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Hypercalcemia: Pathogenesis, Clinical Manifestations, Differential Diagnosis, and Management Chapter 26. Hypercalcemia: Pathogenesis, Clinical Manifestations, Differential Diagnosis, and Management Elizabeth Shane1 and Dinaz Irani2 1Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York; and 2Metabolic Bone Disease Research Program, Columbia University Medical Center, New York, New York INTRODUCTION ities of the kidney to eliminate it and of the skeleton to reclaim it. Less commonly, normal rates of calcium entry into the extracel- The clinical presentation of hypercalcemia varies from a mild, lular fluid may result in hypercalcemia if the process of renal asymptomatic, biochemical abnormality detected during routine excretion or that of bone mineralization is impaired. screening to a life-threatening medical emergency. In this chapter, Accelerated bone resorption by multinucleated bone-resorbing pathogenesis, clinical manifestations, differential diagnosis, and osteoclasts is the primary pathogenetic mechanism in most in- management of hypercalcemia will be discussed. stances of hypercalcemia.(1) Osteoclasts may be stimulated to resorb bone by PTH, PTH-related protein (PTHrP), and 1,25- PATHOGENESIS dihydroxyvitamin D, all of which have been shown to cause The concentration of calcium in the extracellular fluid is critical hypercalcemia.(2,3) A number of cytokines (IL-1␣, IL-1␤, IL-6, for many physiologic processes. Under normal circumstances, the TNF, lymphotoxin, and TGF-␣) also stimulate osteoclastic bone range is remarkably constant, between 8.5 and 10.5 mg/dl (2.1–2.5 resorption either alone or in concert with PTHrP.(4) Although low mM). The exact normal range varies slightly, depending on the levels of PTHrP are expressed by many normal tissues, high levels laboratory. Approximately one-half the total serum calcium is may be secreted from some malignant tumors. Some cytokines bound to plasma proteins, primarily albumin. A small component have been linked to the development of hypercalcemia in human of the total calcium is complexed to anions such as citrate or malignancy.(4) Excessive GI absorption of calcium is a much less sulfate. The remaining one-half circulates as the free calcium ion. common cause of hypercalcemia, although it may play a role in It is only this ionized portion of the total serum calcium that is hypercalcemic states characterized by excess vitamin D, such as physiologically important, regulating neuromuscular contractility, lymphoma or vitamin D intoxication. Whether the primary cause the process of coagulation, and a variety of other cellular activities. of the hypercalcemia is accelerated bone resorption or excessive In a variety of chronic illnesses, there may be a substantial GI tract absorption of calcium, the kidney is the primary defender reduction in the serum albumin concentration. Under such circum- against a rise in the serum calcium. Thus, hypercalcemia is usually stances, the total serum calcium concentration may be low, preceded by hypercalciuria, and it is only when the capacity of the whereas ionized calcium concentrations remain normal. A simple kidney to excrete calcium has been exceeded that the patient correction for hypoalbuminemia may be made by adding 0.8 becomes hypercalcemic.(5) mg/dl to the total serum calcium concentration for every 1.0 g/dl Several other factors may contribute to the pathogenesis of by which the serum albumin concentration is lower than 4.0 g/dl. hypercalcemia. In addition to stimulating osteoclast-mediated Thus, a patient with a total serum calcium of 10.5 mg/dl and a bone resorption, both PTH and PTHrP increase reabsorption of serum albumin level of 2.0 g/dl has a corrected total serum calcium from the distal tubule, thus interfering with the ability of calcium of 12.1 mg/dl. Conversely, falsely elevated serum cal- the kidneys to clear the filtered calcium load. PTH and PTHrP also cium levels may be observed, usually as the result of an elevation increase 1,25-dihydroxyvitamin D synthesis, further contributing of the serum albumin because of dehydration or hemoconcentra- to a hypercalcemic state.