UMLS:C0020438 - FACTA Search

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Query: UMLS:C0020438 (hypercalciuria)
2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical course of the idiopathic juvenile osteoporosis (IJO) was monitored in the group of 45 patients of both sexes with diagnosed disease, verified during follow-up period. The aim of the study was to evaluate the relationship between clinical symptoms and the results of biochemical, anthropometric, and densitometric measurements. An analysis of the obtained data enabled to distinguish the acute and chronic IJO phases. Evolution of the acute phase into chronic one was manifested by the cessation of pain and pathological gait stereotype, normalization of muscular strength, anthropometric parameters and urinary Pyr and DPyr excretion, as well as improvement in bone density. Hypercalciuria and increased urinary excretion of Pyr and DPyr, observed in the acute phase of IJO, may indicate that bone resorption exceeded bone formation. Tendency to maintain of alkaline phosphatase activity within lower limits of the normal values with slight increase during an improvement of densitometric parameters suggested transient osteoblast dysfunction.
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PMID:[Dynamics of the course of idiopathic juvenile osteoporosis]. 830 31

Eight patients (6 women and 2 men) with osteoporosis caused or aggravated by renal acidification defects are presented. Three of the female patients were premenopausal; the others were 9, 20 and 22 years postmenopausal, and two of them were on hormonal replacement therapy. Two patients had nephrolithiasis: one male with recurrent calcium phosphate stones and a left sided staghorn calculus, and one female with nephrocalcinosis due to medullary sponge kidney and hypercalciuria (patients No. 1 and 2, respectively, Table 1). In the remaining subjects, clinical suspicion was based on: a) Hip fracture in a 44-yr-old premenopausal female without any risk factor (No. 3, Table 2). b) Several vertebral compression fractures in a 45-yr-old male without hypogonadism or other predisposing factors (No. 7, Table 2). c) Lack of response to antiosteoporotic therapy in 3 women (patients No. 4, 6 and 8, Table 2). Serum bicarbonate levels and urine acidification capacity were studied in all patients. Three had low serum bicarbonate (two of whom showed high fractional excretion of bicarbonate), four had a distal defect, and one had a mixed form. Serum creatinine and potassium, and venous blood pH were normal in all cases, suggesting incomplete renal tubular acidosis. Bone mineral density in Z-score (means +/- s.e.m.) was - 1.75 +/- 0.08 in the lumbar spine (n = 8), and - 1.57 +/- 0.09 in the femoral neck (n = 4) [Tables 1 and 2; Figs 1 and 2]. Following one year treatment with oral sodium bicarbonate and potassium citrate, total skeletal calcium increased by 3-10% in five of the patients. Whereas the high prevalence of renal acidification defects among renal stone formers with or without hypercalciuria is well acknowledged, renal tubular acidosis is not included in the list of entities causing secondary osteoporosis. As shown in 6 patients of this series, incomplete RTA should be considered as another disease capable of causing osteoporosis or worsening involutional bone loss.
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PMID:[Renal acidification mechanism disorders in patients with osteoporosis]. 854 15

It is well recognized that patients with postmenopausal osteoporosis usually exhibit some degree of calcium malabsorption and commonly have low serum concentrations of 1,25-dihydroxyvitamin D (calcitriol). Administration of calcitriol has been shown to normalize calcium absorption in patients with osteoporosis and, over the long term may have a stimulating effect on bone formation. Clinical trials have shown a significant reduction in osteoporotic fractures among calcitriol-treated patients. Hypercalcemia and hypercalciuria are infrequent complications of calcitriol therapy with physiologic doses (0.25 microgram twice daily), and are most commonly related to excessive calcium intake (i.e., > 1000 mg daily).
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PMID:The role of vitamin D in the pathogenesis and treatment of osteoporosis. 885 46

Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Bone loss occurs soon after corticosteroid therapy is initiated and results from a complex mechanism involving osteoblastic suppression and increased bone resorption. There are a number of factors that may increase the risk of corticosteroid-induced osteoporosis [smoking, excessive alcohol (ethanol) consumption, amenorrhoea, relative immobilisation, chronic obstructive pulmonary disease, inflammatory bowel disease, hypogonadism in men, organ transplantation]. The initial assessment of patients about to start taking corticosteroids should include measurement of spinal bone density, urinary calcium level and plasma calcifediol (25-hydroxycholecalciferol) level; serum testosterone levels should also be measured when hypogonadism is suspected. Many different drugs have been used to prevent osteoporosis in patients receiving long-term corticosteroid therapy, including thiazide diuretics, cholecalciferol (vitamin D) metabolites, bisphosphonates, calcitonin, fluoride, estrogens, anabolic steroids and progesterone. At present, however, published studies have failed to demonstrate a reduction in the rate of fracture using different preventive pharmacological therapies in patients being treated with corticosteroids on a continuous basis. Among the drugs studied, bisphosphonates (pamidronic acid and etidronic acid) and calcitonin appear to be effective in increasing bone density. Cholecalciferol preparations have been reported to be effective in some, but not all, studies. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma. Patients should take as much physical activity as possible, maintain an adequate daily intake of calcium (1000 mg/day0 and cholecalciferol (400 to 800 U/day), stop smoking and avoid excessive alcohol intake. It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. A thiazide diuretic should be considered if hypercalciuria is present (urinary calcium excretion in excess of 4 mg/kg/day). High-risk patients and those with established osteoporosis should be treated with bisphosphonates (cyclical etidronic acid or intravenous pamidronic acid), nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.
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PMID:Corticosteroid-induced bone loss. Prevention and management. 894 96

Calcitriol has been widely used in the management of osteoporosis, but its efficiency is a matter of controversy. It is not known whether combinations of calcitriol and antiresorptive agents such as etidronate and calcitonin are superior to calcitriol alone in the treatment of postmenopausal osteoporosis. To make this determination, 30 Turkish women with postmenopausal osteoporosis between 45 and 68 years of age were randomized to receive either intermittent cyclical etidronate (400 mg/day, for 14 days) followed by 60 days of cyclical calcitriol therapy 0.25 microg twice daily (group 1; n = 10), or calcitriol 0.25 microg twice daily (group 2; n = 10), or calcitriol 0.25 microg/day in combination with 100 IU intranasal salmon calcitonin taken every other day (group 3; n = 10) through a 1-year period. Bone mineral density (BMD) of lumbar spine (L2 to L4) was determined for each patient by dual-photon absorptiometry (153Gd) at baseline, after 6 months, and at the end of the study. There was no significant difference among groups with respect to mean spinal BMD at baseline, after 6, and after 12 months. No significant spinal BMD changes occurred in any group from baseline, after 6 months, and after 12 months. Four patients in groups 1 and 2 and five patients in group 3 developed hypercalcemia at least once during therapy. Hypercalciuria occurred at least once in 9, 10, and 7 patients in groups 1, 2, and 3, respectively. One patient in group 2 developed a renal stone at the end of the study. Mean urine hydroxyproline levels did not change significantly in any group with respect to baseline. The data suggest that one-year treatment with calcitriol, given either alone or in combination with antiresorptive agents, does not improve spinal BMD in Turkish women with postmenopausal osteoporosis, and is associated with a high rate of adverse events.
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PMID:Comparison of calcitriol treatment with etidronate-calcitriol and calcitonin-calcitriol combinations in Turkish women with postmenopausal osteoporosis: a prospective study. 919 11

