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A significant elevation of serum calcium is seen; the level must be interpreted in relation to the serum albumin level (see Hypocalcemia, above) A high serum chloride concentration and a low serum phosphate concentration in a ratio > 33 to 1 is suggestive of primary hyperparathyroidism where PTH decreases proximal tubular phosphate reabsorption A low serum chloride concentration with a high serum bicarbonate concentration, along with elevations of BUN and creatinine, suggests milk-alkali syndrome The highest serum calcium levels (> 15 mg/dL) generally occur in malignancy More than 200 mg/d of urinary calcium excretion suggests hypercalciuria; less than 100 mg/d suggests hypocalciuria Hypercalciuric patients such as those with malignancy or those receiving
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oral active vitamin D therapy may easily develop hypercalcemia in case of volume depletion Serum phosphate may or may not be low, depending on the cause Hypocalciuric hypercalcemia occurs in milk-alkali syndrome, thiazide diuretic use, and familial hypocalciuric hypercalcemia The chest radiograph may reveal a malignancy or granulomatous disease The ECG shows a shortened QT interval Measurements of PTH and PTHrP help distinguish between malignancy-associated hypercalcemia (suppressed PTH, elevated PTHrP) and hyperparathyroidism (elevated PTH)
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Lee CT et al Hypercalcemia in the emergency department Am J Med Sci 2006 Mar;331(3):119 23 [PMID: 16538071] Stewart AF Clinical practice Hypercalcemia associated with cancer N Engl J Med 2005 Jan 27;352(4):373 9 [PMID: 15673803]
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In plasma, phosphate is mainly present as inorganic phosphate, and this fraction is very small (< 02% of total phosphate) However, body phosphate metabolism is regulated through plasma inorganic phosphate Important determinants of plasma inorganic phosphate concentration are its renal excretion, intestinal absorption, and shift between the intracellular and extracellular spaces In general, the kidney is the most important regulator of the serum phosphate level PTH decreases the absorption of phosphate in the proximal tubule while 1,25dihydroxyvitamin D3 increases tubular phosphate reabsorption Renal proximal tubular reabsorption of phosphate is decreased by volume expansion, corticosteroid administration, and proximal tubular dysfunction, such as occurs in Fanconi s syndrome due to myeloma or other diseases Fibroblast growth factor 23 (FGF23) is another potent phosphaturic hormone Intestinal absorption of phosphate is facilitated by active vitamin D PTH, which both stimulates phosphate release from bone and is phosphaturic, can lead to hypophosphatemia and to depletion of bone phosphate store if hypersecretion continues Growth hormone, on the other hand, augments proximal tubular reabsorption of phosphate Cellular phosphate uptake is stimulated by various factors and conditions, including alkalemia, insulin, epinephrine, feeding, hungry bone syndrome, and accelerated cell proliferation Phosphorus metabolism and homeostasis are intimately related to calcium metabolism See sections on metabolic bone disease in 26
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Until the primary disease can be brought under control, renal excretion of calcium with resultant decrease in serum calcium concentration is promoted Excretion of Na+ is accompanied by excretion of Ca2+ The tendency in hypercalcemia is toward volume depletion from nephrogenic diabetes insipidus Therefore, establishing euvolemia and inducing natriuresis by giving saline with furosemide is the emergency treatment of choice In dehydrated patients with normal cardiac and renal function, 045% saline or 09% saline can be given rapidly (250 500 mL/h) Then, intravenous furosemide (20 40 mg every 2 hours) prevents volume overload and enhances Ca2+ excretion Thiazides can actually worsen hypercalcemia (as can furosemide if inadequate saline is given) Bisphosphonates are the mainstay of treatment of hypercalcemia of malignancy They are safe, effective, and normalize calcium in more than 70% of patients, although it may require up to 48 72 hours before their full therapeutic effect is achieved In emergency cases, dialysis with low or no calcium dialysate may be needed The calcimimetic agent cinacalcet hydrochloride suppresses PTH secretion and decreases serum calcium concentration and holds promise as a treatment option See 39 for a discussion of the treatment of hypercalcemia of malignancy and 26 for a discussion of the treatment of hypercalcemia of hyperparathyroidism Typically, if patients with CKD stage 5D who receive long-term dialysis do not receive proper supplementation of calcium and active vitamin D, hypocalcemia and hyperphosphatemia develop On the other hand, hypercalcemia can sometimes develop, particularly in the setting of severe secondary hyperparathyroidism, characterized by high levels of PTH and subsequent release of calcium from bone Therapy may include intravenous vitamin D, which further increases the serum calcium concentration Another type of hypercalcemia occurs when the PTH levels are low In this setting, bone turnover is decreased, which results in a low buffering capacity for calcium When calcium is administered in calcium-containing phosphate binders or in the dialysate, or when vitamin D is administered, hypercalcemia results Hypercalcemia in dialysis patients usually occurs in the presence of hyperphosphatemia, and severe metastatic calcification, eg, involving blood vessels, may occur Malignancy should also be considered as a cause of the hypercalcemia
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Jacobs TP et al Clinical review: Rare causes of hypercalcemia J Clin Endocrinol Metab 2005 Nov;90(11):6316 22 [PMID: 16131579]
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