Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153690 (bone metastases)
 6,382 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma calcitonin was determined in 33 patients with breast carcinoma. Eight patients had bone metastases as revealed at scintigraphy and radiography. Only 3 of the 33 patients had elevated plasma calcitonin, 2 had osteolytic bone metastases. It is concluded that the determination of plasma calcitonin is of no value in the evaluation of patients with breast malignancy and it should not be referred to as a tumor marker.
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PMID:Calcitonin and mammary carcinoma. 625 46

Levels of immunoreactive ACTH and calcitonin (CT), as well as CEA, were determined serially in 144 patients with lung cancer and in 62 patients with metastatic carcinoma to the lungs. Patients with neoplasms not involving the lungs, with nonmalignant blood dyscrasias, and with chronic obstructive pulmonary disease were studied, as were normal control subjects. In 55-91% of lung cancer patients, elevated values of CT were detected; the frequency of elevation varied with cell type and stage. The highest values (mean 1346 +/- 2534 pg/ml) were found in patients with extensive small cell lung carcinoma (SCLC) and were significantly greater than the values for patients with SCLC confined to one hemithorax (196 +/- 287.7 pg/ml, P less than 0.005). ACTH levels were elevated less frequently (24-46%) and were highest (192 +/- 200.9 pg/ml) in patients with extensive small cell carcinoma, although Cushing's syndrome was observed only once. Agreement between all three tumor markers was seen in 25-50% of lung cancer patients; the percentage depended on cell type. Calcitonin levels paralleled changes in the clinical status and tumor burden in 89% of SCLC patients, while ACTH levels reflected the clinical course in 67%. In six patients with small cell carcinoma in remission, rising levels of CT, ACTH, and CEA preceded clinical evidence of relapse, in oe patient, by as long as five months. Among 129 patients with conditions other than primary lung cancer, CT levels were highest (232 +/- 328 pg/ml) in those with cancer metastatic to the lungs and/or pleura; there was no; association between CT levels and the presence of bone metastases.
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PMID:A study of immunoreactive calcitonin (CT), adrenocorticotropic hormone (ACTH) and carcinoembryonic antigen (CEA) in lung cancer and other malignancies. 626 70

Receptors for 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] have been described in several human breast cancer cell lines and more recently in human melanoma. The presence of 1,25-(OH)2D3 receptor (1,25-DR) in two cultured breast cancer cell lines was associated with receptors for calcitonin, another hormone thought to have effects on calcium handling. Therefore, it seemed important to examine a range of established human cancer cell lines for the presence of receptors for 1,25-(OH)2D3 and calcitonin. Thirty-three cancer cell lines were examined. 1,25-DR was found to be present in 23 lines, while calcitonin receptors were not detected in any of them. The 1,25-DR from several cell lines sedimented at about 3.5S in sucrose density gradients, had the appropriate specificity for vitamin D metabolites, had Kds of 0.8 to 2.2 x 10(-11) M, and had receptor concentrations of 12 to 99 fmol/mg protein. Ten malignant melanoma and nine colonic carcinoma lines constituted the largest groups of carcinoma cell lines, and seven and eight, respectively, of these were 1,25-DR positive. The high frequency of 1,25-DR positivity in the cultured colonic carcinoma cells is quite different from the low frequency of 1,25-DR in primary colonic carcinomas. It was also interesting that both of two cell lines derived from patients who had had both bone metastases and malignant hypercalcemia were 1,25-DR positive. These various cell lines may provide useful models for the examination of 1,25-(OH)2D3 action in vitro.
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PMID:Presence of 1,25-dihydroxyvitamin D3 receptors in established human cancer cell lines in culture. 627 75

