Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present paper a 67 years old female with chronic renal failure is reported, who developed at least three episodes of live-threatening hypercalcemia during long-term therapy with calcium carbonate. Results of biochemical and hormonal parameters and of dual x-ray photon absorptiometry (DEXA) were indicative for the presence of adynamic bone disease. Results obtained in this patient and published in the literature suggest, that presence of subnormal plasma concentrations of intact parathyroid hormone seems to be a valuable predictor of hypercalcemia in uremic patients treated with calcium carbonate.
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PMID:[Life threatening hypercalcemia in a patient with chronic renal failure. Case report]. 884 14

We report a 12-year-old boy receiving long-term peritoneal dialysis who developed marked hypercalcemia and pancreatitis. Hypercalcemia was successfully treated by conducting dialysis with non-calcium-containing dialysate fluid. Factors predisposing to the development of hypercalcemia included the presence of adynamic bone disease and the use of vitamin D and calcium carbonate therapy. This case is presented to emphasize potential complications that can be associated with the adynamic bone lesion in patients on peritoneal dialysis.
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PMID:Hypercalcemia and pancreatitis in a child with adynamic bone disease. 909 Jun 72

The observation that some subjects with low PTH had elevated plasma magnesium (Mg) levels prompted us to analyze in 41 patients on maintenance hemodialysis for 44 +/- 36 months, their serum Mg concentrations, and the relationship between plasma Mg and PTH levels. The mean serum Mg concentration was 2.4 +/- 0.2 mg/dl. Twenty-four out of the 41 subjects (58.5%) had hypermagnesemia (serum Mg above 2.5 mg/dl). Patients were classified into 3 groups according to their PTH level: Group A, low PTH (below 120 pg/ml); group B, adequate PTH (120-250 pg/ml); and group C, high PTH (above 250 pg/ml). There were no differences among groups according to number of subjects, age, sex, time on dialysis, renal disease, serum calcium, phosphorus, bicarbonate, vitamin D or aluminum concentrations. Doses of calcium carbonate and aluminium hydroxide were also similar in all groups. Curiously, although the differences were not statistically significant, the total cumulative intake of calcium and aluminium were less in group A than in the other groups. Interestingly, patients with low PTH had a significantly higher serum Mg concentration than patients with adequate or high PTH (2.8 +/- 0.2 mg/dl vs 2.3 +/- 0.1 mg/dl and 2.2 +/- 0.1 mg/dl, respectively, p < 0.01). Moreover, regression analysis showed a negative linear correlation between serum PTH level and plasma Mg concentration (r = -0.6059, p < 0.001). Based on these findings, chronic hypermagnesemia could have a suppressive effect on PTH secretion, and it could be a risk factor for the development of adynamic bone disease in dialysis patients.
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PMID:Serum magnesium concentration and PTH levels. Is long-term chronic hypermagnesemia a risk factor for adynamic bone disease? 924 93

The aim of this study was to evaluate the influence of LCD on bone metabolism, and assess the indication of LCD. Fourteen patients on CAPD (m = 8, f = 6) were converted to LCD following over 1 year on standard calcium dialysate (1.75 mmol/l; SCD) treatment, and followed for 1 year. The biochemical measurements included plasma levels of Ca, P, ALP, and i-PTH. The bone mineral density (BMD) was evaluated using dual energy x-ray absorptiometry. Ca-carbonate and calcitriol were administered to maintain plasma Ca levels within the normal range. The patients were divided into three groups on the basis of the i-PTH levels just before the conversion to LCD. Group 1; n = 5, i-PTH < 65. Group 2; n = 5, 65 < or = i-PTH < 200. Group 3; n = 4, 200 < or = i-PTH (pg/ml). Mean BMD Z scores decreased significantly in group 3. Mean serum i-PTH significantly increased in all groups. These results suggest that LCD is effective for treating adynamic bone disease, which is seen in high frequency in patients undergoing peritoneal dialysis. However, these results also pointed to the disadvantage of worsening the secondary hyperparathyroidism. In conclusion, LCD should be used carefully in patients whose i-PTH levels are high, because of the possibility of bone mineral loss.
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PMID:[The impact of low calcium dialysate (1.25 mmol/l; LCD) on bone metabolism in CAPD patients]. 965 8

