecalciferol and ostocalcin; 8 patients were re-examined in euthyroidism. Total and corrected values of calcaemia (P less than 0.05 and P less than 0.01), phosphoreamie (P less than 0.01), alkaline phosphatase (P less than 0.01), calciuria (P less than 0.01) and hydroxyprolinuria (P less than 0.01) were significantly higher in patients with hyperthyroidism. Osteocalcin also was significantly increased (P less than 0.01) and correlated with thyroid hormone levels, thus confirming its usefulness as marker of bone remodelling in hyperthyroidism. Creatininaemia was significantly lowered (P less than 0.01). The intestinal absorption of calcium after injection of 1 g of calcium was reduced. Parathormone and 25-hydroxycholecalciferol levels were not significantly different in patients and in controls. In patients who were re-examined in euthyroidism, there was a significant increase in parathormone and in 1-25 dihydroxycholecalciferol levels (P less than 0.05). Thus, in situations of hyperthyroidism 2 elements contribute to a deficit in calcium balance: (a) a fall in parathormone level, consecutive to a rise in calcaemia, induces hypercalciuria; and (b) a fall in 1-25 dihydroxycholecalciferol level, consecutive to functional hypoparathyroidism and hyperphosphoraemia, results in a decrease of intestinal calcium absorption.
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PMID:[Phosphorus-calcium metabolism in hyperthyroidism]. 213 61

1. To determine the relationships between parathyroid hormone activity and long-term sodium fluoride therapy in osteoporosis, cytochemical bioassays (for biologically active parathyroid hormone) were performed in 22 osteoporotic control patients and in 18 patients after 15 +/- 10 months of treatment (60 mg of sodium fluoride daily). Ten patients were studied longitudinally by repeated metabolic balances and were therefore common to both groups. All patients were receiving mineral supplements. 2. Cross-sectional data showed a fourfold mean increase in biologically active parathyroid hormone on fluoride treatment (P less than 0.005) together with a 51% increase in serum alkaline phosphatase (P less than 0.005). Longitudinal data showed, in addition, a significant increase in the calcium balance of 2.4 +/- 1.2 (SEM) mmol daily (P less than 0.05) and the development of a positive phosphorus balance (P less than 0.02). 3. Fluoride-treated patients were then analysed in two groups according to the level of biologically active parathyroid hormone. Thirty-two per cent of values were above the upper limit of normal (18 pg/ml). The mean serum alkaline phosphatase level in this group showed no elevation above that of the control patients, the overall rise being accounted for entirely by patients with normal levels of biologically active parathyroid hormone. High levels of biologically active parathyroid hormone were also associated with relative hypophosphataemia (P less than 0.01), relative hypercalciuria (P less than 0.05) and an increased urine/faecal calcium ratio (P less than 0.025). 4. Results show that long-term fluoride and calcium therapy increase biologically active parathyroid hormone in osteoporosis and that excessive parathyroid hormone activity may account for certain features of the refractory state.
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PMID:Fluoride therapy and parathyroid hormone activity in osteoporosis. 216 71

Treatment with 1,25-(OH)2D3 (calcitriol) was compared with placebo in a double-blind, randomized, parallel clinical trial of 24 months' duration. Subjects were white women with postmenopausal osteoporosis. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. Positive slopes were observed in the active treatment group for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. In contrast, negative slopes were observed for the bone mineral measurements in the placebo group. Measurement of urinary hydroxyproline and of serum alkaline phosphatase and osteocalcin suggested that the mechanism of action of 1,25-(OH)2D3 involved reduction of bone resorption. Hypercalciuria occurred regularly and preceded hypercalcemia by about 2 weeks. A decline in creatinine clearance was observed in two patients, one of whom had nephrolithiasis on sonography. Calcitriol is effective in preventing bone loss, but must be used with caution.
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PMID:Role of calcitriol in the treatment of postmenopausal osteoporosis. 218 76

Bone mineral contents of calcium urolithiasis patients (105 males and 52 females) were measured by the microdensitometry (MD) method, and the patients were divided into the MD normal group and the MD abnormal group. The patients were also divided into the group (21 males and 3 females) treated with thiazides for 1 year or more and the nontreated group to examine various factors in blood and urine. [Nontreated group] The rate of MD abnormality was higher in younger males. The rate tended to increase with age in females. Alkaline phosphatase values were significantly higher in MD abnormal group males than in MD normal group males. Urinary calcium excretion and PTH values were significantly higher in MD abnormal group females than in MD normal group females. Comparison of hypercalciuria and normocalciuria revealed no significant difference between the MD normal rate and the MD abnormal rate. Comparison of single of stone formers and recurrent stone formers also revealed no significant difference between the MD normal rate and the MD abnormal rate. [Treated group] PTH and alkaline phosphatase values were significantly higher in the treated group than in the nontreated group. Alkaline phosphatase values were significantly higher in the MD abnormal group. From the viewpoint of stone recurrence prevention, the monitoring of bones where the majority of calcium in the body is present is considered important besides behavior of calcium in blood and urine.
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PMID:[Calcium urolithiasis and bone change]. 230 17