Elevated plasma calcitonin was detected by radioimmunoassay in 19 of 99 unselected cancer patients (19%). The frequency of hypercalcitoninaemia in patients with tumours of lung, uterus, gastrointestinal tract, and urinary bladder was about 40%, in carcinoma of the breast 18%, and in carcinoma of the skin 4%. In 8 patients with bone metastases, 4 were hypercalcitoninaemic. None of 19 patients with non-malignant disorders had elevated plasma calcitonin. The highest plasma calcitonin level in cancer patients was 8200 ng/l. Urinary cyclic AMP was elevated in patients with hypercalcitoninaemia as compared with patients with normal plasma calcitonin. All 6 patients with medullary carcinoma of the thyroid had very high plasma calcitonin levels: more than 50000 ng/l in five and 30000 ng/l in one patient. Of the family members of these patients, raised plasma calcitonin was detected after stimulation with oral alcohol in 6 of 12. It is concluded that plasma calcitonin levels in excess of 10000 ng/l suggest the presence of medullary carcinoma of the thyroid, while levels below 10000 ng/l have a poor diagnostic value but should alert the clinician to look for a possible malignancy.
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PMID:Hypercalcitoninaemia in medullary carcinoma of the thyroid and other malignancies: value of calcitonin as tumour marker. 628 27

Infusion of 200 IU Calcitonin-Sandoz in 20 of 44 hospitalized patients with malignant tumor suffering from chronic severe pain due to bone metastases, reduced the intensity of pain and with it the need for analgesics for an average of 10 hours. The result points to an analgesic potential of salmon-calcitonin.
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PMID:[Salmon calcitonin in metastatic bone pain. Demonstration of acute analgesia in tumor patients]. 637 42

Apart from the search for specific oncological treatments, interesting investigations are currently in progress into methods designed to increase bone resistance against tumoral aggression. Several substances are under study. Here the discussion will chiefly centre on the diphosphonates, their mechanism of action and indication in bone oncology. It has been seen that tumoral hypercalcemias (with or without bone metastases) essentially derive from disturbance of the balance between the huge mineral stores of the bone and the small extracellular space. It has also been learned that osteolysis inhibition is the major step in their treatment, while therapies designed to eliminate the calcium excess through the kidney (saline solutions, furosemide, ethacrinic acid, dialysis) or bind it with chelators (EDTA) can have only transitory effects. Tumoral osteolysis may be inhibited by drugs acting on bone and/or tumoral cells (mithramycin, calcitonin, corticosteroids etc.) or by the diphosphonates. At present the latter are the treatment of choice for tumoral hypercalcemias.
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PMID:[Treatment of hypercalcemias]. 680 27

Clodronate (clodronic acid, dichloromethylene bisphosphonate) is a bisphosphonate which has demonstrated efficacy in patients with a variety of diseases of enhanced bone resorption including Paget's disease, hypercalcaemia of malignancy and osteolytic bone metastases. In addition, early reports demonstrating potential efficacy of clodronate in the treatment of osteoporosis suggest a possible role in this debilitating disease. Short term intravenous administration (usually 300 mg/day for 5 days) or longer courses of oral clodronate (usually 1600 mg/day for 6 months) effectively reduced bone pain and/or improved mobility in most patients with Paget's disease, and these effects persisted for up to 12 months after discontinuing clodronate. When administered intravenously (300 mg/day for up to 12 days) to patients with malignant hypercalcaemia, serum calcium levels declined significantly within 2 days of starting treatment and approximately 70 to 95% of patients became normocalcaemic. While there is less experience with oral administration, clodronate (800 to 3200 mg/day) achieved normocalcaemia in the majority of patients, usually within 1 week, and serum calcium levels remained significantly reduced from baseline for up to 6 months with continued treatment. Clodronate is clearly superior to placebo and, based on a retrospective analysis, appears to produce greater and more sustained reductions in serum calcium levels than calcitonin in patients with malignant hypercalcaemia. The few available prospective comparative trials showed that clodronate is at least as effective as etidronate, but comparisons with alendronate and pamidronate produced results of questionable clinical relevance because of low bisphosphonate dosages used in these trials. Nevertheless, single intravenous doses of clodronate 600 mg or alendronate 7.5 mg (both agents repeated on day 3 if necessary) were comparable in efficacy, whereas a single intravenous dose of pamidronate 30 mg was more effective than a single intravenous dose of clodronate 600 mg. Normocalcaemic patients with osteolytic bone metastases due to advanced breast cancer experienced significant reductions in the number of episodes of hypercalcaemia and terminal hypercalcaemia, incidence of vertebral fractures and overall rate of morbid events, including the need for radiotherapy to treat bone-related pain, following treatment with clodronate 1600 mg/day for 3 years in a large placebo-controlled study. A similar large placebo-controlled trial in patients with multiple myeloma demonstrated that clodronate 2400 mg/day orally for 2 years significantly reduced progression of osteolytic bone lesions. Follow-up data from clinical trials revealed that the effects on development of fractures and hypercalcaemia persisted for at least 12 months after the drug was discontinued.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clodronate. A review of its pharmacological properties and therapeutic efficacy in resorptive bone disease. 752 33

