Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-nine patients with acute hypercalcemia secondary to carcinoma, myeloma and parathyroid adenoma have been treated with large doses of furosemide, mithramycin, or salmon calcitonin perfusion. With furosemide administration the treatment was successful in 6 of 10 patients. Furosemide was injected intravenously at the rate of 125 mg every 3 hours. With mithramycin perfusion only 2 of 8 patients have a return of the serum calcium levels to normal. With salmon thyrocalcitonin 3 of 10 patients obtained a good result. It can be interesting to suggest the association of furosemide and salmon calcitonin infusion to treat hypercalcemia of myeloma.
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PMID:Furosemide, mithramycin, and salmon calcitonin in hypercalcemia. 13 Feb 39

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.
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PMID:Senile and postmenopausal osteoporosis. 76 91

Hypercalcemia of multiple myeloma has been discussed widely in the medical literature. The role of calcitonin and phosphate in the treatment of hypercalcemia of multiple myeloma has not yet been studied to our knowledge, although experimental animal models have been pointing to the role of phosphate supplement to calcitonin treatment in multiple myeloma. A patient had multiple myeloma and hypercalcemia. The usual medical treatment for hypercalcemia failed; however, the treatment with combined orally administered phosphate and calcitonin was successful. The role of phosphate depletion in this setting is brought up as an important factor in the failure of calcitonin therapy.
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PMID:Combined calcitonin and oral phosphate treatment for hypercalcemia in multiple myeloma. 87 32

Hypocalcemic response following the administration of 160 units of porcine calcitonin was investigated in 14 patients with bone lesions caused by myeloma and in 9 control subjects. Significant decrease in blood serum calcium level was found in 85 per cent of myeloma patients, both in those with osteolytic bone lesions and those with generalized osteoporosis. Moreover, in all the patients a significant positive correlation was found between hypocalcemic response and the initial blood serum calcium concentration. Calcitonin administration did not cause any changes in blood serum phosphate level in myeloma patients.
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PMID:[Calcitonin test in patients with bone changes during the course of myeloma]. 136 10

Two cases of myeloma with roentgenographic evidence of bone sclerosis confirmed by iliac histomorphometric measurements are reported. In one patient, increased resorption, major depression of osteoblast activity, initial intense myelofibrosis, and myeloid deposits were found. The other patient had both increased resorption and increased osteoblast activity with clinical manifestations suggestive of POEMS syndrome. These two cases are compared with 116 cases previously published in the occidental medical literature and with five histomorphometric studies demonstrating increased bone trabecula volume (BTV). Conventional histologic studies suggest several mechanisms as possible explanations for the occurrence of bone sclerosis, including increased modeling unit activity, isolated osteoblast activation, metamorphic neoosteogenesis in myelofibrosis foci, and, in exceptional cases, inhibition of resorption due to increased production of calcitonin. The diversity of bone modeling patterns evidenced by the seven histomorphometric studies reviewed in this article is striking. Bone modeling patterns provide only a snapshot of bone modeling units and may vary over time in a given patient. Reported cases are too few to allow conclusions but emphasize the need for performing further histomorphometric investigations.
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PMID:[Condensing myeloma. Apropos of 2 cases with bone histomorphometric study]. 141 Dec 13

Circulating monomeric human calcitonin (hCT-M), parathyroid hormone, osteocalcin, alkaline phosphatase, urinary hydroxyproline, corrected serum calcium and inorganic phosphate were measured in 49 multiple myeloma patients and 49 matched controls. In patients with Durie-Salmon stage III disease hCT-M levels (16.9 +/- 5.8 ng/l, mean +/- SD) were significantly higher than controls and stage I patients (P less than 0.01), and correlated directly with corrected serum calcium (r = 0.74; P less than 0.001). In the same subgroup 14 of 15 patients had plasma hCT-M concentrations higher than the mean + 2SD of the controls. The calcium infusion test induced an increase of hCT-M in normocalcemic patients which was significantly greater in patients with advanced disease than in either controls or stage I patients. These findings suggest that hCT-M may be a biochemical index of bone resorption and disease activity in myeloma patients with osteolysis. In fact, its plasma concentrations were elevated in a large proportion (93%) of patients with severe bone involvement, and correlated directly with serum calcium. Moreover, our findings suggest the presence of a calcitonin-dependent calcium homeostatic mechanism, that protects against hypercalcemia due to tumor osteolysis.
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PMID:Plasma monomeric calcitonin as a marker of disease activity in multiple myeloma patients with osteolysis. 163 26

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

Salmon calcitonin, a polypeptide hormone secreted by the parafollicular C cells of the thyroid gland, lowers serum calcium levels by decreasing bone resorption and renal tubular calcium reabsorption. An analgesic action, possibly mediated via beta-endorphins, is also evident. In the past, parenteral formulations of salmon calcitonin have been used in the management of metabolic bone disorders, but their routine use has been limited by the inconvenience of this route of administration and by poor tolerability. The development of an intranasal preparation of salmon calcitonin will provide a more convenient means of administering the drug. In clinical trials published to date intranasal salmon calcitonin has been effective and well tolerated in small numbers of recently postmenopausal women at risk of developing osteoporosis, and in patients with established osteoporosis, Paget's disease, or osteoporosis secondary to corticosteroid usage, multiple myeloma or ovariectomy. For periods of up to 2 years the drug reduces bone resorption and improves bone architecture, relieves pain and increases functional status. Further research is needed to confirm longer term efficacy (in particular, effects on fracture rate), optimal dosage schedules and the role of intermittent and combination treatment regimens.
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PMID:Intranasal salmon calcitonin. A review of its pharmacological properties and potential utility in metabolic bone disorders associated with aging. 179 28

The author describes the excellent effect of two-years therapy of a female patient suffering from multiple myeloma, using the calcitonin preparation Miacalcic Sandoz. During the two and a half year follow up of the patient only a small progression of the bone affection occurred. The patient who on account of pain was treated with opiates was unable to walk unaided, now walks does not take analgesics.
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PMID:[Plasmacytoma and support therapy with calcitonin]. 179 64

Forty-nine subjects have been included in a randomized cross-over study evaluating acute hypocalcemia induced by calcitonin in the staging of multiple myeloma, and comparing 0.5 mg of human calcitonin and 100 IU of salmon calcitonin. Subjects were divided in 11 controls, 15 myelomas before primary treatment, 11 myelomas in plateau-phase and 12 in relapse. All the subjects had both tests with the two calcitonins at an interval of 3 days. Decrease of calcemia was important and similar in patients before primary treatment and in relapse (0.16 mmol/l mean value). Decrease was moderate in patients in plateau-phase (0.07 mmol/l mean value), similar to the decrease observed in controls. Decrease of calcemia was correlated with tumoral cellular mass in initial phase patients, but not in patients in plateau-phase. Both human and salmon calcitonins had similar effects on onset, magnitude and duration of hypocalcemia inside each group. This study confirms the interest of acute hypocalcemia test induced by calcitonin in the clinical staging of myeloma, and the similar effectiveness of both calcitonins in man.
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PMID:[Evaluation of osteoclastic activity in multiple myeloma: results of a randomized trial studying hypocalcemia induced by human and salmon calcitonin in 49 patients]. 205 1


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