One year of a very low protein diet (VLPD) can reverse secondary hyperparathyroidism in uremic patients. We studied bone histology, bone mineral density (BMD), and dynamic parathyroid function (calcium/PTH curves) in 16 nondialyzed patients with advanced renal failure who had been receiving a VLPD for a mean of 5 yr (mean protein intake, 0.34 +/- 0.12 mg/kg x day; mean phosphorus intake, 8.2 +/- 2.1 mg/kg x day) and daily supplementation with essential amino acids and their ketoanalogs (1000 IU vitamin D2 and 1-2 g calcium carbonate). Three patients exhibited a high bone formation rate (BFR), 7 patients had normal bone remodeling, and 6 patients had a low BFR, including 2 with osteomalacia and 4 with adynamic bone disease without aluminum overload. A longer diet duration and lower caloric intake were associated with low BFR. More than half of the patients exhibited moderate or severe osteoporosis at the appendicular skeleton. The t score of femur BMD explained 65% of the BFR variance. Patients with a low BFR had a dynamic parathyroid function similar to that of patients with a normal BFR, except they had a lower capacity to buffer a calcium load, whereas patients with a high BFR had a higher basal PTH/maximum PTH and a steeper calcium/PTH curve slope; the calcium set-point was identical in the three groups.
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PMID:Bone mass and dynamic parathyroid function according to bone histology in nondialyzed uremic patients after long-term protein and phosphorus restriction. 1002 9

Acute magnesium (Mg) infusion decreases patathyroid hormone (PTH) secretion. However, the effect of chronic hypermagnesemia on PTH levels in dialysis patients is not well established. We studied 110 hemodialysis patients (mean age, 55 +/- 14 years; time on dialysis, 35 +/- 28 months) not receiving vitamin D and undergoing dialysis with an Mg dialysate concentration of 1.2 mg/dL. The primary phosphate binder was calcium carbonate, and 43% of the patients also needed aluminum hydroxide. During a 6-month period, calcium (Ca), phosphorus (P), and total serum Mg were measured every 2 months; intact PTH and aluminum (Al) were measured every 6 months. The mean value of each parameter was computed. Hypermagnesemia (serum Mg > 2.47 mg/dL) was observed in 73% of the patients. Mg and Ca were inversely correlated with PTH levels (r = -0.48; P < 0.001 and r = -0.21; P < 0.05, respectively). After adjusting for Ca and P (partial correlation analysis), Mg and PTH were inversely correlated (r = -0.58; P < 0.001). A stepwise multiple regression analysis showed that PTH levels were predicted by Mg (P < 0.001), alkaline phosphatase (P < 0.01), and P levels (P< 0.05; multiple R = 0.57; P < 0.001), whereas Ca level, sex (dummy variable), diabetes (dummy variable), time on dialysis, and Al level were not predictive. Patients with inadequately low PTH levels (relative hypoparathyroidism, PTH < 120 pg/mL; n = 52) showed greater serum Mg concentrations than the rest (n = 58; 3.01 +/- 0.33 v 2.63 +/- 0.38 mg/dL; P < 0.001). In conclusion, serum Mg concentrations in dialysis patients are independently associated with PTH levels, suggesting that chronic hypermagnesemia may decrease PTH secretion and/or synthesis. In addition, chronic hypermagnesemia of dialysis patients may have a role in the pathogenesis of adynamic bone disease.
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PMID:Relationship between serum magnesium and parathyroid hormone levels in hemodialysis patients. 1040 Oct 14

A 62-yr-old woman with thyroid carcinoma metastatic to bone, and a history of subclinical hypoparathyroidism was admitted to the hospital in hypocalcemic crisis 5 wk after receiving iv pamidronate. The patient had tetany and laryngospasm. An electrocardiogram showed junctional rhythm with QT segment prolongation. The patient had previously maintained a low-normal serum calcium on 500-750 mg of calcium carbonate and 600 IU of vitamin D daily. One week after pamidronate administration the patient's calcium and vitamin D supplementation were inadvertently discontinued. She continued to take daily intranasal calcitonin. At the time of her hospitalization for hypocalcemia, the patient's serum calcium was 4.3 mg/dL. The patient received aggressive calcium and vitamin D supplementation. However, her serum calcium remained below 6 mg/dL for a 2-wk period, and took another week to return to the normal range. In this article, we discuss the counterregulatory responses necessary to maintain calcium homeostasis following osteoclast inhibition by bisphosphonates. We also review the risk factors for hypocalcemia following bisphosphonate administration. Pamidronate and other bisphosphonates are becoming an integral part of the management of normocalcemic patients with malignant bone disease. Therefore, awareness of risk factors for hypocalcemia and familiarity with avenues available for protection from potentially catastrophic hypocalcemia are both crucial.
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PMID:Prolonged, symptomatic hypocalcemia with pamidronate administration and subclinical hypoparathyroidism. 1139 32

