Tag Archives: inflammation

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

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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.

The NUTRIENT Trial (NUTRitional Intervention among myEloproliferative Neoplasms): Results from a Randomized Phase I Pilot Study for Feasibility and Adherence

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Laura F. Mendez Luque1,2, Julio Avelar-Barragan3, Hellen Nguyen1, Jenny Nguyen1, Eli M. Soyfer1, Jiarui Liu1, Jane H. Chen1, Nitya Mehrotra1, Xin (Helen) Huang1, Heidi E. Kosiorek4, Amylou Dueck4, Alexander Himstead1, Elena Heide1, Melinda Lem1, Kenza El Alaoui1, Eduard Mas1, Robyn M. Scherber5, Ruben A. Mesa6, Katrine L. Whiteson3, Andrew Odegaard1, Angela G. Fleischman1

ABSTRACT

Purpose: Chronic inflammation is integral to Myeloproliferative Neoplasm (MPN) pathogenesis. JAK inhibitors reduce cytokine levels, but not without significant side effects. Nutrition is a low- risk approach to reduce inflammation and ameliorate symptoms in MPN. We performed a randomized, parallel-arm study to determine the feasibility of an education-focused Mediterranean diet intervention among MPN patients.

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Identification of Novel Risk Variants of Inflammatory Factors Related to Myeloproliferative Neoplasm: A Bidirectional Mendelian Randomization Study

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Yang Li, Ting Sun, Jia Chen, Lei Zhang

Abstract

Epidemiological and experimental evidence has linked chronic inflammation to the etiology of myeloproliferative neoplasm (MPN). However, it remains unclear whether genetic associations with specific inflammatory biomarkers are causal or due to bias. This study aimed to assess the effect of C-reactive protein (CRP) and systemic inflammatory regulators on MPN within a bidirectional Mendelian randomization design. Genetic associations with MPN were derived from a publicly available genome-wide association study (GWAS) comprising 1,086 cases and 407,155 controls of European ancestry. Additionally, data on inflammation were extracted from two GWASs focusing on CRP and cytokines. The causal relationships between exposure and outcome were explored using the inverse variance weighted (IVW) method. To confirm the final results, multiple sensitivity analyses, including MR-Egger, weighted median, and MR-pleiotropy residual sum and outlier (MR-PRESSO), were simultaneously employed. Our results suggest that lower levels of macrophage-migration inhibitory factor (IVW estimate odds ratio [OR IVW] per SD genetic cytokines change: 0.641; 95% confidence interval [CI]: 0.427–0.964; p = 0.032) and higher levels of interleukin-2 receptor α (lL2Rα, 1.377, 95% CI: 1.006–1.883; p = 0.046) are associated with an increased risk of MPN. Genetically predicted MPN is related to increased levels of RANTES (IVW estimate β: 0.043, 95% CI: 0.002–0.084; p = 0.039) and interleukin-10 (IVW estimate β: 0.030, 95% CI: 0.001–0.060; p = 0.041). This study provides evidence for a causal relationship between CRP, systemic inflammatory regulators, and MPN, and new insights into the etiology, prevention, and prognosis of MPN.

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