Prolonged infusion of magnesium sulfate has been used for the treatment of refractory preterm labor. Long-term magnesium sulfate tocolytic therapy either alone or in combination with other tocolytic agents has been reported to be safe and effective with minimal maternal side effects. There has been only one previous report of a disturbance in maternal calcium homeostasis, which included decreased distal radius bone density and hypercalciuria as a result of prolonged magnesium sulfate infusion. This article reports the first case of bilateral fracture of the calcanei in the postpartum period secondary to osteoporosis associated with prolonged magnesium sulfate tocolysis and bed rest. A 35-year-old white female with a triplet pregnancy of 25 weeks' gestation was admitted in preterm labor. Bed rest, intravenous magnesium sulfate tocolysis, and intermittent subcutaneous terbutaline were necessary to maintain uterine quiescence for 65 days. The patient received weekly betamethasone for 6 weeks for the acceleration of fetal lung maturation. Daily prenatal multivitamins and low-dose subcutaneous heparin for thromboprophylaxis were given. Efforts at tocolysis were ultimately not successful and the patient underwent a cesarean section delivery at 34 2/7 weeks' gestation. The patient's postoperative course was complicated by osteoporosis and bilateral stress fractures of the calcanei. This case report demonstrates that stress fractures secondary to osteoporosis may be associated with prolonged magnesium sulfate therapy and bed rest in higher order multiple pregnancy. Other possible contributing factors to osteoporosis include heparin thromboprophylaxis and suboptimal calcium supplementation. Therefore, in circumstances of prolonged bed rest and magnesium sulfate tocolysis, additional daily calcium supplementation would be well advised.
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PMID:Long-term magnesium sulfate tocolysis and maternal osteoporosis in a triplet pregnancy: a case report. 947 87

Advances in the molecular genetics of inherited renal tubulopathies have allowed some insight into the normal mechanisms of tubular cation and anion reabsorption. It is now possible to view Bartter's syndrome, Gitelman's syndrome and pseudohypoaldosteronism type 1 as having genetic abnormalities which produce tubular defects that are similar to those induced by the pharmacological actions of loop diuretics, thiazide diuretics or potassium-sparing diuretics, respectively. Although these rare monogenic disorders with dramatic phenotypes seem to have little relevance to everyday clinical practice, it is possible that subtle abnormalities of the regulation of the ENaCs may play a role in low-renin forms of 'essential' hypertension. Similarly, subtle abnormalities in the function of the electroneutral sodium-(potassium)-chloride cotransporters (NKCC2 and NCCT) and the renal CLC-type chloride channels (CLC5) may be major determinants of urinary calcium excretion with roles in the pathogenesis of 'idiopathic' hypercalciuria and osteoporosis. Because of the intricate and diverse molecular mechanisms by which tubular reabsorption of water and solutes takes place in each different nephron segment, it is likely that other renal channels and transporters will be implicated in the pathogenesis of further monogenic disorders, and that these will allow additional insights into tubular functioning. Recent studies have demonstrated that in addition to abnormalities in the NKCC2 and ROMK1 genes, mutations at a third genetic locus can also cause Bartter's syndrome. Linkage studies, followed by mutational analyses have found deletions and point mutations in the gene encoding one of the TAL-specific chloride channels, CLCKB, in 17 Bartter's families. This chloride channel is similar in structure to CLC5, and is located on the long arm of chromosome 1. Importantly, there appears to be a phenotypic difference between subjects with Bartter's syndrome due to CLCKB abnormalities and those with NKCC2 or ROMK1 mutations. Despite the fact that all of these Bartter's patients had significant hypercalciuria, nephrocalcinosis was not found in any of the 17 subjects with CLCKB mutations, compared to 19 of 20 patients with NKCC2 or ROMK1 mutations. These findings have also demonstrated a key role for CLCKB as a major basolateral chloride channel involved in mTAL sodium and chloride reabsorption (Figure 2).
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PMID:Straightening out the renal tubule: advances in the molecular basis of the inherited tubulopathies. 951 7