The crystallization of calcium oxalate in the urine of patients with hyperparathyroidism and hyperthyroidism was studied using a mixed suspension mixed product removal (MSMPR) system. In addition, calcium metabolism in hyperthyroidism and its relationship to urolithiasis was investigated. The urines from all the three groups (normal subjects, hyperparathyroid and hyperthyroid patients) showed reduced nucleation rates and increased growth rates in comparison with the control synthetic urine. The nucleation rate was not significantly different between the three human urine groups, while the growth rate was significantly higher in the hyperparathyroid group compared to the normal and hyperthyroid groups. Crystal volume (suspension density) in the hyperparathyroid group was approximately twice that in the other two groups. Serum and ionized calcium levels in hyperparathyroid patients were higher than in normal subjects, while hyperthyroid patients had levels only slightly higher than those in normal subjects. The hyperparathyroid and hyperthyroid groups differed significantly from the normal group in urinary calcium excretion. These two groups also showed significantly higher levels of serum alkaline phosphatase and urinary hydroxyproline than did the normal group. Although hyperthyroid patients have a calcium metabolism similar to hyperparathyroid patients, the incidence of urolithiasis is no different between hyperthyroid and normal subjects. The results of both crystallization and calcium metabolism in hyperparathyroid patients were not significantly different between those with and without urolithiasis. The result of crystallization was also not significantly different between hyperparathyroid patients with and without hypercalciuria. This study suggests that hypercalciuria alone does not produce urinary stones and that urine from hyperparathyroid patients may contain promotors of calcium oxalate crystallization and calcium stone formation.
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PMID:Calcium oxalate crystal formation in patients with hyperparathyroidism and hyperthyroidism and related metabolic disturbances. 230 55

X-Ray signs of hyperparathyroid osteodystrophy (HPOT) have been singled out in analysis of roentgenograms of 86 patients. Hypercalcemia has been detected in 76 +/- 5% of patients presenting an x-ray picture of HPOT, hypophosphatemia has been diagnosed in 66 +/- 5%, hypercalciuria in 72 +/- 6%, and increased alkaline phosphatase activity in 67 +/- 7%. Studies of the P-Ca metabolism should be carried out repeatedly over the course of hyperparathyrosis. Combined analysis of laboratory and x-ray findings will help improve the diagnosis and differential diagnosis of HPOT.
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PMID:[A comparative study of laboratory and x-ray data in the diagnosis of hyperparathyroid osteodystrophy]. 247 66

A study was undertaken in 46 subjects; 21 patients diagnosed as having HRL and 25 volunteers patients. Biochemical and hormonal analyses were performed in the study population, including determination of Ca, P, Mg, Cr in blood and urine, phosphate tubular resorption (PTR), maximum tubular phosphate resorption (MTPR), fasting calcium secretion (FCS), alkaline phosphatase (AP), hydroxyprolinuria (HPR), osteocalcin (BGP), parathormone (PTH), cAMP, and 1-25(OH)2D. The stone formers showed lower calcemia values (p less than or equal to 0.005d), higher phosphaturia, and magnesiuria (p less than or equal to 0.0005), higher FCS (P less than or equal to 0.005) and higher values for PTH (p less than or equal to 0.01) and cAMP (p less than or equal to 0.0025). No significant differences were observed for the other parameters evaluated. Classification of the patient group into 2 subgroups (renal SbR and absorptive SbA) according to FCS values greater or lower that 0.16 mg/dl, the SbR patient group revealed a higher PTH and 1-25(OH)2D values (p less than or equal to 0.05). There appears to be no increase of bone resorption since AP, HPR, and BGP values in our patients fell within normal ranges. The 1-25(OH)2D levels were also normal and, with respect to the control group, were only elevated for the SbR patient group, whose PTH levels were also observed to be elevated. These increments appear to be related and may result in intermediate forms between renal and absorptive hypercalciuria.
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PMID:[Parathormone, cyclic AMP, 1,25 dihydroxyvitamin D and osteocalcin in hypercalciuric renal lithiasis]. 254 53


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