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 cuase for the intestinal hyperabsorptionof calcium (Ca) in various forms of hypercalciurias was explored by a careful measurement of plasma 1 alpha, 25-dihydroxycholecalciferol [1 alpha, 25-(OH)I D] and by an assessment of intestinal Ca absorption and of parathyroid function. In 18 cases of primary hyperparathyroidism (PHPT), the mean plasma concentration of 1 alpha, 25-(OH)2D was significantly increased (4.9 +/- 2.2 SD ng/dl vs. 3.4 +/- 0.9 ng/dl for the control group), and was significantly correlated with fractional Ca absorption (alpha) (r = 0.80, P less than 0.001). Plasma 1 alpha, 25-(OH)2D was also correlated with urinary Ca (P less than 0.05), but not with serum Ca or phosphorus (P), P clearance, urinary cyclic AMP, or serum immunoreactive parathyroid hormone. In 21 cases of absorptive hypercalciuria (AH), plasma 1 alpha, 25-(OH)2D was elevated in one-third of cases, and the mean value of 4.5 +/- 1.1 ng/dl was significantly higher than that of the control group (P less than 0.01). Since relative hypoparathyroidism may be present, the normal absolute value of plasma 1 alpha, 25-(OH)2D, found in two-thirds of cases of AH, may be considered to be inappropriately high. Moreover, in the majority of cases of AH, the data points relating plasma 1 alpha, 25-(OH)2D and alpha fell within 95% confidence limits of values found in non-AH groups (including PHPT). The results suggest that the intestinal hyperabsorption of Ca in PHPT aw AH may be vitamin D dependent. However, the disturbance in vitamin D metabolism may not be the sole cause for the high Ca absorption in AH, since in some patients with AH, the intestinal Ca absorption appears to be inapp
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PMID:The role of 1 alpha, 25-dihydroxyvitamin D in the mediation of intestinal hyperabsorption of calcium in primary hyperparathyroidism and absorptive hypercalciuria. 19 63

In an effort to maintain normal serum calcium levels without inducing hypercalciuria, we treated seven hypoparathyroid patients for up to 25 months with chlorthalidone, a thiazide-like sulfonamide diuretic, plus a salt-restricted diet, without added vitamin D. Mean 24-hour calcium excretion decreased from 179 to 88 mg (P less than 0.001), and mean serum calcium increased from 8.2 to 9.3 mg per deciliter (P less than 0.05). Diuretic therapy or moderate salt restriction alone was not as effective as combined therapy. Beneficial effects were sustained for as long as therapy was maintained. The rise in serum calcium, which involves the filterable and ionized fractions, cannot be due entirely to reduced excretion and may in part be explained by increased intestinal absorption. Oral chlorthalidone plus a low salt diet appears to be an effective alternative to vitamin D in the maintenance therapy of at least some patients with hypoparathyroidism.
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PMID:Treatment of hypoparathyroid patients with chlorthalidone. 62 74

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

In two patients (father and daughter) with idiopathic hypoparathyroidism, one of whom was resistant to the action of vitamin D2 and AT-10, 1alpha-hydroxycholecalciferol (1alpha-(OH)D3) in doses of 2-5 mug/day restored the serum calcium concentration to the normal range. The calcemic effect of 1alpha (OH)D3 was in both patients due to an increased intestinal calcium absorption and increased calcium mobilization from bone. In one of the patients 1alpha-(OH)D3 also increased the renal tubular calcium reabsorption; in the other it did not have this effect, resulting in hypercalciuria as serum calcium rose. The lack of effect on tubular calcium reabsorption probably accounts for the relative resistance to the action of 1alpha-(OH)C3 in this patient compared with other.
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PMID:1alpha-hydroxycholecalciferol in the treatment of hypoparathyroidism. 83 68

Fifty eight patients with thyrotoxicosis were examined as well as 9 patients with hypothyroidism and 40 healthy subjects. A tendence towards hypercalcemia and hyperphosphatemia, hypercalciuria, hyperhydroxiprolinuria, elevated alkaline phosphatase were found in hyperthyroidism. In hypothyroidism--hypocalcemia, hypocalciuria, hypohydroxiprolinuria. The changes are associated with the direct effect of thyroid hormones upon bone system (intensified bone metabolism with predominance of destruction). Calciuria and HOP-uria in thyrotoxicosis depend on the severity of the disease. The elevated calcium excretion in thyrotoxicosis speaks for the presence of ostemalacic component. TRP, PEI, mean diametrically opposite in hyper- and hypothyroidism, support the hypothesis of the secondary hypoparathyroidism in thyrotoxicosis and hyperparathyroidism--in the hypothyroidism.
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PMID:[Studies of calcium-phosphorus metabolism in thyrotoxicosis]. 91 16

The tubular reabsorption of calcium is increased in primary hyperparathyroidism as compared to control subjects and patients with resorptive hypercalciuria. The mean percentage of filtered calcium being reabsorbed by the renal tubules is decreased in primary hyperparathyroidism and hypercalciuria. This might point towards a maximal tubular transport capacity being exceeded in some cases of primary hyperparathyroidism whereas a relative hypoparathyroidism with decreased stimulation of tubular calcium reabsorption might be involved in hypercalciuria.
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PMID:[Renal calcium excretion in primary hyperparathyroidism and idiopathic hypercalciuria (author's transl)]. 105 87

