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)

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.
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PMID:Antacid therapy--changes in mineral metabolism. 629 43

Although the nutritional aspects related to bone development and subsequent bone loss have been appreciated for many years, they are now being reemphasized in view of current information concerning the vitamin D endocrine system, the development of new assay procedures and more sensitive radiologic techniques to assess changes in bone mass, and the realization that clinical problems related to bone loss will increase as individuals live longer. The vitamin D endocrine system is complex, involving the skin, liver, and kidney for synthesis of the vitamin D metabolites and, primarily, the intestine and bone for biologic expression. Numerous factors and disorders affecting the skin, gastrointestinal tract, and kidney will adversely affect vitamin D metabolism. Vitamin D deficiency is common in elderly individuals, especially those who are chronically ill, house-bound, and poorly nourished. Subclinical vitamin D deficiency and osteomalacia may also be complicating problems in elderly patients with osteoporosis and hip fractures. At present the role of the vitamin D endocrine system in the pathogenesis and treatment of osteoporosis is unclear. There is little evidence that vitamin D or its metabolites are helpful in osteoporosis, except perhaps to heal osteomalacia which may be present. It is hoped that encouraging results will follow the use of more potent vitamin D metabolites, either alone or in combination with other agents. Calcium homeostasis is affected by numerous dietary factors (including protein, phosphorus, fiber, and lactose) and drugs (including alcohol, diuretics, and antacids), and calcium absorption in the intestine and the ability to adapt to low-calcium diets will decrease with advancing age. There are conflicting reports concerning the relation between low-calcium intake and osteoporosis, and about the role of calcium intake in the development and then maintenance of bone mass. There is little doubt that many older individuals ingest less calcium than is recommended, especially at a time when even more may be required to maintain bone mass. Several studies show that calcium supplementation producing a total calcium intake of 1,200-1,500 mg/day can slow the rate of bone loss. When the high doses of calcium are given along with vitamin D, periodic monitoring of blood and urine calcium is necessary to avoid hypercalcemia and hypercalciuria.
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PMID:The vitamin D endocrine system, calcium metabolism, and osteoporosis. 636 21

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
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PMID:Vitamin D and bone health in the elderly. 676 68

We have prospectively investigated calcium and bone metabolism in 16 patients receiving total parenteral nutrition for periods ranging from 7 to 89 months. In 12 patients, bone biopsies at 6 to 73 months after the start of parenteral nutrition showed osteomalacia. Plasma 25-hydroxyvitamin D levels were normal in all patients. Seven persons developed hypercalcemia, and 10 had hypercalciuria with a negative calcium balance. Serum phosphorus was normal and plasma parathyroid hormone level, normal or decreased. Three patients with the severest form of the disease had vitamin D withdrawn from their solutions. Subsequently, urinary calcium decreased, and serum calcium became normal; two persons reverted to a positive calcium balance. Thus, patients receiving total parenteral nutrition may develop metabolic bone disease characterized by osteomalacia, hypercalcemia, hypercalciuria, and a negative calcium balance. This may be caused by both defective mineralization and increased bone resorption induced by vitamin D, its metabolites, or another unrecognized factor.
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PMID:Metabolic bone disease in patients receiving long-term total parenteral nutrition. 676 94

A 60-year-old woman was evaluated for bone pain and incapacitating weakness. Initial laboratory studies showed a serum calcium level of 10.1 mg/dL, severe hypophosphatemia (1.1 mg/dL), and an elevated alkaline phosphatase level. X-ray films showed changes consistent with osteomalacia. Further studies revealed hypercalciuria (448 mg/24 hr) but absent urinary phosphorus. These data indicated phosphate malabsorption. Excessive use of an aluminum hydroxide-containing antacid was the cause of this patient's failure to absorb dietary phosphate. The features of this syndrome are reviewed to increase physicians' awareness of this illness, which occurs particularly in the elderly and is easily treated.
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PMID:Osteomalacia and weakness from excessive antacid ingestion. 743 92

