Calcium and Phosphate Metabolism in Patients with Disseminated Breast Cancer: Effect of Androgens and of Prednisone

Gardner, Bernard; Graham, William P.; Gordan, Gilbert S.; Löken, Hans F.; Thomas, Arthur N.; Teal, James S.

doi:10.1210/jcem-23-11-1115

Cited by 24 publications

(9 citation statements)

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“…or less, are worth using in mild to moderate hypercalcemia for prolonged control [12,38,40], Intravenous phosphate is rapidly effective [12], but is not recommend ed because hypocalcemia or metastatic calcifications have been fatal [34]. Corticosteroids have been widely used to treat hypercalcemia in breast cancer [7,19,20,24,26], Steroids lead to renal calcium and phosphate wasting and are vitamin D antagonists [7,31], but this is probably not their primary action in breast cancer. They may act by interfering with tumor metabolism, and objective remissions with corticosteroid treatment suggest this [17].…”

Section: Discussionmentioning

confidence: 99%

Hypercalcemia Complicating Breast Cancer

Belnoue-Davis¹,

Wiseley²,

Ramírez³

et al. 1973

Oncology

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The incidence of significant hypercalcemia in 305 women with disseminated breast cancer was 7.2%. 13 patients developed hypercalcemia spontaneously and eight patients developed hypercalcemia shortly after initiation of additive hormone therapy. One patient developed fatal hypercalcemia shortly after adrenalectomy. All patients had bone metastases documented by X-rays or bone scans. Treatment with volume expansion, diuretics, and steroids was successful in 11 of 19 trials and Mithramycin therapy in very low dosage was successful in 4 of 5 trials. 7 of the 22 hypercalcemia patients expired and four of these deaths were directly as a result of hypercalcemia.

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Section: Discussionmentioning

confidence: 99%

Hypercalcemia Complicating Breast Cancer

Belnoue-Davis¹,

Wiseley²,

Ramírez³

et al. 1973

Oncology

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“…Nassim, Saville, and Mulligan (52) thought that the reduction in serum phosphorus after estrogen administration was entirely a renal effect because renal tubular maximum for phosphate decreased in all of their five patients treated with stilbestrol for 2-3 wk. However, Young et al (51) found no change in the phosphorus excretion index in 15 osteoporotic patients during 5 days of ethinyl estradiol administration, and Gardner et al (55) found no change in the tubular reabsorption of phosphorus in cancer patients receiving pharmacologic doses of androgens. Our renal phosphate excretion data agree with those of the latter workers.…”

Section: Discussionmentioning

confidence: 99%

Effect of sex hormones on bone in primary osteoporosis

Riggs¹,

Jowsey²,

Kelly³

et al. 1969

J. Clin. Invest.

200

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A B S T R A C T The effect of sex hormones on bone tissue was studied in 12 osteoporotic patients. Surfaces of bone undergoing formation and resorption were determined by quantitative microradiography of iliac crest biopsy samples before and after treatment with estrogens in 11 postmenopausal women and with testosterone in one gonadally competent man. Before treatment, bone resorption was greater than normal in all but one patient and bone formation was normal. After treatment, bone resorption decreased to within the normal range in all patients, and bone formation did not change significantly. Biochemical studies showed significant decreases in serum calcium, phosphorus, and alkaline phosphatase levels and in urinary excretion of calcium and hydroxyproline. These changes are believed to be the consequence of the effect of the hormones on bone. The data indicate that the major effect of sex hormones in osteoporosis is an inhibition of bone resorption. INTRODUCTIONAlbright, Smith, and Richardson in 1941 proposed that anabolic sex hormones were necessary for bone matrix synthesis, and that the loss of estrogens at the menopause in women or of androgens with aging in men caused osteoporosis (1). Since then, sex hormones have been used extensively in the treatment of osteoporosis, although their mechanism of action and therapeutic usefulness have not been completely established.Estrogens stimulate intramedullary bone formation in birds (2), but their effect on mammalian bone is variable. Experiments have demonstrated increased endosteal formation in mice (3), decreased endosteal resorption in rats (4), and no specific skeletal response in

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“…1 This decrease in glomerular filtration rate, as measured by the endogenous creatinine clearance in women with far advanced, progressing malignancy, and its improvement during hormone-induced regressions are the subjects of this report.…”

Section: San Franciscomentioning

confidence: 87%