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 effects of glucocorticoids on calcium and bone metabolism were investigated in 11 children (aged 6 months to 13 years) who were treated with dexamethasone, prednisolone and depot-ACTH because of different disorders. Alkaline phosphatase activity and osteocalcin in serum, representing indices of osteoblastic bone synthesis, and urinary hydroxyproline in relation to creatinine in morning fasting urine specimens, an index of osteoclastic bone degradation, decreased by 53-61% from baseline (P less than 0.01), with a highly significant relationship of all 3 indices to each other. Additional influences of glucocorticoids were hyperphosphaturia due to decreased renal phosphate reabsorption not mediated by secondary hyperparathyroidism, as well as marked hypercalciuria. As the consequence of the present study the following prophylactic or therapeutic recommendations are given during steroid-treatment: 1. Approvement of the negative balance of calcium and phosphate by correcting the hypercalciuria with hydrochlorothiazide, and the hypophosphatemia with oral phosphate and 2. in elder children with osteoporosis, stimulation of the decreased osteoblastic bone formation by sodium fluoride.
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PMID:[Disorders of calcium and bone metabolism in glucocorticoid treatment]. 284 91

An 8-year-old boy with idiopathic juvenile osteoporosis and multiple fractures had three abnormalities of bone mineral metabolism: calcitonin deficiency, elevated serum calcitriol concentrations, and hypercalciuria. Calcitonin deficiency was documented by two attempts to stimulate calcitonin secretion with intravenous calcium and pentagastrin. Treatment for 11 months with daily subcutaneous injections of human calcitonin and oral administration of calcitriol failed to reduce the excessive bone resorption observed on bone biopsy, and the fracture rate did not decrease. Treatment was discontinued for two months, then resumed with calcitonin injections and oral calcium supplementation. The fracture rate decreased but bone biopsy continued to show excessive resorption. Therapy was discontinued. After the onset of puberty, endogenous calcitonin was detectable. Exogenous calcitonin therapy may have failed to control bone resorption for several reasons: insufficient dose, reduction of bone receptors from long-term calcitonin exposure, secondary hyperparathyroidism, or lack of association between calcitonin deficiency and the bone disease.
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PMID:Effect of calcitonin replacement therapy in idiopathic juvenile osteoporosis. 317 35

The results are presented of an oral calcium tolerance test with 1,000 mg calcium in 20 patients with recurrent renal calcium calculosis, a woman with primary hyperparathyroidism and incipient renal failure (serum creatinine 1.8 mg%), creatinine clearance 55 ml/min) and 9 healthy persons as controls. The serum osteocalcin level was determined before and after the oral test. The results show that the serum osteocalcin level alone is of no differential diagnostic value for differentiation of the various types of hypercalciuria in patients with recurrent renal calcium calculosis. As a marker of osteoblasts functional state however the determination of serum osteocalcin level is of great importance for the early diagnosis of osteoporosis. In 3 patients with renal hypercalciuria, often leading to general osteoporosis, an acute rise of serum osteocalcin level was found after the oral calcium tolerance test. High osteocalcin level was also found in the patient with primary hyperparathyroidism and incipient renal failure.
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PMID:[Serum osteocalcin level as a marker of the functional state of osteoblasts after oral calcium tolerance test]. 326 44

Calcitriol was compared with placebo in the treatment of postmenopausal osteoporosis in a double-blind, randomized, parallel clinical trial of 24 months' duration. Adjustment was made in dietary calcium to maximize the dose of calcitriol. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. The calcitriol group had positive slopes (compared with negative slopes for the placebo group) for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. The difference between the two groups was statistically significant for each of these measurements. The fracture rate in the treatment group was 250 per 1,000 patient-years as compared with 333 for the placebo group. The mean dose of calcitriol was 0.8 micrograms per day. Hypercalcemia, hypercalciuria, and perhaps nephrolithiasis were observed as complications of treatment. Calcitriol increased bone mineral density by decreasing bone resorption, but not by increasing bone formation. Future studies should concentrate on treatment with oral calcitriol in lower doses. It would also be of interest to examine parenteral administration of calcitriol. It is possible that bone formation can be increased by achieving higher serum levels of the drug, whereas complications may be avoided by using a non-oral route of administration.
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PMID:Calcitriol in the treatment of postmenopausal osteoporosis. 327 69

