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Platelet Function and Markers of Atherothrombotic Risk in Individuals With Parathyroid Disorders
Anda Mihaela Naciu1, Annunziata Nusca2,3, Andrea Palermo1,4
1Unit of Metabolic Bone and Thyroid Disorders, Fondazione Policlinico Universitario Campus Bio-Medico, Rome 00128, Italy.
Insights
Primary hyperparathyroidism (PHPT) and hypoparathyroidism (HypoPT) increase cardiovascular risk by impairing endothelial and platelet function. PHPT significantly elevates oxidative stress and platelet aggregation, suggesting PTH influences platelet reactivity.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Biochemistry
Background:
- Primary hyperparathyroidism (PHPT) and chronic hypoparathyroidism (HypoPT) are linked to cardiovascular diseases (CVDs).
- The precise mechanisms by which parathyroid disorders affect endothelial dysfunction and platelet aggregation, key CVD determinants, remain unclear.
Purpose of the Study:
- To investigate the impact of PHPT and HypoPT on oxidative stress, endothelial function, and platelet activity.
- To compare these effects between PHPT, HypoPT, and healthy controls.
Main Methods:
- A monocentric, cross-sectional study involving 40 PHPT patients, 40 HypoPT patients, and 40 matched controls.
- Assessment of oxidative stress markers, endothelial function (flow-mediated vasodilation - FMD), platelet activation markers, and carotid intima-media thickness (IMT).
Main Results:
- Both PHPT and HypoPT groups exhibited elevated oxidative stress markers compared to controls.
- PHPT patients showed significantly reduced nitric oxide, FMD, and increased IMT compared to both HypoPT and control groups.
- Increased platelet aggregation, soluble P selectin, and thromboxane B2 were observed in parathyroid disorder patients, most pronounced in the PHPT group.
Conclusions:
- PHPT and HypoPT contribute to atherothrombotic risk through endothelial and platelet dysfunction.
- Parathyroid hormone (PTH) appears to play a role in modulating platelet reactivity.
- Further research is warranted to explore personalized antiplatelet therapies for individuals with parathyroid disorders.
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.
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