Hypercalcemia is the most common life-threatening metabolic disorder associated with neoplastic diseases, occurring in an estimated 10% to 20% of all adults with cancer. It also occurs in children with cancer, but with much less frequency (approximately 0.5%-1%).[1,2,3] Solid tumors (such as lung or breast cancer tumors) as well as certain hematologic malignancies (particularly multiple myeloma) are most frequently associated with hypercalcemia. Although early diagnosis followed by hydration and treatment with agents that decrease serum calcium concentrations (hypocalcemic drugs) can produce symptomatic improvements within a few days, diagnosis may be complicated because symptoms may be insidious at onset and can be confused with those of many malignant and nonmalignant diseases. However, diagnosis and timely interventions not only are lifesaving in the short term but also may enhance the patient's compliance with primary and supportive treatments and may improve quality of life. When a patient has a refractory, widely disseminated malignancy for which specific therapy is no longer being pursued, the patient may want to consider withholding therapy for hypercalcemia. For patients or families who have expressed their wishes regarding end-of-life issues, this may represent a preferred timing and/or mode of death (as compared with a more prolonged death from advancing metastatic disease). This option is best considered long before the onset of severe hypercalcemia or other metabolic abnormalities that impair cognition, so that the patient may be involved in the decision making.
In this summary, unless otherwise stated, evidence and practice issues as they relate to adults are discussed. The evidence and application to practice related to children may differ significantly from information related to adults. When specific information about the care of children is available, it is summarized under its own heading.
Thyroid dysfunction, manifested by primary hypothyroidism, hyperthyroidism, goiter, or nodules, is a common delayed effect of radiation therapy fields that include the thyroid gland incidental to treating Hodgkin lymphoma (HL), brain tumors, head and neck sarcomas, and acute lymphoblastic leukemia. Of children treated with radiation therapy, most develop hypothyroidism within the first 2 to 5 years posttreatment, but new cases can occur later. Reports of thyroid dysfunction...
Calcium homeostasis is maintained by two hormones, parathormone (parathyroid hormone or PTH) and calcitriol (1,25-dihydroxy vitamin D). Minute-to-minute regulation of serum-ionized calcium is regulated by PTH. PTH secretion is stimulated when ambient serum-ionized calcium is decreased. PTH acts on peripheral target cell receptors, increasing the efficiency of renal tubular calcium reabsorption. In addition, PTH enhances calcium resorption from mineralized bone and stimulates conversion of vitamin D to its active form, calcitriol, which subsequently increases intestinal absorption of calcium and phosphorus. Pharmacologic doses of calcitonin act as an antagonist to PTH, lowering serum calcium and phosphorus and inhibiting bone reabsorption.
Normal, healthy kidneys are capable of filtering large amounts of calcium, which is subsequently reclaimed by tubular reabsorption. The kidneys are capable of increasing calcium excretion nearly fivefold to maintain homeostatic serum calcium concentrations. Hypercalcemia may occur, however, when the concentration of calcium present in the extracellular fluid overwhelms the kidneys' compensatory mechanisms.