Disorders of calcium metabolism

Calcium is an abundant mineral and has diffuse cellular functions in bone metabolism, cell division, coagulation, enzyme regulation, glycogen metabolism, muscle contraction, neurotransmission, protein synthesis, and degradation. Calcium is ingested in the diet and absorbed in the small intestine. It is distributed throughout the body, but 99% appears in the bone [1–3]. Adult humans contain more than 1 kg of calcium, of which over 99% is skeletal and dental and only 0.1% is in extracellular fluids. About half the calcium in serum is bound to protein, primarily of which is albumin. Decreases in serum albumin are accompanied by decreases in calcium (a drop of 1 g/dL of albumin lowers the calcium by about 0.8 mg/dL). Several calcium determinations and measurement of ionized (physiologically active) calcium levels may be needed to accurately assess calcium status. . Calcium is maintained in a very narrow range by a redundant system of parathyroid hormone (PTH), vitamin D, and calcitonin; all acting at multiple target organs, including bone, kidneys, and the gastrointestinal tract. As ionized (free, metabolically active) calcium levels decrease, the parathyroid glands secrete PTH, which raises calcium levels by stimulating bone resorption, renal calcium reabsorption, phosphate excretion, and renal 1,25-dihydroxycholecalciferol (1,25-[OH] 2 D 3 ) synthesis. Vitamin D, in turn, promotes bone resorption, increases intestinal absorption of dietary calcium and phosphate, and inhibits PTH secretion [1,4–14]. Finally, calcitonin, released by parafollicular cells of the thyroid in response to hypercalcemia, has been shown to transiently inhibit bone resorption [5].