Carotid Plaque Burden and Neutrophil-Lymphocyte Ratio in Patients with Philadelphia Negative Myeloproliferative Neoplasms and Their Relation to JAK2 V617F Mutation

Mahmoud Gaber, Mohamed Ezeldin, Mustafa Adel Younis, Moamen Abdelfadil Ismail, and Asmaa Ahmed Abdel-baset

 

Abstract

Background: Philadelphia negative myeloproliferative neoplasms are characterized by clonal myeloid cell proliferation. The JAK2V617F mutation may influence inflammation and atherosclerosis. Neutrophil-Lymphocyte Ratio and carotid plaque burden are markers associated with inflammation and cardiovascular risk, respectively.

This study aimed to investigate the relationship between NLR, carotid plaque burden, and JAK2V617F mutation in PN-MPN patients.

Patients and Methods: A retrospective case-control study included 90 PN-MPN patients and 60 controls. Data on demographics, comorbidities, thrombosis, laboratory parameters, carotid plaque burden, and JAK2V617F mutation status were collected.

Results: Age, gender distribution, smoking status, and comorbidities did not significantly differ between PN-MPN patients and controls. Thrombosis incidence in PN-MPN patients did not significantly differ from controls. Carotid plaque burden and NLR were significantly higher in PN-MPN patients compared to controls (p=0.024 and p<0.001, respectively). Majority of PN-MPN patients (78.9%) had positive JAK2V617F mutation status. NLR was significantly higher in PN-MPN patients with positive JAK2V617F mutation compared to negative (p=0.001). There was a significant difference in thrombosis incidence between patients with positive and negative JAK2V617F mutation status.

Conclusion: The study identified a significant link between higher N/L ratios and the JAK2V617F mutation in patients with PN-MPNs, proposing the N/L ratio as a potential marker for disease activity or mutation status. Despite observing a higher incidence of thrombosis in MPN patients and increased carotid plaque in PN-MPN patients compared to controls, no significant correlation was found between these cardiovascular risk markers and the JAK2V617F mutation status, suggesting other factors influence thrombosis risk in these patients.

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