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)

We investigated the effects of 1,25-dihydroxyvitamin D3 (1,25-(OH)2-D3) on cultured fibroblasts and keratinocytes from patients with psoriasis and treated 17 patients with psoriasis with orally or topically administered 1,25-(OH)2-D3. Cultured fibroblasts from three of five patients showed a normal response to the antiproliferative activity of a physiologic dose of 1,25-(OH)2-D3, whereas fibroblasts from the other two had a partial resistance to the drug. Cultured keratinocytes from two patients with psoriasis possessed nuclear receptors for 1,25-(OH)2-D3 and the drug caused a dose-dependent inhibition of proliferation and induction of terminal differentiation of these cells similar to effects in normal cultured keratinocytes. Ten of 14 patients with moderate to severe psoriasis who received oral 1,25-(OH)2-D3 showed significant clearing of their hyperkeratotic plaques. Three patients had complete clearing that was sustained with maintenance therapy, but four patients received little or no benefit from the therapy. By the administration of 1,25-(OH)2-D3 as a single oral dose at bedtime, larger doses of the drug could be tolerated without evidence of hypercalciuria or hypercalcemia. Three patients who received topical 1,25-(OH)2-D3 showed a rapid response with complete clearing after 6 weeks of therapy. Therefore, these preliminary findings suggest that orally or topically administered 1,25-(OH)2-D3 may be a safe and effective alternative therapy for the treatment of psoriasis.
J Am Acad Dermatol 1988 Sep
PMID:A novel approach for the evaluation and treatment of psoriasis. Oral or topical use of 1,25-dihydroxyvitamin D3 can be a safe and effective therapy for psoriasis. 245 66

Vitamin D has complex effects in bone: it stimulates matrix formation and bone maturation but also enhances osteoclastic activity and may influence differentiation of bone cell precursors. Calcitonin inhibits the function of osteoclasts, reducing bone resorption, thus, the combination of vitamin D and calcitonin could result in a positive bone balance. We tested the hypothesis that chronic treatment with high doses of vitamin D (150,000 U/week), moderate doses of salmon calcitonin (120 MRC U/week), and adequate Ca supplementation (1 g/day) could be beneficial in osteoporosis. Thirteen women with postmenopausal osteoporosis received this treatment for 2-6 years (mean 3.5 years). No side effects, hypercalcemia, or hypercalciuria occurred. There was marked reduction in bone pain. The fracture rate in 11 patients with vertebral compression fracture was 240/1,000 patient years, threefold lower than the reported 834 fractures for untreated patients of similar age. Single photon bone densitometry of the radius did not change. Iliac crest bone biopsies obtained at the initiation and conclusion of the study showed a 43% increment in trabecular bone volume (P = 0.0003), without changes of the normal osteoid thickness, surface, and volume. Because single photon densitometry reflects mostly cortical bone, the data suggest that the combination of vitamin D and calcitonin increases trabecular bone mass and prevents the fall of cortical bone mass in osteoporosis. Previous reports suggest that calcitonin alone or with small doses of vitamin D increased bone mass for about 2 years. The present study suggests a prolonged beneficial effect of the combination of high doses of vitamin D with rather moderate (less than 150 MRC U/week) doses of calcitonin in postmenopausal osteoporosis.
Calcif Tissue Int 1989 Sep
PMID:Effect of calcitonin and vitamin D in osteoporosis. 250 3

52 patients with Cushing syndrome were studied. According to the appearance of X-ray film of bones, they were divided into three groups: (I) Without osteoporosis, 12 cases (23.1%), (II) Mild osteoporosis, 17 cases (32.7%), (III) Severe osteoporosis with fractured ribs and/or wedge-shaped vertebrae, 23 cases (44.2%). It was found that the mean level of serum calcium in the patients was significantly lower than that in 94 normal subjects (mean +/- S 2.3 +/- 0.2 versus 2.4 +/- 0.1 mmol/L P less than 0.001). The mean concentrations of blood alkaline phosphatase and parathyroid hormone in the patients were much higher than those in normal subjects (65.0 +/- 27.6 versus 42.6 +/- 15.6 IU/L P less than 0.001, 44.6 +/- 22.4 versus 20.6 +/- 8.0 pg/ml P less than 0.001 respectively). The mean level of serum 25 (OH)-D in the patients was significantly lower than that in controls (10.9 +/- 5.6 versus 16.2 +/- 4.6 ng/ml P less than 0.001). Urinary calcium excretion increased in the patients as compared with that in controls (P less than 0.01). The urinary calcium excretion correlated well with the blood total cortisol and urinary free cortisol. It is suggested that hypercalciuria might cause decrease of serum calcium. Thus the parathyroid glands were stimulated and the parathyroid hormone (PTH) secretion was increased. Excess of PTH stimulates bone resorption. All of these factors are involved in the pathogenesis of osteopenia in Cushing's syndrome.
Zhonghua Nei Ke Za Zhi 1989 Sep
PMID:[Metabolism of calcium and phosphorus in Cushing syndrome with osteoporosis]. 262 28