(6) Hypercalcemia interferes with the tion during venipuncture. A similar maneuver can be performed to action of antidiuretic hormone on the distal tubule, causing a form correct the serum calcium in this situation, except that the correc- of nephrogenic diabetes insipidus that results in polyuria. The tion factor must be subtracted from the serum calcium level. thirst mechanism may not be fully operative because of the nausea In contrast to changes in the serum albumin concentration, and vomiting that frequently accompany hypercalcemia; thus, which affect the total but not the ionized calcium level, alterations urinary fluid losses may not be replaced, and dehydration may in pH affect the ionized but not the total calcium concentration. ensue. The resulting reduction in the extracellular fluid volume Acidosis increases the ionized calcium by decreasing the binding and associated reduction in the glomerular filtration rate exacer- of calcium ions to albumin, whereas alkalosis decreases the ion- bate the hypercalcemia. Finally, immobilization may also contrib- ized calcium by enhancing binding of calcium ions to albumin. ute to hypercalcemia by virtue of associated increases in bone Measurement of total serum calcium, particularly if corrected for resorption. the serum albumin, is usually adequate for most situations. How- ever in complex cases (changes in both albumin and pH), a direct measurement of the ionized calcium should be performed. CLINICAL MANIFESTATIONS Under normal circumstances, the plasma calcium concentration The clinical presentation of the hypercalcemic patient(7) may reflects a balance between the flux of calcium into the extracellular involve any of several organ systems (see Table 1). The signs and fluid from the gastrointestinal (GI) tract, the skeleton, and the symptoms tend to be similar regardless of the etiology of the kidney, and the flux of calcium out of the extracellular fluid into hypercalcemia. Because an optimal extracellular calcium concen- the skeleton and the urine. Hypercalcemia develops when the rate tration is necessary for normal neurologic function, symptoms of of calcium entry into the blood compartment is greater than its rate neurologic dysfunction often predominate in hypercalcemic states. of removal. This occurs most commonly when accelerated oste- The patient (or family members) may notice subtle changes in the oclastic bone resorption or excessive GI calcium absorption de- ability to concentrate or an increased sleep requirement. With livers quantities of calcium into the blood that exceed the capac- increasing severity of the hypercalcemia, symptoms may gradu- ally progress to depression, confusion, and even coma. Muscle weakness is common. Dr. Shane has received research funding from Novartis, but not in the Gastrointestinal symptoms are often prominent, with constipa- field of hypercalcemia. Dr. Irani has reported no conflicts of interest. tion, anorexia, nausea, and vomiting present in varying degrees. 176 © 2006 American Society for Bone and Mineral Research HYPERCALCEMIA / 177 TABLE 1. CLINICAL MANIFESTATIONS OF HYPERCALCEMIA moderate hypercalcemia of 12.0–14.0 mg/dl, whereas others may show no overt symptomatology at a similar level. The latter Cardiovascular situation occurs most often in the setting of chronic hypercalce- Shortened QT interval on ECG mia. In other circumstances, the absence of symptoms in the Arrhthymias (rare unless on digitalis) severely hypercalcemic patient should prompt one to measure the Bradycardia ionized calcium level to be certain that hypercalcemia is not Hypertension secondary to excessive binding of calcium to plasma proteins. Bundle branch/AV blocks Cardiac arrest (if severe) DIFFERENTIAL DIAGNOSIS Neuromuscular Emotional lability Detection of an elevated serum calcium requires that the etiol- Confusion ogy be established. The many causes of hypercalcemia are listed Delirium in Table 2, and most will be covered separately in subsequent Psychosis chapters. However, certain general principles that apply to the Stupor differential diagnosis of hypercalcemia are covered here. Muscle weakness Malignancy and primary hyperparathyroidism are by far the Headache most common causes of hypercalcemia, accounting for Ͼ90% of Seizures (rare) hypercalcemic patients.(7) Differentiating between these two diag- Renal noses is generally not difficult on clinical grounds alone. The vast Polyuria Polydispsia Nocturia TABLE 2. DIFFERENTIAL DIAGNOSIS OF HYPERCALCEMIA Hypercalciuria Nephrolithiasis Most common Nephrocalcinosis Primary hyperparathyroidism Renal failure Malignant disease Gastrointestinal PTH-related protein (carcinoma of lung, esophagus, head and neck, Nausea/vomiting renal cell, breast, ovary, and bladder) Anorexia Ectopic production of 1,25-dihydroxyvitamin D (lymphoma) Constipation Lytic bone metastases (multiple myeloma, hematologic Abdominal pain malignancies and breast carcinoma) Peptic ulcers Other factor(s) produced locally or ectopically Pancreatitis Uncommon Skeletal Endocrine disorders Bone pain/arthralgia Thyrotoxicosis Osteopenia/osteoporosis in cortical bone (often seen in wrist) Granulomatous diseases Other Sarcoidosis Shock HIV Death Drug-induced Vitamin D Thiazide diuretics Lithium Pancreatitis and peptic ulcer disease are unusual but have been Estrogens and antiestrogens reported. They may be somewhat more common if the hypercal- Androgens (breast cancer therapy) cemia is caused by primary hyperparathyroidism than other
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