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| Parathyroid glands | |
|---|---|
| Name | Parathyroid glands |
| Latin | Glandulae parathyroideae |
| System | Endocrine system |
| Location | Neck |
| Artery | Inferior thyroid artery, Superior thyroid artery |
| Vein | Superior thyroid vein, Middle thyroid vein, Inferior thyroid vein |
| Nerve | Cervical sympathetic trunk, Recurrent laryngeal nerve |
| Precursor | Third pharyngeal pouch, Fourth pharyngeal pouch |
Parathyroid glands are small endocrine glands located in the neck that secrete parathyroid hormone to regulate mineral homeostasis. They function closely with the Thyroid gland, Kidney, and Bone to maintain serum calcium and phosphate within narrow limits. Disorders of these glands produce clinically important syndromes that intersect with Nephrology, Endocrinology, Surgery, and Oncology.
The typical human complement is four small oval glands embedded on the posterior surface of the Thyroid gland, two superior and two inferior, though anatomical variation occurs in association with the Thymus and along the course of embryologic migration. Each gland measures about 3–8 mm and is supplied primarily by branches of the Inferior thyroid artery and, variably, the Superior thyroid artery. Venous drainage passes to the Superior thyroid vein, Middle thyroid vein, and Inferior thyroid vein, while lymphatic drainage targets cervical nodes within the Neck compartment. Innervation originates from sympathetic fibers of the Cervical sympathetic trunk and is anatomically related to the Recurrent laryngeal nerve, important for surgical preservation during Thyroidectomy and Parathyroidectomy.
Originating from the endodermal derivatives of the third and fourth pharyngeal pouches, superior parathyroid primordia arise from the fourth pouch and inferior from the third, which also forms the Thymus; aberrant migration explains ectopic glands in the mediastinum near the Heart or within the Thymus. Key molecular regulators include transcription factors and signaling pathways shared with other pharyngeal pouch derivatives studied in models such as the Mouse and Zebrafish. Developmental anomalies may associate with syndromes caused by mutations in genes characterized in Human Genome Project–era research and later clinical genetics studies.
Chief (principal) cells secrete parathyroid hormone (PTH), a peptide that increases renal calcium reabsorption and stimulates osteoclastic bone resorption via signaling through the Receptor activator of nuclear factor kappa-Β ligand pathway; oxyphil cells have uncertain function but increase with age and in some pathological states. PTH acts on the Kidney to enhance 1α-hydroxylase activity, increasing conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, which in turn increases intestinal calcium absorption in the Small intestine. Calcium-sensing receptors on chief cells detect extracellular ionized calcium; the molecular identity of this sensor was elucidated in studies involving researchers and institutions such as the Royal Society and laboratories associated with the National Institutes of Health.
Serum ionized calcium provides negative feedback on PTH via the calcium-sensing receptor; low calcium stimulates PTH, while high calcium suppresses it, a control mechanism investigated in classic experiments at institutions like Cambridge University and Harvard University. PTH increases renal phosphate excretion by downregulating sodium-phosphate cotransporters in the proximal tubule, affecting phosphate balance relevant to disorders managed in Nephrology units and dialysis centers described in policy documents of organizations such as the World Health Organization. Vitamin D status, dietary intake, and hormones from endocrine organs studied at centers including Mayo Clinic and Cleveland Clinic modulate the interplay of calcium and phosphate.
Hyperparathyroidism, often due to a sporadic parathyroid adenoma, causes hypercalcemia with symptoms ranging from nephrolithiasis to neurocognitive changes; epidemiologic and therapeutic data have been reported by groups at Johns Hopkins University and in population studies from countries including the United States and the United Kingdom. Secondary hyperparathyroidism results from chronic kidney disease, a major global health problem addressed by nephrology consortia such as the European Renal Association. Hypoparathyroidism, whether postsurgical after Thyroidectomy or autoimmune in origin as described in cohorts from institutions like Massachusetts General Hospital, leads to hypocalcemia with neuromuscular irritability and cardiac effects. Parathyroid carcinoma is rare but recognized in case series published by oncology centers including MD Anderson Cancer Center.
Biochemical testing centers on serum calcium, phosphate, intact PTH assays developed by diagnostic manufacturers and validated in clinical laboratories at institutions like Centers for Disease Control and Prevention–affiliated programs. Imaging for localization uses high-resolution neck ultrasound, 99mTc-sestamibi scintigraphy, and four-dimensional computed tomography performed in radiology departments at hospitals such as Guy's Hospital and the Hospital of the University of Pennsylvania. Intraoperative PTH monitoring, introduced through surgical research at tertiary centers like Mayo Clinic, aids focused parathyroidectomy. Genetic testing for syndromic causes references datasets curated by genomic consortia such as the Human Genome Variation Society.
Definitive treatment for primary hyperparathyroidism is surgical excision of pathological glands via minimally invasive or bilateral neck exploration, procedures refined at centers like Memorial Sloan Kettering Cancer Center and Royal Marsden Hospital. Medical management includes hydration, bisphosphonates studied in randomized trials at Cochrane collaborative reviews, and calcimimetic agents such as cinacalcet approved by regulatory authorities including the Food and Drug Administration. Secondary hyperparathyroidism due to chronic kidney disease may be managed with phosphate binders, vitamin D analogs, and when refractory, parathyroidectomy as practiced in nephrology-surgery partnerships at tertiary referral centers. Long-term follow-up involves endocrine clinics modeled on multidisciplinary programs at institutions like Toronto General Hospital.
Category:Endocrine system