Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151825 (bone pain)
 3,118 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate the effects of calcitonin (CT) treatment on bone pain, osteoporosis, bone fractures and blood chemistry in thalassemic patients. Twenty-four patients with an age range of 10-24 years were included, 14 of whom received 100 IU CT and 250 mg calcium 3 times a week. The others (n = 10) were followed up as a control group with only routine thalassemia therapy. After 1 year of treatment, bone pain disappeared and radiological signs of osteoporosis had improved significantly (p < 0.01) in the treatment group. CT has no important side effects.
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PMID:Effects of calcitonin therapy on osteoporosis in patients with thalassemia. 772 45

3 patients with prolonged, diffuse, bone pain due to Paget's disease were treated with intranasal salmon calcitonin, 200-400 U/d for 12 months. Within the first 3 months, in all 3 bone turnover decreased 31-35% (as assessed by serum alkaline phosphatase activity and urinary hydroxyproline/creatinine ratio). After 1 year of nasal calcitonin the reduction in serum alkaline phosphatase was 24%, and in urinary hydroxyproline 10%. In addition, pain and functional impairment markedly improved during the year. It is concluded that daily nasal calcitonin spray is well tolerated and effective initial treatment for Paget's disease of the bone.
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PMID:[Calcitonin nasal spray for Paget's disease of the bone]. 775 Aug 16

In 1954, when I gave a talk on calcium homeostasis at the first Gordon Conference on Bones and Teeth, it was recognized that the level of ionic calcium in the plasma and body fluids must be maintained with precision, since it is critically important for a number of vital processes. However, very little was known of the mechanisms involved and I decided to make this the focus of my research career. With the assistance of a number of first-year medical students working during the summer, we developed a precise method for measuring calcium, demonstrated the remarkable constancy of plasma calcium in normal human subjects, and found that normal calcium levels were restored quickly after being artificially raised or lowered. We focussed on parathyroid hormone (PTH), which plays a key role in controlling hypocalcemia by stimulating osteolysis. While studying the control of its secretion in 1961, we discovered a second calcium-regulating hormone (calcitonin) which was released by hypercalcemia and lowered plasma calcium by inhibiting osteolysis. It is a straight-chain peptide with 32 amino acids and a 7-membered disulfide ring at the N terminal. It is produced by C cells which arise from the neural crest and is considered a neuropeptide hormone. It is produced in the thyroid of mammals and the ultimobranchial glands of lower vertebrates. We were involved in the isolation of salmon calcitonin, which is the form most widely used in therapy because of its high potency. In addition to inhibiting bone resorption, it is a powerful analgesic agent with a potency in certain circumstances which is 30-50 times that of morphine. It is widely used clinically for the treatment of Paget's disease, hypercalcemia, osteoporosis, and relief of bone pain. World sales in 1992 exceeded US$900 million, of which 85% was for osteoporosis.
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PMID:Calcitonin: discovery, development, and clinical application. 792 3

The studies were carried out assessing the effect of calcitonin in the treatment of bone pain. In the years 1990-1992 43 patients were studied. Pain intensity scale was used with evaluation by doctor and patient.
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PMID:[Use of calcitonin in treatment of bone pain]. 794 53

Paget's disease of bone is characterized by primary osteoclastic dysfunction and prolonged treatment with conventional medications including calcitonin and etidronate, results in a number of patients becoming refractory to treatment. We have evaluated the effectiveness of three dosage regimes of aminohydroxypropylidene bisphosphonate (pamidronate) in 15 patients with extensive Paget's disease who had become refractory to conventional therapy. Nine patients had pamidronate (intravenous infusion of 30 mg over 4-5 hours at monthly intervals) for 6 months. A further four patients received 30 mg of pamidronate infusion daily for 6 consecutive days and another two patients, 60 mg on 3 consecutive days (total dose of 180 mg/patient). In all three groups the bone-specific alkaline phosphatase and urinary hydroxyproline excretion both fell by 75% (P < 0.001). All but one patient showed a marked improvement in clinical symptomatology (pain and mobility) and biochemical parameters indicating decreased bone turnover. Remissions achieved (> 12 months) with all three regimens were comparable. The pagetic bone pain was reduced and the mobility was significantly improved after 3 months of therapy and was continued for up to 1 year. Currently, it may be difficult to justify the use of intravenous bisphosphonate as the first line of therapy for Paget's disease, but it does seem to have a definite place in patients with severe Paget's disease who do not respond to other therapeutic agents. Here we demonstrate that pamidronate is highly effective in patients with extensive Paget's disease who became refractory to conventional treatment. Further studies are necessary to optimize the dosage and frequency of administration of pamidronate.
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PMID:Pamidronate is effective for Paget's disease of bone refractory to conventional therapy. 786 63

