ABSTRACT
The parathyroid glands comprise a group of endocrine structures (usually 4 in number) that either hug the posterior surface of the thyroid gland or are in close proximity to it. Although exceedingly small in size, they play crucial roles in the maintenance of calcium and phosphorus balance. Their function spans a range of activities, including blood coagulation, modulation of membrane permeability, muscle contraction, neuromuscular excitability, and the regulation of various signal transduction processes within cells. Their importance to the surgeon is usually related to states of overactivity in which hypercalcemia may ensue. Occasionally, these glands also become important in surgical practices when a state of hypocalcemia results, as may occur after total thyroidectomy for goiter or neoplasia. The intricate control systems regulated by the parathyroid glands to maintain calcium and phosphorus balance are the subject of this chapter.
Intracellular signaling systems are exquisitely sensitive to the intracellular calcium concentration. Increased intracellular calcium concentrations generate further release of calcium stores in the sarcoplasmic reticulum, triggering the desired cellular response. Calcium-dependent intracellular signaling systems are affected by serum and extracellular fluid calcium concentration, necessitating tight control of serum calcium levels. This is especially true for neuromuscular and secretory cells whose functions are disrupted by small alterations in extracellular calcium concentrations. Serum calcium concentration is tightly regulated by the intestinal tract (absorption), bone (calcium stores), and kidney (excretion). Regulation of these processes occurs through the actions of several hormones, including parathyroid hormone (PTH) and vitamin D 1,25dihydroxy vitamin D (1,25-(OH)2D), calcitonin, estradiol, glucocorticoids, and the growth hormone. Of these, PTH and (1,25-(OH)2D) appear to be the main regulators of calcium homeostasis in humans. Both hormones stimulate bone-resorbing osteoclasts, promoting calcium release into the extracellular fluid. PTH also stimulates renal hydroxylation of 25-(OH)D3 to 1,25-(OH)2D1 and distal renal tubular calcium reabsorption.
