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)

The treatment of rapidly progressive skeletal demineralisation in myelomatosis has been studied with the help of metabolic calcium balance in two patients; In one, osteoporosis accelerated during treatment with melphalan and prednisolone, although he remained normocalcaemic throughout, suggesting that osteoporosis was aggravated by corticosteroid therapy. In the other patient, who was initially hypercalcaemic, conventional treatment produced clinical remission before eventual relapse with more hypercalcaemia and skeletal dissolution. Both patients were then treated with mithramycin alone, and, although neither obtained haematological remission, bone pain was relieved, hypercalciuria and hypercalcaemia were abolished, and calcium balances proved that mithramycin was effective in restoring calcium equilibrium. The results indicate that mithramycin may abolish excessive bone resorption in myelomatosis and that severe bone dissolution may occur in the absence of hypercalcaemia. Regular determination of 24-hour urinary calcium excretion as well as of plasma-calcium is important in monitoring process. Mithramycin should be considered in the early treatment not only of hypercalcaemia but also of severe hypercalciuria, if these complications do not rapidly remit during the first course of conventional myeloma therapy, with or without steroids. Finally, these results add to evidence that a humoral factor may be responsible for osteoclast stimulation in myelomatosis.
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PMID:Treatment of osteolytic myelomatosis with mithramycin. 4 84

A brother and a sister are reported, demonstrating the severe form of childhood idiopathic hypercalciuria associated with dwarfism, renal defects and bone lesions (rickets and osteoporosis). The family are Israeli Beduins from a small village with a highly inbred population. The parents who are first cousins, and the remaining 6 siblings are not affected. This suggests an autosomal recessive form of transmission for the trait.
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PMID:[Familial form of idiopathic hypercalciuria with nanism, bone and renal involvement in children]. 52 1

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

Fifteen patients, 13 women and 2 men (mean age 60 years) with osteoporosis of different types have been under treatment with 1 alpha-hydroxyvitamin D3 and calcium. The responses were observed clinically and by the use of roentgen morphometry, photon absorptiometry and by blood and urine chemical analyses. The treatment had beneficial clinical effect in all but 3 patients. The intestinal calcium absorption rate increased significantly. Slight hypercalcemia and a significant hypercalciuria occurred during treatment. Serum and urine phosphate levels, alkaline phosphatase and parathyroid hormone values were within normal ranges. The bone mineral content increased significantly during treatment. 1 alpha-hydroxyvitamin D3 and calcium was well tolerated by the patients. Three patients had coincidental acute attacks of spinal pain and 2 had further vertebral crush fractures. A period of time longer than one year is necessary to further evaluate the effects of 1 alpha-hydroxyvitamin D3 therapy on the clinical course of severe osteoporosis.
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PMID:Interim report on treatment of osteoporotic patients with 1 alpha-hydroxyvitamin D3 and calcium. 70 36

The calcium tolerance test is of diagnostic importance only in osteomalacia, which it helps to identify before bone biopsy when the static phosphocalcic parameters are not a deciding factor. However, the test does not make it possible to distinguish an osteoporosis from a cortisone osteopathy or an idiopathic hypercalciuria. In the first two diseases, the rates of urinary calcium elimination are comparable to that of normal individuals. It seems that the rate of urinary elimination of I.V. administered calcium is, approximately, all the more elevated as the level of iPTH is low; and, when the level of iPTH is low, the osteoid tissue seems less calcified than normally.
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PMID:[The provoked hypercalciuria test. Significance and limitations]. 74 25

The rate of reversal of hypercalcaemia or hypercalciuria induced by calciferol, dihydrotachysterol, 1-alpha-hydroxycholecalciferol (1-alpha-OHD3), or 1-alpha, 25-dihydroxycholecalciferol (1-alpha, 25-(OH)2D3) was measured in three normal subjects, two patients with osteoporosis, and 14 patients with disorders resistant to vitamin D. The half time for reversal after stopping 1-alpha, 25 (OH)2D3 was less than that after stopping 1-alpha-OHD3, calciferol, or dihydrotachysterol. The differences observed were independent of the dose given or length of treatment. When 1-alpha-OHD3 or 1-alpha-25-(OH)2D3 was stopped patients with vitamin D resistant states (hypoparathyroidism, renal tubular hypophosphataemia, or chronic renal failure) showed less rapid reversal of hypercalcaemia and hypercalciuria than did normal subjects. These studies show one potential advantage of 1-alpha-25-(OH)2D3 over vitamin D, and possibly over 1-alpha-OHD3, in the management of vitamin D resistant states.
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PMID:Rate of reversal of hypercalcaemia and hypercalciuria induced by vitamin D and its 1alpha-hydroxylated derivatives. 83 19

