Hyperparatyreoidism

Hyperparatyreoidism is an endocrine disorder characterized by excessive production of parathyroid hormone (PTH) by the parathyroid glands, typically leading to elevated blood calcium levels (hypercalcemia) and often reduced phosphate levels. It is categorized into primary, secondary, and tertiary forms, each with distinct causes and clinical features.

Primary hyperparatyreoidism arises from autonomous PTH secretion, most commonly due to a single parathyroid adenoma, but it can also result from multiglandular hyperplasia or, rarely, parathyroid carcinoma. Patients may be asymptomatic or experience bone pain, kidney stones, fatigue, gastrointestinal symptoms, or neuropsychiatric manifestations. Laboratory tests usually show hypercalcemia with inappropriately elevated PTH and low to normal phosphate. Imaging such as sestamibi scintigraphy and neck ultrasound can localize the hyperfunctional gland and guide surgical planning; parathyroidectomy is the standard treatment for most patients.

Secondary hyperparatyreoidism is driven by chronic hypocalcemia or phosphate retention, most often due to chronic kidney disease or severe vitamin D deficiency. PTH is elevated in response to low calcium, with calcium levels that may be low or normal. Management focuses on correcting calcium and phosphate balance, supplementing vitamin D, and addressing underlying disease; advanced kidney disease may require dialysis and, in some cases, calcimimetics. If secondary hyperparatyreoidism becomes autonomous and persistently elevated PTH despite treatment, it can evolve into tertiary disease.

Diagnosis relies on measurements of serum calcium, PTH, phosphate, and vitamin D, with imaging used for surgical planning in primary disease. Complications include osteoporosis, nephrolithiasis, vascular calcification, and neuropsychiatric symptoms. Treatment decisions are individualized, ranging from observation in mild cases to surgical removal of abnormal parathyroid tissue.