Treatment of hypercalcemia of malignancy with intravenous etidronate: a controlled, multicenter study

Article Abstract:

Malignant hypercalcemia is an excess of calcium in the blood that occurs in 10 to 20 percent of patients with cancer. It is caused by increased bone loss either due to destruction of the bone by metastatic cancer, or through the production of a parathyroid hormone-like protein. (Parathyroid hormone causes the release of calcium from bone.) The usual treatment is hydration (giving the patient fluids), but this is not always effective. Etidronate sodium belongs to a group of chemicals called the diphosphonates, which bind to bone and prevent its breakdown. It has been shown to be effective in lowering calcium levels in patients with malignant hypercalcemia. A total of 157 cancer patients with hypercalcemia were randomly assigned to one of two groups: one group received hydration with saline solution (43 patients), and the other received an infusion of etidronate in saline solution (114 patients). The infusions were given once a day over a two-hour period for three days. Additional hydration was given to both groups as needed to restore fluid levels. Furosemide (Lasix) was also administered, if needed, to prevent fluid overload. By the fourth day, patients in the etidronate group had significantly lower levels of calcium than those in the saline group. Furthermore, 63 percent (72 of 114) of the patients in the etidronate group responded to the treatment, whereas only 33 percent (14 of 43) of the saline group responded to hydration alone. There were few side effects of etidronate treatment; nausea and/or vomiting occurred in 8.8 percent of patients on etidronate compared with 4.5 percent of patients receiving hydration alone. Twelve percent of the etidronate-treated group experienced mild, temporary impairment of kidney function, compared with five percent of the saline group. However, hypercalcemia and dehydration can cause kidney damage, and the adverse effect of etidronate can be minimized by administering the drug slowly over long periods of time. In fact, etidronate treatment may be more effective if the duration of treatment is increased. The most effective treatment for hypercalcemia of malignancy is cancer therapy, etidronate may be useful in the short-term for lowering elevated calcium levels.(Consumer Summary produced by Reliance Medical Information, Inc.)

Drug therapy

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Malignant hypercalcemia: the choice of therapy

Article Abstract:

Malignant hypercalcemia is an excess of calcium in the blood associated with cancer. It is caused by increased bone loss either due to destruction of the bone by metastatic cancer, or through the production of a parathyroid hormone-like protein. (Parathyroid hormone causes the release of calcium from bones.) Symptoms include muscular weakness, confusion, tremor, and psychosis. The most effective treatment for malignant hypercalcemia is to treat the cancer, but many patients have advanced cancers which have not responded to treatment. Although hydration (giving the patient fluids) remains the most effective short-term treatment, many patients still require additional therapy. Etidronate sodium belongs to a group of chemicals called the diphosphonates; they bind to bone and prevent its breakdown. Previous studies have reported that calcium levels returned to normal in 19 of 26 patients (79 percent) who were given etidronate. In the March 1991 issue of the Archives of Internal Medicine, Singer reports that etidronate and hydration were more effective in reducing calcium levels than hydration alone. It remains to be seen whether etidronate is more effective than other diphosphonates in treating malignant hypercalcemia. Lowering blood calcium levels does not necessarily improve survival, and most patients will die of their cancer. Therefore, treatment of malignant hypercalcemia will be most meaningful in those patients who have an improved chance of survival. (Consumer Summary produced by Reliance Medical Information, Inc.)

editorial

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Bilateral vocal cord paralysis with respiratory failure: a presenting manifestation of bronchogenic carcinoma

Article Abstract:

Obstruction of the upper airway and an inability to breath due to an excess of carbon dioxide in the blood were diagnosed in a patient with lung cancer. Paralysis of both vocal cords, or bilateral laryngeal paralysis, was identified as the primary cause of the patient's respiratory failure. Computed tomography (CT) scanning revealed that the lung tumor had extended into the upper chest and had probably disrupted the pathways of both laryngeal nerves, which were required for an open airway. Such bilateral vocal cord paralysis is usually associated with the continued ability to speak in conjunction with stridor, in which very high pitched sounds are made when inhaling air during airway obstruction; these symptoms can become life-threatening if there are delays in diagnosis and treatment. If the obstruction is severe, urgent intubation, the insertion of a tube into the throat to maintain an airway, is necessary, and long-term laryngeal surgical procedures may be required to maintain the airway.

Airway obstruction (Medicine), Airway obstruction, Lung cancer, Respiratory insufficiency, Vocal cords, Vocal cord paralysis

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