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

Abstract

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: To evaluate the effects of PHPT and HypoPT on oxidative stress, endothelial and platelet function.

Design: Monocentric cross-sectional study.

Setting: Outpatient clinic.

Patients: 40 subjects with HypoPT, 40 with PHPT and 40 age- and sex-matched control subjects.

Main outcome measures: 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 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 markers of atherothrombotic risk due to endothelial and platelet function alterations. Our results suggests that PTH may influence platelet reactivity. Further research is needed to determine if personalized antiplatelet therapy is necessary in subjects with parathyroid disorders.