Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A hypercalcemia frequency of 1.5% was found in patients with malignant disease attending a large oncological center. Eighty per cent of hypercalcemias were of obvious malignant etiology. Hypercalcemia was most frequent in multiple myeloma, renal carcinoma, squamocellular carcinomas of different sites and breast cancer. Most patients had advanced metastasized disease. In 80% of those with solid tumors malignant hypercalcemia was associated with bone metastases. Serum calcium could almost invariably be reduced by treatment, and active treatment was associated with a more favorable prognosis. One year actuarial survival of patients with malignant hypercalcemia was 31%.
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PMID:Malignant hypercalcemia--a hospital survey. 381 29

All patients with carcinoma of the breast seen in this Unit since 1970 were reviewed to study the incidence, prognosis, morbidity and response to treatment of bone metastases. The biological characteristics of the primary tumour were compared in patients relapsing first in bone or liver. Sixty-nine percent of patients dying with breast cancer had bone metastases and bone was the commonest site of first distant relapse. Bone relapse was more common in receptor positive or well differentiated (grade 1) tumours. The median survival was 24 months in those with disease apparently confined to the skeleton compared with 3 months after first relapse in liver. Ten percent of patients with breast cancer developed hypercalcaemia. All had metastatic disease and 85% had widespread skeletal involvement. Fifteen percent of patients with disease confined to the skeleton developed hypercalcaemia. The response in bone to primary endocrine therapy, and chemotherapy, was apparently less than the overall response achieved. A large proportion had apparently static disease reflecting the insensitivity of the UICC assessment criteria. The duration of survival in these patients was similar to responding patients, suggesting a tumour response may occur in the absence of discernable radiological evidence of healing.
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PMID:The clinical course of bone metastases from breast cancer. 381 76

This paper reports the experience at the Royal Victoria Hospital in Montreal with the first 50 Port-A-Cath devices implanted for venous access in patients requiring long-term chemotherapy. There were 25 women and 22 men, ranging in age from 18 to 85 years. Twenty-two devices were implanted for hematologic malignant disease, 26 for solid tumours and 2 for benign disease. The mean operative time was 46.3 minutes, using a percutaneous subclavian stick technique in 94% of insertions. Blood sampling and infusions were easy in 88% and 92% respectively. Seventy-eight percent of the patients accepted the device well. Nine devices were removed, four at the end of therapy (median functioning time of 208.5 days) and five because of sepsis (median time 18 days). The median time of the still-functioning devices in live patients is 141.5 days. Septic complications were seen in 12%, blockage in 6% and skin necrosis in 2%. One death occurred from sepsis in a poor-performance patient with stage IV breast cancer and hypercalcemia. We breast cancer and hypercalcemia. We believe that the Port-A-Cath is efficient, safe and easily accessible for patients on long-term chemotherapy.
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PMID:Implantable device for venous access. 382 9

Patients with advanced breast cancer may develop acute, severe hypercalcemia when treated with estrogens or antiestrogens. In this study, we examined the effects of estrogens and related compounds on the release of bone resorbing activity by cultured human breast cancer cells in vitro. We found that the estrogen receptor positive breast cancer cell line MCF-7 releases bone resorbing activity in response to low concentrations of 17 beta-estradiol. Bone resorbing activity was also released in response to the antiestrogen nafoxidine. Other steroidal compounds had no effect on the release of bone resorbing activity. Estrogen-stimulated release of bone resorbing activity occurred with live bone cultures, but not with devitalized bones, indicating that the effect was bone cell mediated. The breast cancer cell line MDA-231, which does not have estrogen receptors, did not release bone resorbing activity in response to 17 beta-estradiol or nafoxidine. Release of the bone resorbing activity by MCF-7 cells incubated with 17 beta-estradiol was inhibited by indomethacin (10 microM) and flufenamic acid (50 microM), two structurally unrelated compounds that inhibit prostaglandin synthesis. Concentrations of 17 beta-estradiol and nafoxidine that caused increased release of bone resorbing activity by the breast cancer cells caused a four- to fivefold increase in release of prostaglandins of the E series by MCF-7 cells. These data may explain why some patients with advanced breast cancer develop acute hypercalcemia when treated with estrogens or antiestrogens, and why bone metastases are more common in patients with estrogen receptor positive tumors.
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PMID:Estrogens and antiestrogens stimulate release of bone resorbing activity by cultured human breast cancer cells. 385 65

The treatment of hypercalcemia remains a common problem in the management of many patients with cancer. We have used intravenously administered etidronate disodium as a therapy for hypercalcemia in 26 patients with malignant disease. Patients with persistent hypercalcemia despite adequate hydration and a serum creatinine level less than or equal to 1.5 mg/dL were allowed on study. Treatment consisted of intravenously administered etidronate disodium at 7.5 mg/kg/day in 250 mL of saline infused over two hours on 1, 2, 3, or 4 consecutive days. The serum calcium level in 19 (73%) of 26 patients returned to the normal range with a mean response time of 3 +/- 2 days. Similar response rates were seen in patients with a variety of tumors, including breast cancer, non-small-cell lung cancer, and multiple myeloma. Intravenously administered etidronate appears to be safe and effective therapy for hypercalcemia in patients with malignant disease.
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PMID:Intravenous etidronate in the management of malignant hypercalcemia. 391 67

