Hypoparathyroidism and Pseudohypoparathyroidism

Mary Ruppe, MD ■ Martha A. Zeiger, MD ■ Suzanne Jan de Beur, MD

Hypoparathyroidism can result from either decreased secretion of parathyroid hormone (PTH) or target organ resistance to PTH. The etiologies of decreased secretion of PTH include the destruction of the parathyroid glands as a complication of head and neck surgery; genetic defects, such as mutations in the PTH or the calcium-sensing receptor genes; developmental defects, such as DiGeorge's syndrome; autoimmune destruction, as in the polyglandular autoimmune endo-crinopathies (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy [APECED] syndrome); and infiltrative diseases, such as hemochromatosis or Wilson's disease. In contrast with true hypoparathyroidism, hypocalcemia and hyperphosphatemia in pseudohypoparathyroidism (PHP) is accompanied by an elevated serum level of PTH and results from resistance to the action of PTH rather than to PTH deficiency. The etiology of the hormone resistance observed in this group of related syndromes is a G-protein defect that results in impaired signaling in a variety of receptors, including the PTH receptor. Hypomagnesemia, depending on the severity and duration, may also result in either decreased secretion of or resistance to PTH.

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