TABLE 2311 Drugs that Can Cause Hypocalcemia

Postoperative Hypocalcemia HYPOPARATHYROIDISM Currently, more than 10 percent of postparathyroidectomy patients may have hypoparathyroidism as defined by a fasting calcium level of less than 8.5 mg/dL and a simultaneous inorganic phosphorus level of greater than 4.5 mg/dL. Postoperative hypocalcemia can be due to hypoparathyroidism from the permanent surgical removal of parathyroid tissue, from transient ischemia of the parathyroid glands in patients who have extensive bilateral neck surgery, or because of long-term hypercalcemic suppression of the nonadenomatous parathyroid glands.

HUNGRY-BONE SYNDROME The term hungry-bone syndrome was coined by Albright and now indicates postparathyroidectomy hypocalcemia due to rapid remineralization of the skeleton. During this accelerated remineralization, a persistent hypocalcemia and hypophosphatemia may be severe enough to cause tetany. These patients may require vigorous calcium and vitamin D supplementation for prolonged periods of time.

The hungry-bone syndrome may be found in over 10 percent of patients after parathyroid surgery. Patients are at risk if they have a fasting calcium level of less than 8.5 mg/dL and a simultaneous inorganic serum phosphorus of less than 3.0 mg/dL on postoperative day 3 or later.

Renal Failure Hypocalcemia is a frequent finding in renal failure. This may be partially due to the resulting hyperphosphatemia, but there is also decreased production of 1a,25-(OH)2-vitamin D in the kidney, which, in turn, causes decreased intestinal absorption of calcium. Secondary hyperparathyroidism with increased PTH levels often results from the chronic hypocalcemia. If PTH levels remain elevated and hypercalcemia develops in spite of cure of the renal failure by renal transplantation, the patient is said to have tertiary hyperparathyroidism.

Phosphate Overload Phosphate overload from nonrenal causes may also lead to hypocalcemia. This is the presumed mechanism in the acute rhabdomyolysis of hyperpyrexia and major trauma. Excessive use of phosphate cathartics and sodium phosphate enemas can cause significant hyperphosphatemia in patients with renal disease, in children with Hirschsprung disease, and in small infants.

Hypomagnesemia Hypomagnesemia in association with hypocalcemia may be seen in alcoholism, diuretic use, epilepsy, and renal failure. Neonatal hypomagnesemia leads to low PTH secretion, decreased responsiveness of bone cells to PTH, and decreased calcium mobilization from bone.

Idiopathic Hypoparathyroidism Idiopathic hypoparathyroidism is probably an autoimmune disorder in which pernicious anemia, exostoses, moniliasis, Hashimoto disease, sterility, and Addison disease may be seen. This syndrome may also be associated with cataracts, mental retardation, intracranial calcifications, and papilledema due to increased intracranial pressure.

Nonsurgical Primary Hypoparathyroidism Hypocalcemia with primary hypoparathyroidism has been reported from parathyroid infarction, metastases to the parathyroids, and hemochromatosis of the parathyroids.

Pseudohypoparathyroidism Pseudohypoparathyroidism is a familial disorder characterized by decreased end-organ responsiveness to PTH resulting in hypocalcemia, hyperphosphatemia, parathyroid hyperplasia, and excessive serum PTH concentrations. These patients usually have a very low urinary cyclic AMP excretion that only slightly increases with infusion of parathormone. This condition may be inherited as an X-linked dominant trait with variable penetrance; the male to female ratio is 2 to 1. Patients are short and have round faces; brachycephaly; a short, thick neck; short, pudgy fingers and toes; and growth failure of the fourth and fifth metacarpals. Mental retardation, seizures, and subcutaneous soft tissue calcification may be seen. The skin can be dry and coarse, and the hair is often brittle.

Vitamin D Deficiency Hypocalcemia due to vitamin D deficiency is rare in the United States. Infants born to vitamin D-deficient mothers who lack sunlight exposure and receive no vitamin D supplementation may have rickets. Breast milk has low vitamin D content, and breast milk feeding without sunshine exposure in unsupplemented infants may result in infantile rickets.

PHYSIOLOGIC EFFECTS Although normal ionized calcium levels are 2.1 to 2.6 meq/L (1.05 to 1.3 mmol/L), serious physiologic changes do not usually occur until ionized levels in serum are less than 1.4 to 1.6 meq/L (0.7 to 0.8 mmol/L). Below those levels, hypocalcemia can cause a wide variety of signs and symptoms ( Table 2,3-12).

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