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)

Vitamin D and its metabolites are well-established regulators of bone mineral homeostasis. Their clearest role is in the prevention and treatment of rickets and osteomalacia, bone diseases characterized by inadequate bone formation, and mineralization. Much of the effectiveness of vitamin D and its active metabolite 1,25(OH)2D in treating such disorders rests with their ability to increase serum levels of calcium and phosphate principally by stimulating intestinal calcium and phosphate absorption. Osteoporosis is not a disease resulting from obvious deficiencies in vitamin D, calcium, and phosphate. More subtle deficiencies, however, may be found, especially among the elderly with decreased intake of dairy products, reduced sunlight exposure, and less efficient intestinal absorption of bone minerals. Such subtle deficiencies may account for the ability of vitamin D and calcium supplementation to have a beneficial effect on bone mineral density in this population. Estrogen administration to postmenopausal females raises 1,25(OH)2D levels, presumably through increased renal production, and this increase is associated with increased intestinal calcium transport. Serum measurements of the vitamin D metabolites in general, however, and 1,25(OH)2D in particular do not consistently show evidence of a decrease at the time of menopause. Although most studies show a fall in intestinal calcium transport with age, which can be reversed with 1,25(OH)2D or estrogen, even these observations have not been found consistently. Thus, some investigators have addressed the issue of tissue resistance to 1,25(OH)2D and have noted decreased VDR in the intestine and reduced 1,25(OH)2D accumulation by bone with age. Despite no obvious deficiency of vitamin D in most patients with osteoporosis, clinical trials with vitamin D or 1,25(OH)2D show promise. Vitamin D treatment will probably prove most efficacious in populations with marginal vitamin D intake and/or limited sunlight exposure; high doses would not be required, and the treatment would be safe. This would be a physiologic and not a pharmacologic use of vitamin D. The use of 1,25(OH)2D for treatment of osteoporosis in individuals with adequate nutrition and sunlight exposure may require somewhat higher than physiologic doses to be effective. Perhaps such doses are necessary to stimulate osteoblast activity and/or differentiation; by raising the serum calcium level, such doses of 1,25(OH)2D might block its otherwise stimulatory effect on osteoclast number and activity. Such doses run the risk of hypercalcemia and hypercalciuria, leading to nephrolithiasis and/or nephrocalcinosis. These undesirable side effects appear to be less common with the use of 1 alpha OHD compared with 1,25(OH)2D, but this may be because of the lower levels of calcium consumption in Japan where 1 alpha OHD is widely prescribed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of vitamin D, its metabolites, and analogs in the management of osteoporosis. 798 88

Decreased bone density and increased fracture risk are seen in patients with SCI. The bone resorption rate is markedly increased. Hypercalciuria, low PTH, and low 1,25 (OH)2 vitamin D are commonly seen. Bed-rest studies show similar findings, but of lesser magnitude. Therapies to treat or prevent osteoporosis include optimal nutrition (with care to avoid exacerbating hypercalciuria). Weight-bearing or functional electrical stimulation cycle ergometry may prevent some of the bone loss, especially in acutely injured patients. Estrogen should be considered in postmenopausal or amenorrheic women, but not if they are at high risk of thromboembolism. More research on effects of estrogen is needed in this population. Bisphosphonates may also help prevent the acute bone loss; oral routes must not be used in recumbent patients. Thiazides could be useful as adjunct therapy.
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PMID:Osteoporosis in women with spinal cord injuries. 1185 32

The effect of estrogens on human growth hormone (HGH) and serum sulfation factor was studied in 4 acromegalic and 3 growth hormone-deficient men. Estrogen treatment (.5-1 mg/day) of acromegalic patients for 7-18 days reduced elevated sulfation factor levels, hypercalciuria, and hydroxyprolinuria levels without markedly affecting HGH levels. Increases in blood urea nitrogen and urinary nitrogen reflected the antianabolic effect of estrogen. Subnormal sulfation factor concentrations in HGH-deficient patients were increased to normal or high levels during 4-6 days of HGH administration and returned to pretreatment levels within 2 days of the last treatment. Combined estrogen and HGH treatment inhibited the elevation of serum sulfation factor, urinary calcium, and hydroxyproline excretion, but did not affect the anabolic response to HGH. Urinary calcium and hydroxyproline levels varied in a fashion similar to serum sulfation factor. The response to HGH in estrogen-treated hypopituitary patients seems to indicate that the stimulation of serum sulfation factor is not required for the anabolic action of HGH.
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PMID:Suppression of growth hormone-dependent human serum sulfation factor by estrogen. 1233 22

During pregnancy and lactation women have to form and maintain fetus and newborn skeleton. These processes require maternal hormonal and metabolic adjustments. During the first weeks of pregnancy, calcium intestinal absorption rise and reach a maximum in the last trimester. Hypercalciuria can be detected until lactation is stopped. During lactation, calcium that is present in maternal milk, results from lowering maternal calcium excretion and increasing bone resorption. Plasma 1,25 (OH)(2) D(3) levels increase two-fold early in pregnancy due to high placental 1-alpha-hydroxilase activity, remain high until delivery and decline to normal values during lactation. Estrogen, prolactin and placental lactogen, which are involved in calcium absorption, increase at the same time. Normal or even low levels of parathyroid hormone (PTH) can be detected during pregnancy. This suggests that their physiological actions could be mimicked by the parathyroid- related-peptide (PTHrP), which increases in late stages of pregnancy and remain high during delivery and lactation. Calcitonin levels increase during pregnancy, decline during lactation and return to normal values after lactation is stopped. The physiological roll of tumor necrosis factor, interleukin 6 and osteoprotegerin has not been elucidated yet. The above mentioned changes can exceptionally lead to generalized or regional osteoporosis. The aim of this article is to review the published bibliography concerning the physiopathology of these diseases.
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PMID:[Osteoporosis during pregnancy and lactation]. 1643 84