| [ Summary ] |
Secondary hyperparathyroidism (SHPT) is a common complication in patients receiving long-term chronic dialysis therapy. The pathophysiological features of this condition are diffuse / nodular hyperplasia, downregulation of vitamin D receptors (VDR) and calcium sensing receptors (CaR), along with abnormal expression of cell-cycle regulators. Therapeutic strategies should be focused on various molecular targets, such as VDR, CaR and / or tyrosine kinase in tumor growth factor (TNF) α / epidermal growth factor receptor (EGFR) cascade.
Primary hyperparathyroidism (PHPT) has similar pathophysiological features similar to SHPT. Genetic profiling analysis, however, has highlighted HRPT2 genetic mutations in relation to parathyroid cell carcinoma as well as hyperparathyroidism-jaw tumor syndrome. Molecular-based strategies for both diagnosis and treatment will be advanced for better outcomes in patients with both types of hyperparathyroidism. |