Platelet function and markers of atherothrombotic risk in subjects with parathyroid disorders: a cross-sectional study

Context Both primary hyperparathyroidism (PHPT) and chronic hypoparathyroidism (HypoPT) are associated with the onset and development of cardiovascular diseases (CVDs). 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. Objective This work aimed to evaluate the effects of PHPT and HypoPT on oxidative stress and endothelial and platelet function. Methods This monocentric cross-sectional study at an outpatient clinic included 40 individuals with HypoPT, 40 with PHPT, and 40 age- and sex-matched control participants. Main outcome measures included circulating levels of markers of oxidative stress, endothelial function, and platelet activation, calcium metabolism parameters, flow-mediated vasodilation (FMD), and carotid intimal-media thickness (IMT). Results HypoPT and PHPT patients showed increased oxidative stress markers as compared to control participants (P < .001). Among patients with parathyroid disorders, those with PHPT demonstrated the highest reduction of nitric oxide (P < .001 vs HypoPT and controls) and FMD (P < .001 and P = .001) and a marked increase of IMT (P < .001 and P = .001). We also observed an increased platelet aggregation in patients with parathyroid disorders, with the highest values in PHPT patients (P < .001, PHPT vs controls; P = .006, HypoPT vs controls; P < .001, PHPT vs HypoPT), along with increased levels of soluble P selectin and thromboxane B2. Conclusion PHPT and HypoPT patients have increased markers of atherothrombotic risk due to endothelial and platelet function alterations. Our results suggests that parathyroid hormone may influence platelet reactivity. Further research is needed to determine if personalized antiplatelet therapy is necessary in individuals with parathyroid disorders.