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 study was undertaken to find our the biological profile of bone symptomatology of decompensated coxarthrosis and gonarthrosis. In a group of 77 patients and in 48 individual patients the levels of calcium, phosphorus, hydroxyproline and nitrogen were studied for four successive days. Calcium was administered by the intravenous route on the third day (186 mg). The results were compared to 16 healthy controls. Analysis was made with reference to the differences in sex, age, stature and anabolic therapy. The products eliminated were referred in absolute amounts to the body surface and to the period of 1 minute. 91 patients and 17 healthy controls were subjected to a provoked hypercalciuria test. Five patients were followed up in a 47Ca kinetic study and its result was compared to the content of Ca/P and P/Ca in serum and urine found in the same patients and in 21 healthy controls. The biological profile was also compared to a group of patients with gonarthrosis and varose deformity and to 127 patients with inflammatory joint diseases. From the results it is assumed that in women with decompensated coxarthrosis and gonarthrosis the syndrome of disease is a bone manifestation which affects the mineral bone substrate and particularly its calcium level. Phosphorus and the organic products of bone (nitrogen and hydroxyproline) of these patients are susceptible to intravenous administration of calcium. In women the metabolism of collagen appears to be more active than that seen in controls, and tends to resemble that of phosphorus. With its lower activity calcium tends to relate to noncollagenic products, such as osseomucoid (glycoprotein, proteoglycan) and osseoalbumoid. In accord with the findings, the patients show a higher miscible pool of calcium (47Ca), and its lower elimination (in urine and stools) and lower accretion to bone. There are a number of factors (sex, stature, age, clinical compensation of disease) that must be taken into consideration when evaluating the results.
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PMID:The study of calcium, phosphorus, hydroxyproline, and nitrogen in decompensated coxarthroses and gonarthroses. 98 58

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

Thirty-eight patients with collagen diseases undergoing chronic glucocorticoid treatment were studied to assess the effect of a 24 month administration of oral 1 alpha-hydroxyvitamin D (1 alpha-OHD), calcium and thiazide on bone and mineral metabolism. All patients were premenopausal women (mean age = 35 y.o.) and had been treated with prednisolone (mean dose = 11 mg/day). Patients were randomly divided into three groups. Fourteen patients were treated with 0.75 micrograms of 1 alpha-OHD and 400 mg of calcium daily (1 alpha-OHD group). Eleven patients were treated with 1 alpha-OHD, calcium and 4 mg of trichlormethiazide (thiazide group). Thirteen patients did not have any treatment for osteoporosis and served as a patient control group. There were no significant differences in age, underlying disease, dose of glucocorticoid, or pretreatment values of indices of osteoporosis among the three groups. Twenty-four hour urinary calcium excretion had increased above 300 mg/g creatinine at 12 or 24 months after the start of the treatment in 9 patients of the 1 alpha-OHD group, and asymptomatic renal stones developed in 2 of them. However, neither hypercalciuria nor renal stones developed in the thiazide group or the control group. Serum iPTH levels were suppressed significantly in the thiazide group, but did not change in the 1 alpha-OHD group or the control group. Metacarpal index (MCI) and sigma GS/D, indices of microdensitometry method which indicate bone mineral content, had significantly increased after 12 and 24 months in the thiazide group, while these indices did not change significantly in the 1 alpha-OHD group and deteriorated in the control group at 24 months. Seven patients of the control group and 4 of the 1 alpha-OHD group showed deteriorations in Singh's grade compared to only 2 in the thiazide group. Vertebral bone fractures developed in 5 vertebras of the 2 patients in the control group and 4 of the 3 patients in the 1 alpha-OHD group during the 24 months. But none of the thiazide group suffered from bone fractures. It may be concluded that combination therapy with 1 alpha-OHD, calcium and thiazide is effective in the prevention of glucocorticoid-induced osteoporosis. Long-term administration of 1 alpha-OHD and calcium should be avoided in patients undergoing chronic glucocorticoid therapy because of the risk of the development of nephrolithiasis.
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PMID:[Long-term effect of 1 alpha-hydroxyvitamin D, calcium and thiazide administration on glucocorticoid-induced osteoporosis]. 279 61