The authors analyse the results obtained during 54 radioisotope investigations using 45Ca in 13 cases of idiopathic hypercalciuria, 12 cases of osteoporosis, 3 cases of Paget's disease, and 2 cases of osteomalacia including one of Fanconi's disease in an adult. In 12 patients, repetition of the radio-isotope test two, three or four times; permitted the authors to study the effects of the treatments administered: calcitonin, phosphate, vitamin D, parathormon, oestrogen. Calcitonin increases intestinal absorption and reduces bone reabsorption and also accretion. Phosphate greatly increases accretion and bone reabsorption in vitamin-resistant osteomalacia of adults. The synthetic fragment 1--34 of human parathormone increases accretion and reabsorption but does not modify the calcium balance. The addition of estrogen reduces reabsorption and slightly increases accretion in two osteoporotic patients producing a positive calcium balance. This method of investigation is of great interest to assess the effects of a drug on calcium metabolism and on the two processes of bone remodelling.
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PMID:[Calcium metabolism study performed by means of Ca-45 in bone diseases and idiopathic hypercalciuria]. 745 4

A 12-year-old girl had a severe genu valgum deformity and osteomalacia with hypophosphatemia, hypercalciuria, and modestly elevated levels of 1,25-dihydroxyvitamin D3 and intact parathyroid hormone. This patient seems to have a different type of hypophosphatemic osteomalacia from that previously described.
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PMID:Osteomalacia with hypophosphatemia and hypercalciuria: a possible new variant of osteomalacia. 875 86

A 41-year-old man presented with back pain, osteoporosis and vertebral crushing. Laboratory studies revealed persistent hypophosphatemia, normocalcemia and elevated levels of 1,25-dihydroxy-vitamin D. Other mineral metabolism tests showed a low tubular maximal phosphate reabsorption per glomerular filtrate, an absorptive hypercalciuria and a normal intestinal absorption of phosphate. Hyperparathyroidism was ruled out by an intravenous calcium loading test. Bone histopathology was consistent with osteomalacia. Treatment with phosphate supplements resulted in resolution of symptoms and normalization of laboratory parameters. To our knowledge, this can be a sporadic form of a disorder recently described: hereditary hypophosphatemic rickets with hypercalciuria.
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PMID:Hypercalciuria secondary to chronic hypophosphatemia. 770 Feb 12

Careful examination as well as biochemical and hormonal investigations should be performed in men suffering from vertebral crush fractures, in order to detect a destructive skeletal process (multiple myeloma, bone metastatic lesions, lympho and myeloproliferative disorders), a mineralization defect (osteomalacia) or a secondary osteoporosis: primary hyperparathyroidism, hypogonadism, hyperthyroidism, renal hypercalciuria, alcoholism and tobacco smoking. The diagnosis of idiopathic osteoporosis should be made only after these causes have been excluded; the pathogenesis of the disease is unclear but risk factors have been identified: family history of osteoporosis, low dietary calcium intake, delayed puberty, ethanol use, tobacco smoking, inactive lifestyle and lean body build. Correction of risk factors, calcium supplementation, regular program of weight bearing physical activity, in some instances correction of testosterone deficiency may be of benefit to reduce bone loss. Severe osteopenia or osteoporosis may require sodium fluoride therapy.
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PMID:[Male osteoporosis]. 793 30

Phosphate plays a central role in many of the basic processes essential to the cell and organism. In particular, skeletal mineralisation is dependent on the appropriate regulation of phosphate in the body, and any disturbances in phosphate homeostasis can have severe repercussions on the integrity of bone. The kidney regulates the serum levels of phosphate by tubular mechanisms which are not fully understood. Furthermore, the processes involved in regulating renal tubular phosphate reabsorption are complex, and involve a large number of factors. It is not surprising therefore that defects in renal phosphate handling result in a failure of bone mineralisation. There are three well characterised conditions which are associated with renal tubulopathies resulting in a phosphate leak, with consequent bone disease. Two are familial, hypophosphataemic rickets (HYP), and hereditary hypophosphataemic rickets with hypercalciuria (HHRH). The third is acquired via a tumour, oncogenic hypophosphataemic osteomalacia (OHO), and may well have relevance to the inherited hypophosphataemias. Recent advances in molecular genetics are permitting the identification of genes involved in human diseases from their chromosomal location. These approaches are now being applied to the analysis of the hypophosphataemias. The isolation of the genes responsible for the renal tubulopathies will be an important achievement. Ultimately this will help to increase our understanding of the mechanisms involved in the control of phosphate handling in the body.
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PMID:Molecular biology of hypophosphataemic rickets and oncogenic osteomalacia. 795 77


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