Hypercalcemia of malignancy is most commonly due to the effects of parathyroid hormone-related peptide, which acts as a humoral factor to cause generalized osteoclast-mediated bone resorption and reabsorption of calcium by the kidney tubule, and may also act as a local resorptive factor adjacent to bone metastases. Local resorptive mechanisms are less common causes of malignant hypercalcemia than previously believed. Treatment begins with intravenous fluid rehydration, followed by a furosemide diuresis and the bisphosphonate pamidronate, 60-90 mg, intravenously. Gallium nitrate is an efficacious but inconvenient alternative to pamidronate. Calcitonin combined with pamidronate is a reasonable initial therapy for severe hypercalcemia to hasten normalization of the serum calcium. Steroids should be reserved for hypercalcemia due to tumor production of 1,25 dihydroxyvitamin D, or for steroid-responsive malignancies. Oral or parenteral bisphosphonates can be used to maintain normocalcemia. In addition to improving the morbidity of acute hypercalcemia, bisphosphonate therapy has been shown to reduce bone pain and pathological fractures in patients with bone metastases, and calcitonin also has a potent analgesic effect in these patients. Treatment for hypercalcemia should therefore be considered in the majority of patients in the palliative care setting.
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PMID:Hypercalcemia of malignancy in the palliative care patient: a treatment strategy. 754 27

In 16 patients with pain caused by diffuse osteolytic or osteoplastic-osteolytic metastases, salmon calcitonin was used as pain relieving treatment. All patients were pretreated with opiate type analgesics without a satisfactory effect. In 2 patients it was possible to withdraw completely previous opiate intake. In most of the patients the analgesic effect of salmon calcitonin consisted in decrease of pain with identical or decreased intake of opiate type analgesics. In 3 patients the pain relieving treatment with salmon calcitonin completely failed. Our investigation seems to demonstrate that there is a subpopulation of patients with bone metastases, resistant to opiate type analgesics, in which salmon calcitonin can be administered as an additional useful pain relieving drug.
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PMID:[Anti-pain effect of salmon calcitonin in bone metastases of malignant tumors with the exception of breast and prostatic carcinoma]. 757 28

Hypercalcemia is the most common paraneoplastic syndrome associated with cancer. This paper addresses the etiology and pathogenesis of hypercalcemia of malignancy and discusses the relative contributions of local and humoral effects on bone and renal calcium homeostasis. The roles of parathyroid hormone-related protein and other osteolytic cytokines are outlined. New biochemical markers that enable more specific monitoring of the response of bone metastases to treatment are introduced, including urinary excretion of the collagen crosslinks pyridinoline and deoxypyridinoline. The clinical management and prevention of hypercalcemia is systemically outlined, including indications for bisphosphonate, glucocorticoid, and calcitonin therapy. The results of recent trials of bisphosphonate therapy for the prevention of tumor progression and its subsequent problems such as bone pain, fracture, and hypercalcemia also are discussed.
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PMID:Hypercalcemia and bone resorption in malignancy. 763 18


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