Overview of hypercalcemia of malignancy.
The etiology, pathophysiology, and diagnosis of hypercalcemia associated with malignant diseases are discussed. In humans, calcium is controlled by three mechanisms: parathyroid hormone, which regulates bone resorption and renal reabsorption of calcium; calcitonin, an antagonist of parathyroid hormone; and cholecalciferol, which regulates calcium absorption from the gastrointestinal tract. Hypercalcemia of malignancy (HCM) results primarily from increased bone resorption by osteoclasts and, to a lesser extent, from increased renal tubular reabsorption. In most tumors, parathyroid hormone-related protein (PTHrP) is the primary mediator of calcium. PTHrP stimulates increased bone resorption by osteoclasts. This stimulation also activates transforming growth factor-beta (TGF-beta), which stimulates tumor cells, thus perpetuating the cycle. Hypercalcemia is usually defined as a serum calcium concentration greater than 12 mg/dL, corrected for the serum albumin concentration. In diagnosing HCM, it is important to rule out other causes of hypercalcemia, such as primary hyperparathyroidism.
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D001862:Bone Resorption / Q000209:etiology / Q000378:metabolism; D001943:Breast Neoplasms / Q000150:complications / Q000378:metabolism; D002116:Calcitonin / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002762:Cholecalciferol / Q000378:metabolism; D005260:Female; D019337:Hematologic Neoplasms / Q000150:complications / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D006934:Hypercalcemia / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008175:Lung Neoplasms / Q000150:complications / Q000378:metabolism; D008297:Male; D009101:Multiple Myeloma / Q000150:complications / Q000378:metabolism; D009369:Neoplasms / Q000150:complications* / Q000378:metabolism; D010281:Parathyroid Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism
D010281:Parathyroid Hormone; D002762:Cholecalciferol; D002116:Calcitonin; D002118:Calcium