Some children with Bartter syndrome have hypercalciuria. To determine the mechanism for this phenomenon, we studied tubular function and calcium metabolism in six such children. All patients had hypokalemic alkalosis, normotension, hyperreninemia, growth retardation, low fractional distal chloride reabsorption (4/5), and elevated urinary prostaglandin E2 excretion (5/6). In addition, all had hypercalciuria (urinary calcium 6.5 to 25.0 mg/kg/day), with evidence of nephrocalcinosis in five. None, however, had evidence of rickets or hyperparathyroidism. There was a marked elevation in the serum concentration of 1,25-dihydroxyvitamin D in all, and four patients had a response to oral calcium loading suggestive of absorptive hypercalciuria. Five children have had long-term therapy with indomethacin. They have had improvement in hypokalemia and reduced urinary prostaglandin E2 excretion as well as reductions in the serum concentration of 1,25-dihydroxyvitamin D and in urinary calcium excretion. These data suggest that hypercalciuria in some children with Bartter syndrome is associated with an excess of 1,25-dihydroxyvitamin D. The improvement in hypercalciuria with prostaglandin synthesis inhibition may result in part from correction of this vitamin D abnormality.
J Pediatr 1989 Sep
PMID:Hypercalciuria with Bartter syndrome: evidence for an abnormality of vitamin D metabolism. 267 27

The endogenous overproduction of active vitamin D sterols plays a central causative role in the hypercalcemic/hypercalciuric state associated with granuloma-forming diseases, most notably sarcoidosis, as well as with some human lymphomas. In sarcoidosis, the offending metabolite is most likely 1,25-(OH)2-D and the synthetic source is the disease-activated macrophage. About 50% of hypercalcemic patients with lymphoma harbor frankly elevated or inappropriately high serum 1,25-(OH)2-D concentrations. The source of the hormone in patients with lymphoma is not yet known. The endogenous synthesis of 1,25-(OH)2-D in patients with active sarcoidosis and lymphoma is not subject to regulation by those factors that normally control the production of 1,25-(OH)2-D by the renal 25-OH-D-1-hydroxylase. Treatment and prevention of vitamin D metabolite-mediated hypercalcemia/hypercalciuria consist of pharmacologic inhibition of the abnormal 1-hydroxylation reaction and limitation of substrates for the reaction. The former is best accomplished by the administration of anti-inflammatory concentrations of glucocorticoids and the latter by controlling vitamin D intake and sunlight exposure in susceptible hosts.
Endocrinol Metab Clin North Am 1989 Sep
PMID:Vitamin D metabolite-mediated hypercalcemia. 267 72

Increased gut calcium absorption or reduced renal tubular calcium reabsorption have been alternatively reported in idiopathic hypercalciuria with kidney calculi. The present study aimed to investigate the handling of an exogenous calcium load in hypercalciuric stone formers to detect possible differences with regard to tissue calcium metabolism in vivo. A constant rate intravenous calcium infusion (0.2 mmol kg bodyweight per two hours) was carried out on six absorptives and six renals, defined according to the reported criteria, as well as on normal controls from clinical staff. Serum ionized calcium concentration were determined at regular intervals during the infusion and in the four hours after the end of calcium load. Over the same period, urinary calcium excretion was evaluated in timed urine collections. Absorptive and renal hypercalciurics had lower serum ionized calcium levels compared with normal controls at all experimental times, a finding that suggests a faster disappearance of calcium from the circulation. The total body calcium clearance calculated from the area under the curve of the serum calcium concentrations was enhanced in hypercalciuric patients (P less than .001). Although renal calcium excretion was higher in hypercalciurics, renal calcium clearance accounted for only a minor fraction of the total body clearance, suggesting that the reduced serum calcium levels found in the hypercalciurics could not be explained by the renal calcium leak. The enhanced total body calcium clearance found in hypercalciuric subjects is therefore due to an increased tissue calcium uptake. This finding provides indirect evidence of altered cell calcium handling in idiopathic hypercalciura with no difference between the so-called absorptives and renals in terms of the pathophysiologic mechanism.
Metabolism 1989 Sep
PMID:Altered kinetics of an intravenous calcium load in idiopathic hypercalciuria. 277 May 33

