Circulating IL-17A Levels in Postmenopausal Women with Primary Hyperparathyroidism.

E Dozio,C Eller-Vainicher,M Corsi Romanelli,S Corbetta,E Passeri,S Palmieri,E Vianello

doi:10.1155/2020/3417329

Abstract

Background Primary hyperparathyroidism (PHPT) is a common cause of secondary osteoporosis in postmenopausal women. Th17 lymphocytes and the released cytokine IL-17A play an important role in bone metabolism. Th17 cells have been shown to be activated by PTH, and peripheral blood T cells from patients affected with PHPT express higher levels of IL-17A mRNA than controls. Aim To investigate circulating levels of IL-17A and the ratio RANKL/OPG, as markers of osteoclastogenesis, in 50 postmenopausal PHPT women compared with postmenopausal osteoporotic non-PHPT women (n = 20). Results Circulating levels of IL-17A were similarly detectable in most PHPT and non-PHPT osteoporotic women (12.9 (8.4-23.1) vs. 11.3 (8.3-14.3) pg/ml, median (range interquartile), P = 0.759), at variance with premenopausal women where IL-17A was undetectable. In PHPT women, any significant correlations could be detected between circulating IL-17A levels and PTH levels. Nonetheless, significant negative correlations between circulating IL-17A and ionized calcium levels (r = ‐0.294, P = 0.047) and urine calcium excretions (r = ‐0.300, P = 0.045) were found. Moreover, PHPT women were characterized by positive correlations between IL-17A levels and femur neck (r = 0.364, P = 0.021) and total hip (r = 0.353, P = 0.015) T-scores. Circulating IL-17A levels did not show any significant correlation with sRANKL, OPG, and sRANKL/OPG ratio in PHPT women. Conclusions In postmenopausal PHPT women, circulating IL-17A levels were similar to those detected in postmenopausal non-PHPT women, showing a disruption of the relationship observed in postmenopausal osteoporosis among circulating PTH, sRANKL, OPG, IL-17A, and bone demineralization in postmenopausal PHPT women. The data support an osteogenic effect of IL-17A in postmenopausal PHPT women.

Highlights

Primary hyperparathyroidism (PHPT) is a common cause of secondary osteoporosis in postmenopausal women [1]
Continuous PTH stimulates T cell production of TNFα, which increases the differentiation of IL-17Aproducing Th17 cells via TNF receptor 1 (TNFR1) signaling in CD4+ cells [6]
We showed that serum IL-17A levels in PHPT postmenopausal women (1) were similar to those detected in normocalcemic non-PHPT postmenopausal women, (2) negatively correlated with biochemical parameters of PHPT, and (3) correlated with the bone mineral density status

Summary

Introduction

Primary hyperparathyroidism (PHPT) is a common cause of secondary osteoporosis in postmenopausal women [1]. Disruption of the interaction of the immune-skeletal system interface is recognized to play an important role in the common estrogen deficiency-related postmenopausal osteoporosis [3] and in PHPT-related osteoporosis [4]. Aim. To investigate circulating levels of IL-17A and the ratio RANKL/OPG, as markers of osteoclastogenesis, in 50 postmenopausal PHPT women compared with postmenopausal osteoporotic non-PHPT women (n = 20). In PHPT women, any significant correlations could be detected between circulating IL-17A levels and PTH levels. Circulating IL-17A levels did not show any significant correlation with sRANKL, OPG, and sRANKL/OPG ratio in PHPT women. In postmenopausal PHPT women, circulating IL-17A levels were similar to those detected in postmenopausal non-PHPT women, showing a disruption of the relationship observed in postmenopausal osteoporosis among circulating PTH, sRANKL, OPG, IL17A, and bone demineralization in postmenopausal PHPT women. The data support an osteogenic effect of IL-17A in postmenopausal PHPT women

Methods

Results

Conclusion