Ingestion of alcohol evokes hypoparathyroidism, hypercalciuria, and hypermagnesuria. The dose-dependency of these changes has not been assessed before. We measured the serum concentrations of intact parathyroid hormone (PTH), and serum and urine calcium and magnesium in six normal men before and at intervals up to 6 h after the ingestion of fruit juice (control) and 0.5, 1.0 and 1.3 g of alcohol per kg of body weight. As compared with the control experiment the maximum reductions in the mean PTH concentration were 31% (P = 0.19), 31% (P = 0.20) and 45% (P = 0.01) with the three alcohol doses, respectively. After stopping drinking, the urinary excretion of calcium was 85%, 142% and 207% higher during the three alcohol experiments than during the control session (P < 0.05, < 0.01 and < 0.01, respectively), also urinary magnesium increased up to threefold. We conclude that in nonalcoholic subjects acute alcohol intake induces hypoparathyroidism, hypercalciuria, and hypermagnesuria, the latter two being dose-dependent. The direct renal effects of alcohol are the major mechanisms for hypercalciuria and hypermagnesuria, but hypoparathyroidism contributes to hypercalciuria at high levels of alcohol intoxication.
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PMID:The dose-dependency of alcohol-induced hypoparathyroidism, hypercalciuria, and hypermagnesuria. 142 7

Hundred thirty patients with surgical hypoparathyroidism were followed up. Group I involved 45 patients with mild and group II--85 patients with severe surgical hypoparathyroidism. A delay in vitamin D3 therapy was X +/- SD = 4.2 +/- 8.1 years. A delay in introducing vitamin D3 therapy correlated with the duration of hypoparathyroidism (r = 0.93; 8.9 +/- 9.6 years). Follow up period lasted for 15 years and was 4.3 +/- 3.8 years out of which the attempts to establish ultimate and effective dose of vitamin D3 lasted 1.8 +/- 2.4 years. Dose of vitamin D3 was adjusted 5 times, on the average. Effective daily dose was 4,200-22,500 IU (9,311 +/- 7,252) in group I, and 30,000-195,000 IU (51,385 +/- 32,978) in group II whereas maximum daily dose was 75,000 and 250,000 IU respectively (p < 0.001). Some patients were given 25-OH-D3 in daily doses of 50-225 micrograms or 25(OH)2-D3 in daily dose of 0.10-0.75 micrograms. Calcium oral doses of 400-1600 mg daily were administered to 115 patients. In case of high hypercalciuria (over 350 mg/24 h) hydrochlorothiazide (43 +/- 17 mg a day) or chlorthalidone (60 +/- 22 mg a day) normalized calciuria. Low phosphate diet and aluminium oxide (4.4 +/- 1.7 g a day) were more frequently used in group II. Period of time necessary to establish an effective dose of vitamin D3 is long in patients with surgical hypoparathyroidism. Several dose adjustments are required. Maximum daily vitamin D3 dose required for normocalcemia is approximately higher by 1/3 in the early period of the treatment than the effective maintenance dose. A decrease in diet phosphate content, inhibition of phosphates absorption in the gut or blocking increased calcium loss with the urine are necessary in some patients, only.
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PMID:[Postoperative hypoparathyroidism: long term observation and therapy]. 166 67

For assessing the risk of adverse complications of surgery the group of 130 patients with post-operational hypoparathyroidism was analysed. Surgical hypoparathyroidism has been diagnosed in 51% of operated on thyroid gland patients. Laryngeal nerves have been damaged in 46.6% of patients. The injury to laryngeal nerves has been irreversible in 2/3 of patients, and reversible in the remaining 1/3. Cataract, nephrolithiasis and vitamin D3 intoxication have been observed in some cases before surgery. Their incidence increased in severe surgical hypoparathyroidism. Osteoporosis of the spine has been diagnosed in 49% of patients including some with vertebral fractures. No correlation between the degree of spine osteoporosis and diagnosis before surgery, number of operations on thyroid gland, and type of therapy has been noted. The symptoms of hypercalcemia have been diagnosed in 5 patients out of which hypercalcemia has been transient in 2 patients, and lasted for 1-5 months in the remaining 3 patients. The results of 7,873 analyses of mineral metabolism have been assessed. Hypocalcemia has been found in 38.4%, hypercalcemia in 1.6%, hypomagnesemia in 25.7%, hyperphosphatemia in 41.5%, decreased alkaline phosphatase serum activity in 28.7%, and hypercalciuria in 22.4% of cases. Surgical hypoparathyroidism is frequently accompanied by surgical hypothyroidism and injury to the recurrent laryngeal nerves.
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PMID:[Postoperative hypoparathyroidism: risk of complications]. 166 68

Abuse of alcohol is considered to be an important risk factor for fractures and osteoporosis. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density. These changes may also be produced by factors commonly associated with alcohol abuse, e.g., nutritional deficiencies, liver damage, and hypogonadism. Thus the etiology of alcohol-associated bone disease is multifactorial. Alcohol has, however, clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcemia and hypercalciuria. Prolonged moderate drinking elevates serum parathyroid hormone (PTH) levels, whereas chronic alcoholics are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria. Independently of whether alcohol consumption is of short duration, social, or heavy and chronic, it seems to suppress the function of osteoblasts, as evidenced by low serum levels of osteocalcin. It has recently been reported, however, that alcohol can also have a beneficial effect on bone. Among postmenopausal women, moderate alcohol consumption correlates positively with central and peripheral bone mineral density, and with serum estradiol levels.
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PMID:Alcohol and bone. 193 4


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