The effects of endocrine disease on bone mass continue to attract attention. Investigations include the effects on the skeleton of thyroid disease, primary hyperparathyroidism, and their treatment. The effect of growth hormone replacement in adults with panhypopituitarism has also been investigated; children with treated growth hormone deficiency appear to reach adulthood with low bone mass. The indications for surgery in asymptomatic primary hyperparathyroidism have recently been reviewed. The associations between autoimmune thyroid disease and connective tissue disease have been investigated. Although patients with Graves' disease are frequently positive for antinuclear antibodies, there appears to be no increased risk of systemic autoimmune disease. The possible pathogenesis of diabetic bone disease via calcium malabsorption, hypercalciuria, reduced bone formation, and collagen abnormalities has been reviewed. A long-term study has clarified the links among diabetic control, limited joint mobility, nephropathy, and retinopathy. The possible mechanisms by which pregnancy may induce remission in rheumatoid arthritis have been discussed.
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PMID:Endocrine disease. 843 94

Hypercalcemia and hypercalciuria observed both in humans and in animals who were on long-term theophylline therapy, prompted us to investigate whether oral theophylline treatment at optimal doses causes any adverse side effects on bone metabolism in mild asthmatics. Therefore, serum osteocalcin (BGP) and total alkaline phosphatase (TALP, EC 3.1.3.1) as bone formation markers, serum prolidase I (EC 3.4.13.9) activity as a marker for collagen metabolism, urinary deoxypyridinoline (Dpd), hydroxyproline (Hyp) and fasting urinary calcium as bone resorption markers, were measured in 18 mild asthmatics who had been treated with theophylline over 1-10 years. Among measured bone turnover markers, BGP, TALP, and Hyp levels were found to be increased in mild asthmatics; and BGP showed the greatest percent mean increase (98%) over the healthy subjects. However, these increments did not exceed the upper reference limits. Serum prolidase I activity was also increased in mild asthmatics receiving theophylline. Our results indicate that theophylline therapy at optimal doses may not exert adverse side effects on bone homeostasis, but patients receiving supratherapeutic doses of theophylline should be under close examination in order to predict future bone mass status.
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PMID:Evaluation of the effect of low-dose oral theophylline therapy on some bone turnover markers and serum prolidase I activity in mild asthmatics. 1043 80

Advanced tumor osteopathy is characterized by abnormal bone turnover. Using a rat model of parathyroid hormone-related peptide (PTHrP)-mediated tumor osteolysis, the aim of the present study was to define the sequential changes in, and the association between, biochemical and histomorphometric indices of bone metabolism during the early stages of developing tumor osteopathy. Eight-month-old Wistar rats (n = 48) were subcutaneously inoculated with either 2 x 10(6) cells of the Walker carcinosarcoma 256, or saline on day 0, and treated with either saline or the bisphosphonate ibandronate until killing on day 8. Serum calcium (sCa), alkaline phosphatase (sTAP), and osteocalcin (sOC) and urinary calcium (uCa), deoxypyridinoline (uDPD), and pyridinoline (uPYD) were measured daily. In a second semilongitudinal experiment (n = 70), the number of osteoclasts and osteoblasts (N.Oc, N.Ob), trabecular bone volume (BV/TV), and osteoid volume (O.Ar) were assessed by histomorphometry. In untreated tumor-bearing animals, osteoclast numbers increased by 74% on day 3 (5.4 +/- 2.4 vs. 3.1 +/- 1.5/mm(2), p < 0.05), and trabecular bone volume fell by 24% on day 4 (12.5 +/- 2.0 vs. 15.8 +/- 1.2%, p < 0.05). Both time course and magnitude of these changes were closely reflected by an increase in uDPD (0.46 +/- 0.14 vs. 0. 31 +/- 0.15 nmol/12 h, p < 0.05) and uPYD on day 4 (1.44 +/- 0.25 vs. 1.03 +/- 0.3 nmol/12 h, p < 0.05), sCa (3.8 +/- 0.52 vs. 3.0 +/- 0. 13 mmol/L, p < 0.01), and uCa (0.13 +/- 0.08 vs. 0.03 +/- 0.01 mmol/12 h, p < 0.001) on day 6, and sTAP (254 +/- 127 vs. 120 +/- 40 U/L, p < 0.001) on day 7 (mean +/- SD), whereas sOC remained unchanged until day 8. When combining the results of the two experiments, a high correlation was found between the number of osteoclasts and the urinary excretion of PYD (r = 0.91) and DPD (r = 0.89). Treatment with ibandronate delayed hypercalcemia, abolished hypercalciuria, and accelerated bone resorption. We conclude that osteoclast activation is an early event in PTHrP-mediated osteolysis, which is closely reflected by the renal excretion of pyridinium cross-links of type I collagen. Therefore, specific biochemical markers of collagen breakdown may be useful as early indicators of developing tumor osteopathy.
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PMID:Association between histomorphometry and biochemical markers of bone turnover in a longitudinal rat model of parathyroid hormone-related peptide (PTHrP)-mediated tumor osteolysis. 1077 87