The elimination of calcium, phosphorus, hydroxyproline and nitrogen was studied in 127 patients with inflammatory joint diseases and )6 healthy controls for 4 days. On the third day, 186 mg of calcium was administered intravenously. Provoked hypercalciuria tests were made in 35 males, 116 females with rheumatiod arthritis (RA), 18 males with ankylosing spondylitis (ASp), 8 postinfectious arthritis (PA) and 18 healthy controls (C). In 120 patients comparison was made between the ratios of eliminated P/hydroxyproline, Ca/hydroxyproline and P/Ca with regards to the results obtained in healthy controls. The kinetics of 47Ca were studied in 7 males with ASp and 4 C. The ratios Ca/P in serum and P/Ca in urine were studied in the same patients and compared with 21 C. The results show that the bone symptomatology of PA manifests itself by elimination of elevated amounts of all of the indicators studied, especially phosphorus. In RA there may be considerable oscillations of flow of urine due to the perspiration of patients. RA differs from decompensated coxarthrosis and gonarthrosis in that the patients eliminate significantly less calcium and phosphorus. Corticosteroids stimulate the elimination of hydroxyproline. Younger patients with RA (25-44) show changes compatible with osteoporosis, older females (45-64) display changes similar to those seen in osteomalacia, the oldest female patient (65-84) appear to have insufficient binding capacity for calcium. The hyposthesis is proposed that at the disease onset RA is characterized by an extremely marked syndrome of osteopathy. ASp is characterized by significantly reduced elimination of hydraxyproline, higher metabolic pool of calcium, lower elimination of calcium in urine and faeces and lower accretion to bone.
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PMID:[Calcium, phosphorus, hydroxyproline and nitrogen in inflammatory joint diseases]. 84 46

Case report of a 18 year old boy with short stature, microceophaly, mental retardation and multiple dysmorphic signs. At the age of 9 years a severe generalised osteoporosis was discovered. A pathological fracture of the greenwoor type healed without proper callus formation. The osteoporosis persists without signs of either deterioration or improvement. The serum phosphorus is slightly decreased, while serum calcium, alkaline phosphatase and renal functions are normal. The main biochemical finding is a constant hyperclaciuria of 6-13 mg/kg/24 h, which can be corrected by treatment with oral sodium phosphate. No other chronic disease could be found which would explain the bone disease. The complex disease of this boy does not fit into the known pictures of osteogenesis imperfecta, idiopathic juvenile osteoporosis or of idiopathic hypercalciuria, and might therefore be another type of demineralising bone disease. It is suggested, that the cause might be an impairment of the calcium fixation of collagen fibres during desmal ossification.
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PMID:[Uncommon form of idiopathic osteoporosis with hypercalciuria, growth retardation and mental retardation]. 115 69

The influence of insulin on plasma and bone mineral homeostasis was studied in the BB rat model, which develops an autoimmune form of diabetes at the age of about 100 days. Untreated diabetes of short duration resulted in hypercalciuria and intestinal calcium malabsorption despite increased free concentrations of serum 1,25-dihydroxyvitamin D. The concentrations of two vitamin D-dependent calcium-binding proteins were also decreased: a low duodenal calbindin-D 9K concentration corresponding to the low intestinal active calcium absorption and a low serum osteocalcin concentration, corresponding to a low bone formation and highly correlated with serum IGF-I concentration. Indeed, on bone histology a very low number of osteoblasts and low osteoblast activity (osteoid formation and mineral apposition rate) were observed. Similar abnormalities persisted in rats with long-standing diabetes resulting in markedly decreased bone mass and increased brittleness of bone. Diabetes therefore resulted in low-turnover osteoporosis. Several hormones (testosterone, growth hormone and 1,25-dihydroxyvitamin D) and growth factors (IGF-I and its binding proteins) with known effects on bone were markedly decreased in diabetic rats. A continuous infusion of testosterone, GH or 1,25-(OH)2D3 for 14 d by miniosmotic pumps could not improve the biochemical or histomorphometric abnormalities. Insulin infusion for 2 weeks, however, rapidly increased and overcorrected the number of osteoblasts, normalized serum osteocalcin and IGF-I concentrations but could not yet normalize bone mineralization. Continuous infusion of IGF-I alone did not improve the osteoblast number of osteocalcin but markedly stimulated bone mineralization. From these data we can conclude that both insulin and IGF-I are potent bone growth factors but with different mode of action. In human type 1 diabetes, a similar decrease in serum osteocalcin and IGF-I was observed. A reduction of regional bone mass, both in long and trabecular bones, is frequently observed in human diabetes. Cumulative data from case control studies indicate that the life-time fracture risk is increased in diabetes.
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PMID:Diabetic bone disease. Low turnover osteoporosis related to decreased IGF-I production. 146 60

A decrease in bone density of the spine has been reported in individuals with hypercalciuria and the finding of the latter in osteoporosis patients is not uncommon. We studied 21 men and 8 women (mean age 47 +/- 13) with idiopathic hypercalciuria (IHCU) defined by an urinary calcium of more than 7.5 mmol/24 h in men and 6.25 mmol/24 h in women. The duration of IHCU was 10 (+/-) 8 years. Among the 29 patients, 24 had one or more renal calculi. Twenty one had been treated, by low calcium diet only (and diuresis), combined with a thiazide diuretic, or sodium phytate, or phosphorus. Bone mineral content (BMC) was measured in the lumbar spine and the upper end of the femur using an ORIS ODC 200 densitometer and compared with 29 control subjects paired for age and sex. No difference was found between the two groups concerning BMC values in either the spine or the 3 femoral sites (neck, Ward, trochanter). BMC was not correlated with urinary calcium. Thus individuals with IHCU showed no decrease in their bone mass, among this group seen in a department of nephrology. The influence of the treatment of IHCU remains to be defined.
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PMID:[Idiopathic hypercalciuria and bone density]. 157 44


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