Hyperparathyroidism and Hypoparathyroidism

Abstract

Parathyroid hormone and active vitamin D control calcium homeostasis; dysregulation of this system leads to abnormal calcium measurements and a spectrum of clinical disorders. Primary hyperparathyroidism can present clinically with abdominal pain from peptic ulceration or renal calculi, mood disorders, fractures and loss of height from osteoporosis or on blood tests with reduced kidney function and hypercalcemia in the setting of normal or elevated parathyroid hormone. It is managed primarily with surgery although asymptomatic patients may elect to have serial monitoring for deterioration or clinical sequelae of hyperparathyroidism. International consensus guidelines are regularly updated to reflect research on the benefits of surgery or medical management of asymptomatic patients with primary hyperparathyroidism. Parathyroid carcinoma is a rare cause of primary hyperparathyroidism that is associated with a genetic mutation causing hyperparathyroidism-jaw tumour syndrome. Secondary hyperparathyroidism is usually a complication of chronic kidney disease or vitamin D deficiency. Hypoparathyroidism is a complication of thyroid or parathyroid surgery, a manifestation of one of a number of genetic disorders or may be one of a number of autoimmune diseases in an individual patient. Patients with hypoparathyroidism suffer from lower quality of life; undertreatment manifests as symptomatic hypocalcemia and overtreatment can result in renal calculi or reduced kidney function. Pseudohypoparathyroidism is a condition of resistance to circulating PTH, which is high; this can co-exist with skeletal abnormalities described collectively as Albright’s hereditary osteodystrophy. A case history, a patient perspective and clinical notes on two particular aspects of care of patients with parathyroid disorders are included with this chapter.