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.
Vnitr Lek 1989 Sep
PMID:[Diabetic osteopathies. 3. The effect of diabetic complications on bone mineralization]. 281 5

Previous studies of 1,25-dihydroxyvitamin D [1,25-(OH)2D] kinetics in normal subjects using the pulse injection technique have led to conflicting results, and only limited data are available concerning 1,25-(OH)2D kinetics in hypercalciuric patients. We developed an infusion equilibrium technique that measures the metabolic clearance and production rates of 1,25-(OH)2D and applied this technique in 13 normal subjects and 9 well characterized patients with absorptive hypercalciuria; all subjects were studied after 10 days on a 400-mg calcium intake. All subjects received a constant infusion of [3H]1,25-(OH)2D3 (20,000 dpm/min). Purified plasma radioactivity reached steady state levels after 15 h, and between 15 and 19 h, serial measurements of purified plasma radioactivity and endogenous 1,25-(OH)2D were made for calculation of metabolic clearance and production rates. In the 13 normal subjects, the MCR values were within a narrow range, with a mean +/- SD value of 37 +/- 6 ml/min, which, when combined with the mean steady state concentration of endogenous 1,25-(OH)2D (42 +/- 6 pg/ml), yielded a mean production rate of 2.2 +/- 0.5 micrograms/day. In the 9 patients with absorptive hypercalciuria, MCR values also were tightly clustered, with a mean of 35 +/- 4 ml/min. However, the mean endogenous steady state 1,25-(OH)2D level was significantly elevated in these patients, such that the calculated mean 1,25-(OH)2D production rate was significantly elevated at 3.4 +/- 0.5 micrograms/day. In 7 of the 9 patients with absorptive hypercalciuria, production rates exceeded the highest values found in the normal subjects. These data demonstrate disordered 1,25-(OH)2D production as opposed to metabolic clearance in the syndrome of absorptive hypercalciuria.
J Clin Endocrinol Metab 1985 Sep
PMID:Elevated production rate of 1,25-dihydroxyvitamin D in patients with absorptive hypercalciuria. 299 23

To examine the effects of mineralocorticoidism on calcium (Ca) absorption and to define the mechanism, rats received a high-salt diet and injections of vehicle or deoxycorticosterone acetate (DOCA). Net (44.2 vs. 31.4 mg/day) and percent Ca absorption (28.1 vs. 20.1%) was increased after 5 days of DOCA. This was associated with increased duodenal 45Ca uptake. Thus despite the hypercalciuria, Ca balance was similar. Although the hypercalciuria persisted chronically, the gut effects were sustained, which maintained normal ionized Ca, bone Ca, and Ca balance. Urinary cyclic adenosine monophosphate was elevated by DOCA. Compared with appropriate controls, neither DOCA alone nor polydipsia (elicited by dextrose) produced similar magnitudes of hypercalciuria as DOCA plus high-salt diet. These maneuvers also failed to increase Ca absorption. Neutralization of the metabolic alkalosis neither attenuated the DOCA-induced hypercalciuria nor abolished the Ca hyperabsorption. In vitamin D-deprived rats, the hypercalciuria but not the intestinal effects of DOCA were reproduced. Serum 1,25-dihydroxyvitamin D3 levels were increased during chronic DOCA treatment (224 vs. 139 pg/ml). These data best fit the hypothesis that increased Ca absorption is secondary to the calciuric effects of DOCA and high-salt diet and is mediated via the increased parathyroid hormone and 1,25-dihydroxyvitamin D3 activities.
Am J Physiol 1986 Sep
PMID:Chronic DOCA treatment increases Ca absorption: role of hypercalciuria and vitamin D. 301 51

Poorly controlled type II diabetic patients with hypomagnesaemia, hypermagnesuria, and hypercalciuria were allocated to treatment with either metformin or glipizide, to determine the effects on some indices of mineral metabolism. Despite comparable improvement in glycaemic control, assessed by glucose and haemoglobin A1, there were significant differences between the two groups in the handling of magnesium. Patients receiving metformin showed a reduction in magnesium excretion but remained hypomagnesaemic and hypercalciuric. In contrast, patients receiving glipizide exhibited little change in either magnesium or calcium excretion but showed a significant rise in serum magnesium.
J Clin Pathol 1988 Sep
PMID:Effects of improved glycaemic control on calcium and magnesium homeostasis in type II diabetes. 319 52


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