It was the aim of the present study to investigate whether a 2-month prophylaxis of postovariectomy bone loss with low-dose calcitriol would have long-lasting beneficial effects on cancellous bone mass or structure after its withdrawal in rats. Six-month-old female Fischer 344 rats were either ovariectomized (OVX) or sham-operated (SHAM). Groups of SHAM and OVX rats were orally treated with either 0.05 microgram calcitriol/kg per day or vehicle for 2 months postovariectomy, starting immediately after ovariectomy. Thereafter, the rats were maintained without treatment for another 4 months. Half the animals in each group were killed 2 months postovariectomy; the rest of the rats were killed 6 months postovariectomy. Cancellous bone histomorphometry was performed on the first lumbar vertebral body and on the proximal tibial metaphysis. Administration of low-dose calcitriol to SHAM and OVX rats resulted in hypercalciuria, but not hypercalcemia. By 2 months postovariectomy, calcitriol treatment of OVX rats had completely prevented tibial trabecular bone loss, and had increased vertebral cancellous bone mass in SHAM and OVX rats by about 30% over the level observed in SHAM vehicle controls. However, at the end of the experiment, i.e. 4 months after withdrawal of calcitriol, cancellous bone mass and structure in both the vertebrae and the tibiae of calcitriol-treated OVX rats were almost identical to those of vehicle-treated OVX rats. We conclude that prevention of bone loss with low-dose calcitriol during the phase of acute estrogen deficiency, when bone turnover is maximally increased, does not provide long-term beneficial effects on cancellous bone mass or structure in OVX rats. If extrapolated to postmenopausal women, this study would suggest that prophylaxis against postmenopausal bone loss with short-acting antiresorptive substances during only the first few years after menopause will probably not reduce the risk of postmenopausal osteoporosis later in life.
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PMID:Short-term prophylaxis against estrogen depletion-induced bone loss with calcitriol does not provide long-term beneficial effects on cancellous bone mass or structure in ovariectomized rats. 969 82

AN UPCOMING PUBLIC HEALTH PROBLEM: There has been a considerable focus on osteoporosis in men recently. Bone mass is high in men who have larger bones than women. The frequency of fractures is also higher due to post-trauma lesions. Femoral neck fractures have also increased over the last few years although the F/M ratio remains about 2.8. Overall, there is a trend towards an increased incidence of masculine osteoporosis (and vertebral fractures) due to population aging. FAVORING FACTORS IN MEN: The most important factors are hypoandrogenism, hypoestrogenism (pre or post-puberty), the alcohol-smoking association, malnutrition, lack of sun exposure and chronic liver disease. Other causes of osteoporosis (hyperthyroidism, Cushing's disease, hemochromatosis, gastrectomy, inflammatory rheumatic disease, tubulopathy, hypercalciuria and iatrogenic causes) should also be taken into consideration. PRETHERAPY WORK-UP: All the different possible etiologies should be investigated. Therapeutic protocols should provide hormone replacement when required, withdrawal of causal drugs, better nutrition and reduced alcohol and tobacco use.
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PMID:[Male osteoporosis]. 981 8

The author demonstrates on a group of 292 patients (207 women, 85 men) treated on account of various diseases with corticoids laboratory parameters and bone density and records of bone fractures. The bone metabolism is negatively influenced by the action of corticoids on the vitamin D transformation into its active metabolites; as a result of reduced calcium absorption from the gut the reduced calcium level in blood causes secondary hyperparathyroidism and osteoclastic bone resorption is enhanced. On the other hand, corticoids inhibit new formation of bone by suppressing the proliferation of osteoblasts and by interfering with osteoid formation. One quarter of the patients suffers moreover from osteoporomalacia. Two and a half times as many women have steroid osteoporosis, and bone demineralization is enhanced also by other factors caused by the basic disease (immobilization, hypercalciuria, lactose intolerance). By comprehensive treatment using a combination of Ca + F, vitamin D, exercise, thyrocalcitonin, Osteogenon and recently also the third series of bisphosphonates it proved possible to increase within one year the bone density on average by 4.5% of normal values. The number of fractures declined dramatically.
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PMID:[Steroid osteoporosis]. 982 82

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