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)

Serum calcitonin (CT) levels and other aspects of calcium metabolism were investigated in 40 epileptic children receiving long-term treatment with phenytoin and/or other anticonvulsant drugs, and in 38 age-matched controls. In the patients CT levels were significantly lower. Immunoreactive parathyroid hormone (iPTH) was significantly elevated exceeding the upper limit of controls in 11 patients. We also observed a highly significant correlation between iPTH and urinary cyclic AMP (cAMP) excretion but a lack of such a correlation with the renal handling of phosphate; this indicates to us a dissociation between cAMP production and phosphaturia. A significant correlation between iPTH levels and urinary hydroxyproline excretion points to a normal action of PTH on bone in the patients. The low CT levels are not due to hypocalcemia and may be directly attributed to the effects of anticonvulsant drugs. As the primary effect of CT is a direct inhibition of PTH induced calcium loss from bone, the drug-related low CT levels in association with secondary hyperparathyroidism possibly is an additional factor in anticonvulsant bone disease.
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PMID:Parathyroid function and serum calcitonin in children receiving anticonvulsant drugs. 624 59

Calcitonin in pharmacologic doses influences the renal handling of electrolytes, especially phosphate and sodium. High-affinity receptors exist for calcitonin in the kidney and are probably linked to adenylate cyclase activation. Calcitonin accumulates in the serum in renal failure, and may have a role in modifying the expression of the bone disease of chronic renal failure. In chronic renal failure, calcitonin is present in the serum in multiple molecular forms but the biologic activity of each form is not known. Some immunoreactive calcitonin appears in the urine. The amount appearing in relation to calcitonin secretion rates requires further exploration.
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PMID:Calcitonin and the kidney. 625 58

Osteoporosis is the reduction of expected bone mass. This results in structural failure with an increased risk of fracture and it is the most common bone disorder encountered. Bone mass declines with age, and in some people will fall below the threshold for easy fracture. This loss is accelerated in the postmenopausal period. Trauma and the internal trabecular structure of bone are additional determinants of risk of fracture. Effective management of osteoporosis depends on identifying and treating those at risk before reaching the critical bone mass and presenting with skeletal failure. There are limitations to methods available for assessing bone loss, and the final arbiter of any treatment is prevention of fracture. Primary prevention involves maximising peak adult bone mass and reducing the rate of bone loss. This may be attained by exercise, adequate dietary calcium, and the identification and treatment of risk factors such as postmenopausal hormone replacement. Once skeletal failure has occurred, long term treatment is required to have a clinically significant effect. Increasing bone mass cannot be assumed to reduce the risk of fracture, and such a reduction has not been directly demonstrated for several agents. Calcium supplements, hormone replacement therapy and fluoride are probably effective in reducing fracture rate, particularly when used in combination, whereas the efficacy of anabolic steroids, calcitonin and diphosphonates is yet to be established. Vitamin D is only of use in coexistent osteomalacia. The limitation of significantly strengthening the skeleton during the life expectancy of the elderly must be realised.
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PMID:Osteoporosis. An update on management. 639 66

The efficacy of salmon calcitonin and etidronate disodium was compared in the therapy of Paget's bone disease in 37 patients. Nineteen patients received etidronate for six months with a mean alkaline phosphatase reduction to 53% of initial values. Bone scintophotographs improved in 12 and were unchanged in seven. Symptoms improved in 11 subjects, were unchanged in seven, and worsened in one. Twelve of these patients were then treated with calcitonin for six months with continued improvement in alkaline phosphatase values to 36% of initial values. All bone scintophotographs improved compared with initial studies. Seven patients continued to improve symptomatically; five described no change. Eighteen individuals were treated initially with calcitonin for six months. During therapy, the alkaline phosphatase level fell to 76% of initial values. Bone scintophotographs were worse in two patients, did not change in seven, and improved in nine. Eleven patients reported improvement in symptoms and seven reported no change. Seventeen of these patients were then treated with etidronate for six months with a decrease in alkaline phosphatase levels to 64% of initial values. Compared with initial tests, bone scintophotographs were worse in three with no change in five and improvement in nine. Symptomatically, three patients reported improvement; four noted no change, and ten reported increasing pain. Although the reason for the poor response to initial calcitonin therapy and/or subsequent etidronate therapy is not apparent, we have concluded that patients fare better when treated with an etidronate calcitonin sequence when compared with those treated with a calcitonin/etidronate sequence.
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PMID:Alternate calcitonin and etidronate disodium therapy for Paget's bone disease. 642 94

Biochemical and radiologic indices of bone disease were assessed in 26 insulin-dependent diabetic patients and 28 nondiabetic patients with endstage kidney disease. The two groups were comparable in age, sex, duration of renal failure, and length of time on dialysis. Diabetic patients showed significantly lower serum calcium and immunoreactive parathyroid hormone (iPTH) levels than nondiabetic patients. iPTH was not related to total serum calcium, but was positively correlated with serum phosphorous (r = 0.37, P less than 0.05 and r = 0.54, P less than 0.005, in nondiabetic and diabetic patients, respectively). iPTH correlated with alkaline phosphatase (r = 0.59, P less than 0.0009) and calcitonin (r = 0.51, P less than 0.05) only in nondiabetic patients. Osteitis fibrosa was noted radiologically in 30% of nondiabetic patients and in none of the diabetic patients (P less than 0.03). Bone morphology in eight diabetic patients who underwent iliac bone biopsy was characterized by reduced trabecular and osteoid bone volume, no woven bone, and marked reduction in indices of bone formation and resorption. The small amount of bone and lack of osteomalacia are a unique feature of the diabetic patient with chronic renal disease. The long-term sequelae of low bone turnover and reduced circulating iPTH may present a special problem to the long term diabetic survivor on the current therapies of uremia.
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PMID:Parathyroid and bone response of the diabetic patient to uremia. 648 71

