| Theme | Progress in parathyroid research : Pathophysiology and treatment | |
|---|---|---|
| Title | Molecular pathogenesis of hyperparathyroidism | |
| Publish Date | 2017/10 | |
| Author | Yasuo Imanishi | Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine |
| [ Summary ] | Primary hyperparathyroidism (PHPT) causes hypercalcemia, usually through a single benign hyperfunctioning parathyroid adenoma with somatic mutations. Secondary uremic hyperparathyroidism (SHPT) is common in patients with chronic kidney disease (CKD), especially in maintenance hemodialysis patients (CKD5D). Alterations in calcium and phosphate metabolism contribute to the advance of SHPT in early CKD. Subsequent to continuous growth stimulation due to CKD affecting parathyroid cells, these cells develop somatic mutations, which lead to growth advantages for non-mutated cells. In this review, the molecular pathogenesis in PHPT and SHPT is discussed. | |