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Antibodies targeting the calcium sensing receptor: acquired hypoparathyroidism—an autoimmune disease at last?

Medical terminology provides many terms for diseases of yet unknown etiology, including idiopathic, essential, or cryptogenic. Fortunately, some of them at some point in time need to be renamed, when their true identity becomes better known. Idiopathic acquired hypoparathyroidism might be such an example. This disorder, characterized by decreased levels of intact parathyroid hormone, usually affects children in their first decade of life, with a female preponderance, and eventually leads to hypocalcemia and hyperphosphatemia. Clinically, individuals with acquired hypoparathyroidism may display neuromuscular signs and symptoms of persistent hypocalcemia, including episodes of tetany, calcification of the basal ganglia, increased prevalence of seizures, mental retardation, and papilledema, as well as cataract formation and dental abnormalities (1).

In search of an autoimmune etiology of acquired hypoparathyroidism (AH), investigators have rounded up several suspects during recent years. First, autoantibodies directed against parathyroid tissues have been detected in some individuals with AH (1, 2). Second,