Clinical details are given of 8 patients who complained of severe pain from metastatic bone disease or from multiple myeloma. Four of the patients were included in a double-blind pilot trial designed to compare the effectiveness of salmon calcitonin (200 i.u. intramuscularly) and placebo given twice daily for 4 days. Two of these patients experienced pain relief and were found to have been given salmon calcitonin; the other 2 had no pain relief and had been given placebo. The other 4 of the 8 patients were treated with salmon calcitonin and also had relief of their pain. It would appear, therefore, that salmon calcitonin may be dramatically effective in the treatment of intractable pain from advanced malignancy and its use warrants further study.
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PMID:Calcitonin in the treatment of intractable pain from advanced malignancy. 666 91

Eleven patients with Paget's disease of bone, treated intermittently for 2-4 years with porcine calcitonin (pCT) and clinically resistant to pCT [no modifications of serum alkaline phosphatase (ALP) and urinary hydroxyproline ( uHOP ) during pCT administration] were treated with 0.5-0.25 mg/day of human calcitonin (hCT) for 3-6 months. Nine of our patients showed biochemical improvement during the first 2 months of treatment, with reduction in ALP and uHOP . In one patient with slightly increased ALP and uHOP , and in another one during the second treatment course, hCT treatment did not modify the biochemical indices of bone disease. However all patients, including those with biochemical resistance, experienced a remarkable diminution of bone pain, which had not been observed during previous pCT treatment courses. Therefore, hCT appears to be indicated for therapeutic use in patients who are resistant to foreign calcitonins.
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PMID:Response of Paget's disease to human calcitonin in patients resistant to porcine calcitonin. 672 70

Twenty-one patients with chronic renal failure and bone disease or hypercalcaemia were studied before and following single (twenty patients) or repeated (fourteen patients) intravenous injection of synthetic salmon calcitonin. Significant correlations were noted before treatment between bone surfaces occupied by osteoblasts or osteoclasts and plasma levels of immunoreactive parathyroid hormone, alkaline phosphatase and hydroxyproline. Following a single injection of 2--200 i.u. salmon calcitonin, plasma levels of calcium and phosphate fell for 6--8 h, but rose subsequently to pre-injection levels at 24 h. The magnitude and duration of the hypocalcaemic response was not clearly dose-dependent, but correlated with measured indices of bone cell activity. Repeated administration of calcitonin (10--200 i.u. thrice weekly for up to 2 months) lowered plasma calcium in the majority of patients and restored plasma calcium to normal in four previously hypercalcaemic patients. Mean levels of alkaline phosphatase increased but no significant changes in plasma phosphate, immunoreactive parathyroid hormone and calcitonin, or hydroxyproline occurred. Calcium absorption (six studies) did not change during treatment. We conclude that synthetic salmon calcitonin is an effective short-term inhibitor of bone resorption in patients with chronic renal failure. Its use as a possible treatment for hypercalcaemia and hyperparathyroid bone disease in chronic renal failure is discussed.
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PMID:Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover. 679 36

The therapy of Paget's bone disease is essentially based on the use of calcitonin and diphosphonates: both drugs, if used in large doses for long periods, have shown themselves able to provoke particular side-effects. It was, therefore, decided to study the therapeutic efficacy of combined low-dosage treatment using synthetic salmon calcitonin and sodium-etidronate on a group of patients with Paget's osteodystrophy. A clear evident diminution in plasma alkaline phosphatase, hydroxyprolinuria and whole body retention (WBR) of MDP-Tc99m was observed, demonstrating a reduction of metabolic turnover in the bone. No changes in the bone mass (BMC), evaluated by bone mineral detector, were observed at the end of treatment. With this treatment the plateau effect was shown to be appreciably less than normally occurs when either calcitonin or sodium etidronate are used alone.
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PMID:[Effects of the combined calcitonin and sodium etidronate therapy in Paget's disease of bone]. 680 55

Twelve patients with chronic renal failure and osteitis fibrosa were treated for periods of 1-9 months with thrice-weekly injections of 10-200 iu salmon calcitonin. Treatment had no significant effects on symptoms of bone disease and side effects were common. A transient fall in plasma alkaline phosphatase levels occurred in only three patients, and both plasma alkaline phosphatase and hydroxyproline levels rose in the majority of patients. Radiographic signs of hyperparathyroidism increased in seven of the nine patients treated for longer than 3 months. Paired bone biopsy specimens in nine patients showed significant increases in osteoblast counts, but no changes in the indices of resorption. These treatment-induced changes were reversed when treatment with 1,25-dihydroxyvitamin D3 was substituted for calcitonin. The use of this regimen of salmon calcitonin is not recommended in the long-term management of hyperparathyroid bone disease in chronic renal failure.
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PMID:Deterioration of renal bone disease in patients treated with salmon calcitonin. 704 29


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