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)

Using the method of assessment of clavicular corticodiaphyseal indices, the authors investigated the mineralization of bones in a group of 215 type II diabetics and in 40 type I diabetics. From both groups patients were selected without detectable complications and these were compared with a sub-group of patients who had some complications. Furthermore the authors investigated the number of fractures of vertebral bodies and other bones. The poorest results as regards mineralization were found in complications which interfere with calcium absorption: enteropathies, chronic pancreatitis, gastrectomies, renal disease and in women also liver disease, in both with impaired vitamin D conversion. An adverse effect was exerted also by a reduced dietary calcium intake in subjects with lactose intolerance or increased urinary calcium excretion in idiopathic hypercalciuria. Low values were recorded in all patients with motor disorders in angiopathies, otherwise this complication alone did not cause major decalcification. Hysterectomy with ovariectomy were manifested by decalcification only in women where the operation was performed during a certain period before the menopause. Neuropathy and retinopathy alone without impaired locomotor activity do not cause deterioration of the bone mineralization in diabetics. Surprisingly good results were achieved also in a group of diabetics with steatosis of the liver but without severe damage of liver function. With a exceptions the number of fractures of vertebral bodies and other bones correlated with the level of their mineralization.
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PMID:[Diabetic osteopathies. 3. The effect of diabetic complications on bone mineralization]. 281 5

Although corticosteroids are effective in the treatment of hypercalciuria and hypercalcemia in chronic sarcoidosis, complications of their long-term use frequently limit therapy. We studied the efficacy of chloroquine in two patients with sarcoidosis who were unable to tolerate the dosage of corticosteroids required to control hypercalciuria and prevent the formation of renal stones. Over a three-year period, each patient received a 6-month and a 10-month course of oral chloroquine phosphate (500 mg per day) while continuing to receive corticosteroids at a fixed dose. Chloroquine therapy was associated with a significant reduction in levels of serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and urinary calcium. We observed a direct correlation between serum 1,25-(OH)2D levels and 24-hour urinary calcium excretion, supporting the hypothesis that excessive serum 1,25-(OH)2D is responsible for the hypercalciuria in sarcoidosis. Serum levels of 25-hydroxyvitamin D (25-(OH)D) did not change with therapy, suggesting that chloroquine may act by inhibiting the conversion of 25-(OH)D to 1,25-(OH)2D. Current dosage guidelines and ophthalmologic-surveillance techniques, which allow chloroquine to be administered with little risk of retinopathy, should permit an expanded role for this agent in the treatment of the calcium abnormalities of sarcoidosis.
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PMID:The effects of chloroquine on serum 1,25-dihydroxyvitamin D and calcium metabolism in sarcoidosis. 375

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