To investigate the role of the pro alpha 2(I) collagen chains of type I collagen in mineralization we used the oim (osteogenesis imperfecta model) mouse as our model system. The oim/oim mouse (homozygous for a null mutation in its COL1A2 gene of type I collagen) fails to synthesize functional pro alpha 2(I) collagen chains, synthesizing only homotrimers of pro alpha 1(I) collagen chains. To evaluate the role of pro alpha 2(I) collagen in type I collagen structure/function in mineralized tissues, we examined age-matched oim/oim, heterozygous (oim/+), and wild-type (+/+) mouse femurs and incisors for mineral composition (calcium, phosphorus, magnesium, fluoride, sodium, potassium, and chloride) by neutron activation analyses (NAA), and bone mineral content (BMC) and bone mineral density (BMD) by dual-energy X-ray absorptiometry (DEXA) in a longitudinal study (7 weeks to 16 months of age). NAA demonstrated that oim/oim femurs had significant differences in magnesium, fluoride, and sodium content as compared with +/+ mouse femurs, and oim/oim teeth had significant differences in magnesium content as compared to +/+ teeth. The ratio of calcium to phosphate was also significantly reduced in the oim/oim mouse femurs (1.58 +/- 0.01) compared with +/+ femurs (1.63 +/- 0.01). DEXA demonstrated that oim/oim mice had significantly reduced BMC and BMD as compared to oim/+ and +/+ mice. Serum and urine calcium, magnesium, and phosphorus levels, and Ca(47) absorption across the gut were equivalent in oim/oim and +/+ mice, with no evidence of hypercalciuria. These studies suggest that the known decreased biomechanical properties of oim/oim bone reflect both altered mineral composition as well as the decreased BMD, which further suggests that the presence of alpha2(I) chains plays an important role in mineralization.
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PMID:Oim mice exhibit altered femur and incisor mineral composition and decreased bone mineral density. 1091 14

Both diabetes and fractures affect a large proportion of older adults. Recent cohort studies indicate that diabetes itself is associated with increased risk of fracture of the hip, proximal humerus, and foot. Observational studies and animal models suggest that decreased bone strength in diabetes may contribute to fracture risk but this remains a controversial issue. Type 1 diabetes is associated with modest reductions in bone mineral density (BMD) but type 2 diabetes is often characterized by elevated BMD. This paradox of higher BMD but increased fracture risk in type 2 diabetes may be explained by a combination of more frequent falls and poorer bone quality. Diabetes can impact bone through multiple pathways, some with contradictory effects, including obesity, changes in insulin levels, higher concentrations of advanced glycation end products in collagen, hypercalciuria associated with glycosuria, reduced renal function, lower insulin-like growth factor-I, microangiopathy, and inflammation. A better understanding of how diabetes metabolism and treatments affect bone would improve fracture prevention efforts in older diabetic adults.
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PMID:Diabetes Mellitus: Does it Affect Bone? 1451 15

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

Diabetes mellitus and osteoporosis are chronic diseases with an elevated and growing incidence in the elderly. Recent epidemiological studies have demonstrated an elevated risk of hip, humerus and foot fractures in elder diabetic subjects. While type 1 diabetes is generally associated with a mild reduction in bone mineral density (BMD), type 2 diabetes, more prevalent in old subjects, is frequently linked to a normal or high BMD. Studies on experimental models of diabetes have suggested an altered bone structure that may help to explain the elevated risk of fractures observed in these animals and may as well help to explain the paradox of an incremented risk of fractures in type 2 diabetic elderly in the presence of normal or elevated BMD. In addition, diabetic elderly have an increased risk of falls, consequent at least in part to a poor vision, peripheral neuropathy, and weaken muscular performance. Diabetes may affect bone tissue by different mechanisms including obesity, hyperinsulinemia, deposit of advanced glycosilation end products in collagen fibre, reduced circulating levels of IGF-1, hypercalciuria, renal function impairment, microangiopathy and chronic inflammation. A better understanding of these mechanisms may help implement the prevention of fractures in the growing population of mature diabetics.
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PMID:[Osteoporosis and diabetes]. 1564 75


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