18 French women with bone metastases of breast cancer were treated with norethisterone 60 mg per day (except 1 woman given 20 mg daily) for 2 months or until the end of the remission from 1969-1972. The patients ranged from 39-84 years (mean 57.7). In 16 breast cancer had 0een diagnosed 6 months to 16 years before (mean 43 months). Calcemia was less than 102 mg per 1; calcuria was above 250 mg per 24 hours in 3. The bone lesions were lytic in 13 and mixed in 5. Progestagens were the first treatment for bone metastases in 10; others had ovariectomy, androgens, cortisone, chemotherapy, adrenalectomy, and hypophysectomy. Since the response of these metastases is difficult to evaluate, the authors chose criteria of disappearance of pain and stabilization of radiographic lesions. In 6 patients pain was relieved within 2-4 weeks, and lesions stabilized or recalcified in 2. In 5 of the 6 erythrocyte sedimentation rate became normal in 2 months; calcemia normalized in 1; calcuria decreased in 4. Remission lasted 3-9 months (mean 5.6). After remission, androgens were effective in 3 or 4. In 6, norethisterone was stopped because it was ineffective. 6 others had to stop for intolerance: vomiting in 1, jaundice in 2, hypercalcemia in 3.
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PMID:[Treatment of bone metastases of breast cancer with progestogens]. 482 May 23

Thirty-four normocalcaemic women with multiple osteolytic bone metastases from breast cancer were randomly allocated to treatment with disodium dichloromethylene diphosphonate (Cl2MDP) 1600 mg/day orally (17) or placebo (17) for 3-9 months. Fasting urinary hydroxyproline/creatinine and calcium/creatinine ratios declined in the Cl2MDP group but not in the placebo group. Four patients in the placebo group died from hypercalcaemia. New bone metastases were more common in patients on placebo and these patients also required more analgesic drugs than those on Cl2MDP. Cl2MDP seemed to reduce bone pain and bone resorption and prevent the development of hypercalcaemia caused by osteolytic metastases. The formation of new bone metastases and the growth of old ones seemed to be retarded by Cl2MDP.
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PMID:Long-term controlled trial with diphosphonate in patients with osteolytic bone metastases. 613 Jan 97

Ten women with skeletal metastases from breast carcinoma received dichloromethylene diphosphonate (Cl2MDP), an inhibitor of osteoclast function, in a placebo-controlled, double-blind, crossover study. Eight of these patients had either hypercalcemia or hypercalciuria, and all 10 had elevated urinary hydroxyproline levels as evidence of active skeletal disease. Eight patients had moderate to severe bone pain. After eight weeks of oral dichloromethylene diphosphonate treatment (3,200 mg per day), either preceded by or followed by an eight-week placebo period, seven of eight patients with hypercalciuria had significant reductions in urinary calcium levels, and nine of 10 had reductions in urinary hydroxyproline levels (significant in eight) when the dichloromethylene diphosphonate treatment periods were compared with prestudy or placebo periods. Additionally, seven of eight subjects had decreased pain with dichloromethylene diphosphonate. There were no adverse effects other than transient diarrhea in some patients. We conclude that oral dichloromethylene diphosphonate can significantly inhibit osteoclast-mediated bone destruction in patients with bone metastases from breast cancer.
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PMID:Effects of dichloromethylene diphosphonate in women with breast carcinoma metastatic to the skeleton. 621 77

Dichloromethylene diphosphonate (Cl2MDP), an inhibitor of osteoclast-mediated bone resorption, lowers serum calcium in hypercalcemia associated with malignancies and with primary hyperparathyroidism. We have evaluated the effectiveness of Cl2MDP in three patients who had multiple osteolytic bone metastases due to breast cancer and coincident primary hyperparathyroidism and who refused neck exploration. Cl2MDP was added to the tamoxifen treatment and was given orally at a dose of 1600 mg/day for 12 months. All patients had a reduction in serum calcium level which was accompanied by a decline in the fasting urinary calcium and hydroxyproline excretion. Administration of Cl2MDP was not associated with any changes in parathyroid hormone levels. New bone metastases were observed neither during the treatment nor in the follow-up period. No side effects were observed.
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PMID:Long-term effects of dichloromethylene diphosphonate in patients with osteolytic bone metastases and coincident primary hyperparathyroidism. 623 89

We have demonstrated that a variety of cultured breast cancer cell lines, human breast cancers, non-malignant breast tumours and normal rabbit breast tissue contain specific, high-affinity, low-capacity receptors for 1,25-(OH)2D3. Considered with the ability of normal breast tissue to transport calcium from blood into breast milk, which has recently been shown to be stimulated by 1,25-(OH)2D3, the presence of this receptor could explain the high incidence of hypercalcaemia in this common disease and has important implications for the management of metastatic breast cancer. Finally these findings suggest that breast is a normal target organ for 1,25-(OH)2D3 action.
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PMID:Presence of 1,25-dihydroxy vitamin D receptor in normal and abnormal breast tissue. 625 52


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