Hypocalcemia and Hypercalcemia

Abstract

Calcium is the fifth most abundant inorganic element of the body, the principal component of the human skeleton, and a vital participant in normal neuromuscular function, blood coagulation, membrane function, and multiple enzyme reactions. Its transmembrane flux plays a critical role in hormone secretion and metabolic coordination. Exquisitely sensitive homeostatic mechanisms have evolved to monitor and regulate the calcium ion in plasma while allowing an enormous reservoir to exist in bone where it principally serves a mechanical function. The normal adult human has roughly 25 g of total body calcium per kg of lean body mass (about 1–1.5 kg). Ninety-nine percent of it is present in bone as calcium phosphate while only 1% of skeletal calcium is freely exchangeable with the extracellular fluid. Mobilization of extensive amounts of skeletal calcium requires active resorption such as that promoted by vitamin D and parathyroid hormone (PTH). Perhaps the most frequent challenge to calcium homeostasis occurs with dietary calcium deprivation. When this occurs, a triad of efficient systems join to combat any tendency to hypocalcemia (Figure 1). Hormonally-induced bone resorption probably represents the most important mechanism by which sudden deficits in calcium homeostasis are overcome. Reduction in urinary excretion of calcium and increased efficiency of calcium absorption from the gut (in response to calcium deficiency) serve as additional mechanisms for maintaining extracellular fluid calcium; the renal effect is probably more important than previously realized. Renal reabsorption of calcium can rise to essentially 100% but this occurs only if the calcium level drops below 7 mg/dl. If calcium is low but above this level, PTH seems to be the principal effector involved in renal calcium conservation (1–10).