Between 1981 and 1983, 49 children aged 2 to 15 years were diagnosed as having idiopathic hypercalciuria (IH). They were divided into 3 groups based on their response to dietary manipulation: group I (32/49) had absorptive hypercalciuria; group II (8/49) had renal hypercalciuria and group III (6/49) had sodium-dependent hypercalciuria. Response to diet was more reliable than Pak's test in differentiating between the three groups. A control group (CG) of 45 healthy, age matched children determined baseline levels for all metabolic parameters. At the time of presentation IH children did not differ from the CG in height or weight. Fifty percent of IH children had first degree relatives with urolithiasis. Yet, only 16% of the IH children had urolithiasis, the majority presenting with gross hematuria and urinary tract infections (UTI). With few exceptions the clinical symptoms resolved when urine calcium excretion was controlled. Severe calcium restriction in a few patients produced osteoporosis and delayed bone age although growth velocity was unaffected. Thiazide therapy in a few patients produced some metabolic derangements. The authors conclude that IH in childhood is a benign disease which may present with UTI or hematuria. They further propose a new classification method based on response to dietary manipulation.
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PMID:Idiopathic hypercalciuria in children. Classification, clinical manifestations and outcome. 359 Dec 93

There is evidence that prolactin (PRL) excess plays a role in the etiology of osteoporosis associated with human prolactinoma. Calcium balance in human hyperprolactinemia has not been thoroughly investigated. In the present study, rats with excess circulating PRL levels (male anterior pituitary-grafted Fischer 344 rats) had urinary calcium excretion twice that of control rats (4.16 +/- 0.43 v 2.25 +/- 0.30 mg/24h X 100 g BW). Calcium excretion expressed per mg of calcium intake was also high in pituitary-grafted rats. The excess calcium excretion in hyperprolactinemic rats was not accompanied by a concomitant rise in sodium excretion. This dissociation suggests that PRL has an effect on the renal handling of calcium. Since thiazide diuretics have a well-described hypocalciuric action, their effect was tested in these rats. In normal rats, benzthiazide, a long-acting agent, significantly reduced urinary calcium excretion in a dose-dependent fashion. Hyperprolactinemic rats responded to benzthiazide in a manner similar to control rats. In pituitary-grafted rats, benzthiazide also decreased the calcium excretion to intake ratio and normalized the calcium to sodium excretion ratio. Since the hypercalciuria of experimental hyperprolactinemia can be corrected by thiazide diuretics, these agents may have therapeutic potential in human PRL excess.
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PMID:Hypercalciuria in hyperprolactinemic rats: effects of benzthiazide. 372 59

The authors presented the results of a study of the indices of phosphorocalcium homeostasis, metabolism of osseous tissue and calcium regulating hormones in 44 patients with Icenko-Cushing's syndrome with regard to severity of disease and expression of osteoporosis. It was shown that disturbances of phosphorocalcium homeostasis and an increase in the level of the parathyroid hormone were characteristic for the active stage of Icenko-Cushing's disease and were most noticeable in a severe course of disease accompanied by sharply marked osteoporosis. Hypocalcemia, hypophosphatemia, hypercalciuria, a decrease in phosphate maximum resorption and an increase in AP activity in the blood serum were revealed in this form of disease. Patients with the average gravity of disease and weakly pronounced osteoporosis were characterized by hypercalcemia and an increase in calcium intestinal absorption. Patients with the active stage of hypercorticism were characterized by hypermagnesemia. Secondary hyperparathyrosis was found in 25% of patients with the active stage of Icenko-Cushing's disease.
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PMID:[Phosphorus-calcium metabolism and calcium-regulating hormones in endogenous hypercorticism]. 380 24

