Calcium-sensing receptor and apoptosis in parathyroid hyperplasia of patients with secondary hyperparathyroidism
- Authors
- Lee, Hye-Jeong; Seo, U-Hyoung; Kim, Woo-Young; Woo, Sang-Uk; Lee, Jae-Bok
- Issue Date
- Feb-2013
- Publisher
- SAGE PUBLICATIONS LTD
- Keywords
- Calcium-sensing receptor; chronic kidney disease; parathyroid gland; parathyroid hormone; secondary hyperparathyroidism
- Citation
- JOURNAL OF INTERNATIONAL MEDICAL RESEARCH, v.41, no.1, pp 97 - 105
- Pages
- 9
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
- Volume
- 41
- Number
- 1
- Start Page
- 97
- End Page
- 105
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/11003
- DOI
- 10.1177/0300060513476600
- ISSN
- 0300-0605
1473-2300
- Abstract
- 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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Collections - 2. Clinical Science > Department of Breast and Endocrine Surgery > 1. Journal Articles
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