Parathyroid Hormone and Vitamin D Replacement Therapy

Abstract

Calcium is a critically important mineral necessary for both intracellular and extracellular processes. Calcium circulates in the blood in an ionized state, bound to albumin and other serum proteins, and chelated to citrate, sulfate, and lactate. Only the free, ionized form of calcium is biologically active. Generally, total serum concentrations of calcium reflect the ionized calcium available to cells. However, there are two clinically important exceptions to this rule: 1) alkalosis will decrease ionized calcium concentration owing to an increase in the binding of calcium ions to albumin; and 2) in many chronic illnesses, substantial reductions in serum albumin concentrations occur, and this may lower total serum calcium concentrations while the ionized calcium concentration remains normal. The circulating level of ionized calcium is maintained in the physiologic range through the concerted actions of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D, which mobilize calcium stores from bone and increase the efficiency of intestinal calcium absorption and renal calcium reabsorption. Hypocalcemia, in general, is an uncommon disorder. However, defects in the production or recognition of either PTH or 1,25-dihydroxyvitamin D, or a chronic deficiency of vitamin D, can precipitate hypocalcemia. Additionally, the removal of calcium from the circulation occasionally can exceed the capacity for correction by PTH and 1,25-dihydroxyvitamin D. In this section, the clinical presentations and appropriate therapeutic approaches for disorders associated with either deficient PTH or vitamin D action will be discussed.