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.

Circulating IL-17A levels in postmenopausal women with primary hyperparathyroidism / E. Dozio, E. Passeri, E. Vianello, S. Palmieri, C. Eller-Vainicher, M. Corsi Romanelli, S. Corbetta. - In: MEDIATORS OF INFLAMMATION. - ISSN 0962-9351. - 2020(2020 Jan 17), pp. 3417329.1-3417329.6. [10.1155/2020/3417329]

Circulating IL-17A levels in postmenopausal women with primary hyperparathyroidism

Dozio E.;Vianello E.;Corsi Romanelli M.;Corbetta S.
2020-01-17

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.
Settore MED/05 - Patologia Clinica
Settore MED/13 - Endocrinologia
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/714988
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