SUN-766 Increased atherothrombotic risk in primary hyperparathyroidism and hypoparathyroidism

Abstract Disclosure: A. Naciu: None. A. Nusca: None. F. Piccirillo: None. G. Tabacco: None. A. D'Amico: None. A. Di Tommaso: None. G. Sterpetti: None. M. Viscusi: None. F. Bernardini: None. M. Forte: None. L. D’Ambrosio: None. G. Frati: None. C. Nocella: None. N. Napoli: None. R. Carnevale: None. S. Sciarretta: None. F. Grigioni: None. A. Palermo: None. Objective. Both primary hyperparathyroidism (PHPT) and chronic hypoparathyroidism (HypoPT) are associated with the onset and development of cardiovascular diseases (CVDs). Endothelium is a recognized target tissue of PTH and there is an increasing body of evidence that PTH affects functional and structural properties of arteries. However, the molecular mechanisms underlying the effects of parathyroid disorders on endothelial dysfunction and platelet aggregation, two main determinants of CVDs, are not completely understood. Aim. To evaluate the effects of PHPT and HypoPT on oxidative stress, endothelial and platelet function. Material and methods: in a monocentric, cross-sectional study we enrolled hypoPT patients treated with calcium and calcitriol, PHPT subjects and age-matched controls. All patients underwent a biochemical examination including calcium-phosphorus metabolism, inflammation markers, circulating levels of markers of oxidative stress, endothelial function, and platelet activation. Moreover, we evaluated brachial artery endothelial function (flow-mediated dilation-FMD), common carotid intima-media thickness (ccIMT), diastolic function and global strain measures with ultrasound. Results. These are the results of this project that included 120 subjects (40 hypoPT, 40 PHPT and 40 age- and sex-matched control subjects). HypoPT and PHPT patients showed increased oxidative stress markers as compared to control subjects (p<0.001). Among patients with parathyroid disorders, those with PHPT demonstrated the highest reduction of nitric oxide (p<0.001 versus HypoPT and controls) and FMD (p<0.001 and p=0.001) and a marked increase of IMT (p<0.001 and p=0.001). We also observed an increased platelet aggregation in patients with parathyroid disorders, with the highest values in PHPT patients (p<0.001, PHPT vs controls; p=0.006, HypoPT vs controls; p<0.001, PHPT vs HypoPT), along with increased levels of soluble P selectin and thromboxane B2. Conclusions. PHPT and HypoPT patients have increased atherothrombotic risk due to endothelial and platelet function alterations. Our results suggest that PTH may influence platelet reactivity. Further research is needed to determine if personalized antiplatelet therapy is necessary in subjects with parathyroid disorders Presentation: Sunday, July 13, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.714
Primary Topic
Parathyroid Disorders and Treatments
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article
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article

SUN-766 Increased atherothrombotic risk in primary hyperparathyroidism and hypoparathyroidism

Alfonso Maria Di Tommaso, Francesco Piccirillo, Nicola Napoli, Francesco Grigioni et al.
Journal of the Endocrine Society
Parathyroid Disorders and Treatments
article

SUN-766 Increased atherothrombotic risk in primary hyperparathyroidism and hypoparathyroidism

Alfonso Maria Di Tommaso, Francesco Piccirillo, Nicola Napoli, Francesco Grigioni, Gaia Tabacco, Sebastiano Sciarretta, Maurizio Forte, Giulia Sterpetti, Anda Mihaela Naciu, Annunziata Nusca, Federico Bernardini, Alessandra D’Amico, Michele Mattia Viscusi, Roberto Carnevale, Andrea Palermo, Luca D’Ambrosio, Cristina Nocella, Giacomo Frati
article en

Abstract

Abstract Disclosure: A. Naciu: None. A. Nusca: None. F. Piccirillo: None. G. Tabacco: None. A. D'Amico: None. A. Di Tommaso: None. G. Sterpetti: None. M. Viscusi: None. F. Bernardini: None. M. Forte: None. L. D’Ambrosio: None. G. Frati: None. C. Nocella: None. N. Napoli: None. R. Carnevale: None. S. Sciarretta: None. F. Grigioni: None. A. Palermo: None. Objective. Both primary hyperparathyroidism (PHPT) and chronic hypoparathyroidism (HypoPT) are associated with the onset and development of cardiovascular diseases (CVDs). Endothelium is a recognized target tissue of PTH and there is an increasing body of evidence that PTH affects functional and structural properties of arteries. However, the molecular mechanisms underlying the effects of parathyroid disorders on endothelial dysfunction and platelet aggregation, two main determinants of CVDs, are not completely understood. Aim. To evaluate the effects of PHPT and HypoPT on oxidative stress, endothelial and platelet function. Material and methods: in a monocentric, cross-sectional study we enrolled hypoPT patients treated with calcium and calcitriol, PHPT subjects and age-matched controls. All patients underwent a biochemical examination including calcium-phosphorus metabolism, inflammation markers, circulating levels of markers of oxidative stress, endothelial function, and platelet activation. Moreover, we evaluated brachial artery endothelial function (flow-mediated dilation-FMD), common carotid intima-media thickness (ccIMT), diastolic function and global strain measures with ultrasound. Results. These are the results of this project that included 120 subjects (40 hypoPT, 40 PHPT and 40 age- and sex-matched control subjects). HypoPT and PHPT patients showed increased oxidative stress markers as compared to control subjects (p<0.001). Among patients with parathyroid disorders, those with PHPT demonstrated the highest reduction of nitric oxide (p<0.001 versus HypoPT and controls) and FMD (p<0.001 and p=0.001) and a marked increase of IMT (p<0.001 and p=0.001). We also observed an increased platelet aggregation in patients with parathyroid disorders, with the highest values in PHPT patients (p<0.001, PHPT vs controls; p=0.006, HypoPT vs controls; p<0.001, PHPT vs HypoPT), along with increased levels of soluble P selectin and thromboxane B2. Conclusions. PHPT and HypoPT patients have increased atherothrombotic risk due to endothelial and platelet function alterations. Our results suggest that PTH may influence platelet reactivity. Further research is needed to determine if personalized antiplatelet therapy is necessary in subjects with parathyroid disorders Presentation: Sunday, July 13, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Università Campus Bio-Medico (IT), Istituto Neurologico Mediterraneo (IT), Campus Bio Medico University Hospital (IT), Sapienza University of Rome (IT)
Openalex Percentile: Top 66%
Parathyroid Disorders and Treatments
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