Hypocalcemia has a number of primary and secondary causes. Primary causes involve some defect in PTH availability, including (1) lack of production (surgical removal of parathyroid gland or hypoparathyroidism from autoimmune disease), (2) impaired secretion (with profound hypomag-nesemia), and (3) end-organ resistance. With the first two, there is a deficit in circulating PTH, but with the third, PTH is elevated, in contrast to a low serum calcium and hyperphos-phatemia. An example of end-organ resistance is Albright's syndrome. Secondary causes include severe vitamin D deficiency, "hungry bone syndrome" with chondrosarcoma, and HIV/AIDS (Box 35-13).

Signs and symptoms are generally lacking in the outpatient setting. The primary clinical findings are caused by neuromuscular irritability. If hypocalcemia is suspected, although negative responses do not rule out hypocalcemia, two physical tests may assist in the diagnosis: Chvostek sign (tapping the facial nerve across the cheek with contraction of the facial muscle) and Trousseau's sign (carpal spasm via BP cuff). Deep tendon reflexes may be hyperactive, and the patient may appear anxious, confused, demented, or psychotic. The signs and symptoms of hypocalcemia are related to the level of ionized calcium rather than total calcium, as well as the rapidity of decline (Levine, 2006). Alkalosis, either primary or compensatory, can cause a shift in ionized calcium to a bound state, thus exacerbating a borderline hypocalcemia situation.

Cardiac changes caused by hypocalcemia include prolongation of the QT interval, resulting in life-threatening dysrhythmia and cardiac dysfunction. Generalized seizures are also possible. The cardiac dysfunction is generally reversible with normalization of the ionized calcium levels. In acute and severe cases, IV calcium is the treatment of choice. Concurrent management of hyperphosphatemia, alkalosis, and hypomagnesemia is required. Long-term management is with oral calcium and vitamin D. Although use of thiazide diuretics is contraindicated in patients with hypercalcemia, they can be used with hypocalcemia and may have a beneficial effect. On the other hand, loop diuretics must be used cautiously because they increase renal excretion of calcium and may exacerbate the problem.

Pseudohypoparathyroidism is a rare phenomenon representative of several congenital endocrinologic disorders in which tissue resistance to PTH is present. The classic form of this disorder is Albright's hereditary osteodystrophy (AHO). The AHO patient has short stature, mental retardation, brachydactyly, and PTH resistance (elevated PTH levels). Another form of AHO does not involve PTH dysfunction, called pseudo-pseudohypoparathyroidism. Although the clinical course of these diseases may vary and in some cases is protracted, AHO usually is associated with a shortened life expectancy. Treatment is primarily supportive (Levine, 2006).

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