The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5'-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4.6 pmol human PTH(1-34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middle- and carboxyl-terminal region of the PTH molecule (r = 0.503, P less than 0.001). A positive correlation (r = 0.572, P less than 0.05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P less than 0.01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0.390, P less than 0.01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance. 394 39

An apparently unique presentation of osteoporosis was encountered in eight postmenopausal women (mean age, 56.8 yr). They had renal hypercalciuria, since they had fasting hypercalciuria [0.17 +/- 0.04 (+/- SD) mg/100 ml glomerular filtrate (GF)] in the setting of normocalcemia and parathyroid stimulation (high serum immunoreactive PTH and/or urinary cAMP). Serum 1,25-dihydroxyvitamin D was not significantly different (28 +/- 7 vs. 34 +/- 2 pg/ml) from that in a nonelderly control group, but fractional intestinal calcium (Ca) absorption was significantly lower (0.382 +/- 0.123 vs. 0.49 +/- 0.06; P less than 0.025). Thus, the patients did not have compensatory intestinal hyperabsorption of Ca despite PTH excess. Treatment with hydrochlorothiazide (50 mg/day) produced a decline in fasting urinary Ca (to 0.07 +/- 0.02 mg/100 ml GF; P less than 0.01), serum PTH (from 39 +/- 19 to 21 +/- 1 microliters eq/ml; P less than 0.05), and urinary cAMP excretion (from 5.30 +/- 0.57 to 3.57 +/- 0.59 nmol/100 ml GF; P less than 0.0025). The results suggested that hyperparathyroidism was secondary. Histomorphometric analysis of bone showed reduced trabecular bone volume without mineralization defect, compatible with osteoporosis. Four of eight patients had high or high normal fractional resorption surfaces, fractional formation surfaces, and fractional osteoid volumes. That these abnormalities may reflect PTH-dependent osteoclastic resorption and bone turnover was supported by the reduction of these indices after correction of secondary hyperparathyroidism with hydrochlorothiazide therapy. The remaining four patients, however, had normal histomorphometric results. In summary, postmenopausal osteoporosis may occur sometimes with renal hypercalciuria and secondary hyperparathyroidism. The lack of compensatory intestinal hyperabsorption of Ca predisposes to negative Ca balance, and the hyperparathyroid state may be manifested by stimulated osteoclastic and osteoblastic activities.
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PMID:Postmenopausal osteoporosis as a manifestation of renal hypercalciuria with secondary hyperparathyroidism. 400 11

Monophotonic absorption densitometry of the forearm is an exact method for the evaluation of the bone mineralisation, provided the positioning of the forearm is strictly controlled. It is also able to demonstrate progressive enlargement of the bones with age, up until the ages of about 60 to 70 years. The measurements should be performed in two sites: diaphyseal (cortical bone) and epiphyseal (cortical and trabecular bone). The curves obtained from 1,011 controls are in agreement with the current state of knowledge concerning the variations in bone mass during life in both sexes. In women, the number of pregnancies has no influence on the mineralisation index (MI). The values obtained in 156 osteoporotic patients and in 53 subjects with idiopathic hypercalciuria were appreciably lower than those obtained in age-matched controls. In individual subjects, this method appears to be much more discrimination than the measurement of the trabecular bone volume (TBV) for the diagnosis of osteoporosis and no statistically significant correlation was observed between the MI and the TBV. In male controls, there was a depression of the mean curves around the age of 45 years in all four sites of measurement. This depression was also observed in male subjects with hypercalciuria. They correspond to the generations born between 1930 and 1940. The responsibility of a relative nutritional deficiency affecting growing boys during the 1939-45 war is proposed.
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PMID:[Bone densitometry by monochromatic photon absorption. Study of a normal population and values obtained in various pathological conditions]. 409 71


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