The principal pathophysiologic alteration in severe hypercalcemia accompanying hyperparathyroidism and malignancy is enhanced osteoclastic bone resorption. Hypercalcemia impairs renal mechanisms that lead to sodium and calcium excretion; PTH and PTHrP acting on renal tubules enhance further calcium reabsorption. Although rehydration is often necessary as an initial therapy of hypercalcemia, the cornerstone of therapy is to inhibit osteoclastic bone resorption. The bisphosphonates, plicamycin, gallium, and calcitonin all inhibit osteoclastic bone resorption. Calcitonin is the most rapidly acting agent. Toxicities of calcitonin are minimal, yet its therapeutic efficacy is limited by lack of potency and tachyphylaxis. The second-generation bisphosphonates such as pamidronate represent a class of compounds that are extremely effective in inhibiting the metabolic function of the osteoclast. Given in a single infusion, a significant majority of patients will have normalization of corrected serum calcium lasting, on average, 1-2 weeks. Therapeutic benefit will be of greater duration because most patients remain only minimally symptomatic until corrected serum calcium rises above 11.5 mg/dL. Side effects of low-grade fever, hypophosphatemia, hypomagnesemia, and hypocalcemia may occur. Gallium nitrate is a potent inhibitor of bone resorption and may be of increased clinical value when more efficient administration protocols can be developed. Plicamycin, available for two decades, has cumulative toxicities and is less potent than the aminobisphosphonates. Renal insufficiency often accompanies severe hypercalcemia. The nephrotoxicity of gallium nitrate and plicamycin should preclude their use when there is moderate impairment of renal function, and amino bisphosphonates become the treatment of choice in these patients. Although several authors have advocated individualized approaches to the management of hypercalcemia, the potency and duration of action of the aminobisphosphonates make them a reasonable treatment choice for most patients with symptomatic hypercalcemia. Most importantly, the most effective therapy for hypercalcemia is to recognize and treat the underlying disease. Acute primary hyperparathyroidism requires surgery. The effective treatment of hypercalcemia of malignancy allows the introduction of tumor-specific therapy, limits morbidity, and shortens and deintensifies hospitalization. At times, the most appropriate and compassionate decision (particularly in patients with malignancy who have exhausted all therapeutic options and have relentless bone pain) is to withhold therapy for hypercalcemia. Future therapies directed at the osteoclast, such as more potent later-generation bisphosphonates; inhibitors of osteoclast attachments and inhibitors of peptides, which stimulate osteoclastic bone resorption, may permit safe, easily administered, outpatient therapies that will improve the quality of life for hypercalcemic patients.
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PMID:Pathophysiology and management of severe hypercalcemia. 832 91

Paget's disease of bone is characterized by an anarchic bone turnover starting with excessive resorption caused by structural and functional abnormalities involving osteoclasts. Calcitonin and bisphosphonates are now considered as the main therapeutic approaches for this disease. Daily parenteral administration of calcitonin to patients with Paget's disease of bone results in a significant fall in serum alkaline phosphatase and urinary hydroxyproline levels. This treatment has also been reported to be effective in relieving clinical symptoms of the disease, mainly bone pain. The drawbacks of injectable calcitonin have stimulated interest in alternative routes of delivery. Substantial evidence of calcitonin bioavailability and bioefficacy equivalent to those of parenteral administration is currently available for only two alternative routes: nasal spray and rectal suppository. Since many results have been published showing a dramatic effect of several bisphosphonates in Paget's disease of bone, nasal and rectal calcitonin are no longer considered as the treatments of choice in this condition. A major advantage of the use of bisphosphonates over calcitonin in Paget's disease is that biochemical and histologic suppression of disease activity may persist for many years after the cessation of treatment. Oral etidronate and intravenous pamidronate have been extensively used and have provided satisfactory benefits to the patient. Since the risk/benefit ratio of alendronate does not appear to be completely positive, it is likely that the future of treatment of Paget's disease of bone will be based on the oral formulation of the new bisphosphonates, including tiludronate, risedronate or dimethyl-pamidronate.
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PMID:Efficacy and safety of drugs for Paget's disease of bone. 857 23