Hyperphosphataemia is prevalent among chronic renal failure and dialysis patients. It is known to stimulate parathyroid hormone and suppress vitamin D3 production, thereby inducing hyperparathyroid bone disease. In addition, it may independently contribute to cardiac causes of death through increased myocardial calcification and enhanced vascular calcification. Hyperphosphataemia is also associated with cardiac microcirculatory abnormalities. Therefore, phosphate control is of prime importance. It is important to control phosphate levels early in the course of chronic renal failure in order to avoid and treat secondary hyperparathyroidism, and cardiovascular and soft tissue calcifications. Dietetic restrictions are often difficult to follow long term. Because of its large sphere of hydration and the complex kinetics of phosphate elimination, phosphate is not easily removed by dialysis. Long, slow dialysis may be effective, but this needs logistics and acceptance by patients. Thus, oral phosphate binders are generally required to control serum levels. None of the existing phosphate binding agents is truly satisfactory. Aluminium-containing agents are highly efficient but many clinicians have abandoned their use because of the potential toxicity. Despite of the wide use of calcium-containing agents, there was a link with hypercalcaemia and soft tissue calcifications. Novel phosphate binders in the form of polyallylamine hydrochloride, polyuronic acid derivatives and lanthanum carbonate appear promising. In this review, we discuss causes of hyperphosphataemia, pathological consequences and modalities of treatment.
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PMID:Hyperphosphataemia in renal failure: causes, consequences and current management. 1265 55

The choice of an appropriate dialysate calcium (Ca) concentration is crucial in the management of dialysis patients: an excessive Ca load has been associated with vascular calcifications, whereas Ca depletion can worsen secondary hyperparathyroidism (HPT) and decrease bone mass. In haemodialysis (HD), Ca transfer by diffusion depends on the concentration gradient between dialysate and blood, and a gain of Ca is expected when the dialysate Ca is >1.5 mmol/l. However, Ca losses by convective transport (ultrafiltration rate) can even exceed the amount of Ca gained by diffusion. Dialysis Ca balances, in normocalcaemic patients with a mean weight loss of 2-4 kg per session, have been shown to be positive, moderately negative or clearly negative using a dialysate Ca of 1.75, 1.50 or 1.25 mmol/l, respectively. Serum ionized Ca increases during sessions with a dialysate Ca of 1.5 and 1.75mmol/l, and decreases to the lower limits of normal after HD with 1.25 mmol/l. In haemodiafiltration (HDF), Ca mass transfer is strongly affected by the Ca content in the replacement solutions. Bicarbonate-containing bags are Ca free so that dialysate Ca needs to be increased above 1.75 mmol/l to overcome the convective losses and avoid markedly negative balances. Ca mass transfer in HDF is also affected by the infusion mode. Ca balance in post-dilution HDF, for a given concentration gradient between blood and dialysate, does not differ from HD. Conversely, in pre-dilution HDF, dialysate Ca concentration should be increased by approximately 0.25 mmol/l to maintain comparable balances. A given dialysate Ca concentration should be prescribed considering the dialysis Ca mass balance, other concomitant therapies (Ca salts, vitamin D metabolites) and the type of bone disease. The current strategy of maintaining normal Ca levels by ensuring an adequate intestinal Ca absorption with large doses of Ca-containing phosphate binders and concomitantly avoiding positive Ca balances from dialysis by using a low Ca dialysate has been questioned recently because of the risk of either worsening HPT or accelerating the progression of vascular calcifications. A dialysate Ca of 1.5 mmol/l seems to be suitable for the majority of patients on HD or post-dilution on-line HDF because the moderately negative dialysis balances can be easily counterbalanced by the administration of mild doses of Ca-containing phosphate binders in order to ensure a neutral total body Ca balance. If necessary, aluminium-free and Ca-free binders can be added to achieve a satisfactory control of hyperphosphataemia, while avoiding an excessive Ca load.
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PMID:The choice of the dialysate calcium concentration in the management of patients on haemodialysis and haemodiafiltration. 1295 28

As adults with cystic fibrosis (CF) have enjoyed incremental increases in longevity over the last few decades, they have also been suffering from low bone density and its clinical manifestations, fractures and kyphosis. We conducted a placebo-controlled, randomized, double-blinded trial of alendronate (10 mg/day orally) (n = 24) compared with placebo (n = 24) for 1 year in 48 patients to improve bone mineral density at the spine as the primary endpoint. All patients received 800 IU of cholecalciferol and 1,000 mg of calcium carbonate. Both groups were similar in age, sex, CF mutations, bone density T scores, renal function, and body mass index at study onset. The alendronate-treated patients gained (mean +/- SD) 4.9 +/- 3.0% and 2.8 +/- 3.2% bone density after 1 year versus placebo, which lost (mean +/- SD) 1.8 +/- 4.0% and 0.7 +/- 4.7%, in spine and femur bone density, respectively (p < or = 0.001 for the spine; p = 0.003 for the femur). Urine N-telopeptide, a bone resorption marker, levels declined in the treatment group more than in the control group (p = 0.002), consistent with the known antiresorptive effects of bisphosphonates. Alendronate was more effective than placebo in improving spine and femur bone mineral density and is a promising agent for the long-term prevention and management of bone disease in patients with CF.
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PMID:Efficacy of alendronate in adults with cystic fibrosis with low bone density. 1456 54


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