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Updated: May 12, 2026

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
Published on: March 14, 2017
Calcium-sensing receptor and apoptosis in parathyroid hyperplasia of patients with secondary hyperparathyroidism
Hye-Jeong Lee1, U-Hyoung Seo, Woo-Young Kim
1Department of Surgery, Korea University College of Medicine, Seoul, Republic of Korea.
Objective:
This retrospective study investigated the characteristics of secondary hyperparathyroidism (SHPT) by examining the presence of the calcium-sensing receptor (CaSR) and the rate of cell proliferation and apoptosis in parathyroid glands.
Methods:
Eighteen diffuse and 57 nodular hyperplastic parathyroid glands from 24 patients with SHPT were compared with 14 primary adenomas and 33 normal parathyroid glands using immunohistochemical staining of CaSR and a marker of proliferative activity (Ki67 antigen). Apoptosis was measured using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling assay.
Results:
The mean ± SE labelling index (LI) of CaSR (12.8% ± 1.5%) in nodular hyperplasia was significantly lower than that in normal parathyroid glands (26.8% ± 0.8%), whereas the mean ± SE LI of CaSR in diffuse hyperplasia was similar to that in normal parathyroid glands (23.3% ± 1.8%). The mean ± SE LI of Ki67 antigen was significantly higher in primary adenoma and nodular hyperplasia than in normal parathyroid glands.
Conclusion:
These results indicate that downregulation of CaSR, and a higher rate of proliferation over apoptosis, could contribute to the pathological progression of SHPT.
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