The variability of different primary tumors in the susceptibility to metastatic bone disease is poorly understood. Factors that determine the viability of metastatic cells are also poorly understood, but may depend in part upon gene expression of PTHrP and the vitamin D receptor. In contrast, much more is known of the manner in which metastatic disease affects bone remodeling to induce osteolytic bone disease. Mechanisms include a generalized increase in activation frequency at sites close to metastatic tissue, an imbalance between the amount of bone formed and that resorbed within resorption cavities, and uncoupling of bone formation from bone resorption. The greatest morbidity from metastatic bone disease arises from osteolytic disease and gives rise to hypercalcemia, bone pain, and fractures. Because osteolysis is primarily mediated by the activation of osteoclasts, there has been a great deal of interest in the use of agents which primarily affect bone metabolism to alter the natural history of metastatic bone disease. Nonsteroidal antiinflammatory agents and cytotoxic agents are capable of inducing responses in bone, but are limited by their toxicity when effective doses are utilized. The use of calcitonin in the long-term suppression of osteolysis has also been disappointing. The bisphosphonates are, however, capable of inducing sustained decreases in osteoclast activity and numbers in patients with osteolytic bone disease. There are now several studies which have examined the effects of the bisphosphonates on skeletal morbidity in breast cancer. Both clodronate and pamidronate decrease the incidence of hypercalcemia, bone pain, and pathological fractures, but do not significantly alter mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone and cancer: pathophysiology and treatment of metastases. 857 90

For virtually all asymptomatic postmenopausal women, moderate exercise and supplementation with calcium and vitamin D are recommended. In addition, most postmenopausal women without contraindications would benefit from estrogen replacement therapy, primarily because of its cardiovascular benefits. In patients with contraindications or an aversion to hormone therapy, bone densitometry should be performed to determine risks before expensive nonhormonal treatment is initiated. Therapy with alendronate sodium (Fosamax) or calcitonin (Calcimar, Miacalcin) is clearly indicated in women with established osteoporosis and may be appropriate for early postmenopausal women with osteopenia. Calcitonin is a good option in patients with disabling spinal bone pain. Slow-release sodium fluoride, although still considered experimental, may eventually be given for vertebral fracture in patients with mild to moderate disease.
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PMID:Osteoporosis. Current pharmacologic options for prevention and treatment. 900 93

The variability of different breast cancers in the susceptibility to metastatic bone disease is poorly understood. Factors that determine the viability of metastatic cells are also poorly understood, but may depend in part upon gene expression of PTHrP and the vitamin D receptor. In contrast, much more is known of the manner in which metastatic breast disease affects bone remodelling to induce osteolytic bone disease. Mechanisms include a generalized increase in activation frequency at sites close to metastatic tissue, an imbalance between the amount of bone formed and that resorbed within resorption cavities, and uncoupling of bone formation from bone resorption. The greatest morbidity from metastatic bone disease arises from osteolytic disease and gives rise to hypercalcaemia, bone pain and fractures. Since osteolysis is primarily mediated by the activation of osteoclasts, there has been a great deal of interest in the use of agents which primarily affect bone metabolism to alter the natural history of metastatic bone disease. Non-steroidal anti-inflammatory agents and cytotoxic agents are capable of inducing responses in bone, but are limited by their toxicity when effective doses are utilized. The use of calcitonin in the long-term suppression of osteolysis has also been disappointing. The bisphosphonates are, however, capable of inducing sustained decreases in osteoclast activity and numbers in patients with osteolytic bone disease. There are now several studies which have examined the effects of the bisphosphonates on skeletal morbidity in breast cancer. Both clodronate and pamidronate decrease the incidence of hypercalcaemia, bone pain and pathological fractures, but do not significantly alter mortality. Given, however, the unchanging survival in patients with metastatic bone disease, significant improvements in the quality of remaining life is an important therapeutic effect.
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PMID:Rationale for the use of bisphosphonates in breast cancer. 914 69


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