Inflammatory Markers in Lipedema: A Comparative Analysis of Neutrophil-to-Lymphocyte Ratio, Platelet-to-Lymphocyte Ratio, and Mean Platelet Volume.

Abstract

Background/aim: Although various distinctive morphological features such as hyperproliferation of adipocytes, fibrosis, and inflammation have been described in the progression of lipedema, the underlying mechanisms of these changes are not yet fully understood. In this study, we aimed to investigate the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), mean platelet volume (MPV), and platelet distribution width (PDW) to demonstrate the role of inflammation in lipedema.

Methods: The retrospective study consisted of 60 lipedema patients (Group 1) and 40 healthy controls (Group 2). The age, height, weight, and body mass index (BMI) of all participants were recorded, along with the lipedema type and stage for Group 1. Laboratory results, including complete blood count, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), were obtained for all participants. Hemoglobin, leukocyte, lymphocyte, neutrophil, and platelet counts, NLR, PLR, MPV, PDW, CRP, and ESR were evaluated.

Results: The mean age was 45.45 ± 10.17 years in Group 1 and 44.90 ± 10.69 years in Group 2; the BMI was 32.15 ± 5.05 in Group 1 and 30.94 ± 4.98 in Group 2, with no significant difference between the groups (p > 0.05). The most common type was Type 2 lipedema. Platelet counts, CRP, NLR, and PLR levels were significantly higher in Group 1 than in Group 2 (p < 0.05). There was no difference between groups in MPV and PDW values (p > 0.05). There was a positive correlation between BMI and both leukocyte count and CRP levels (p < 0.05).

Conclusion: In our study investigating inflammation in lipedema-an etiology that is still not fully understood-NLR, PLR, platelet count, and CRP levels were found to be significantly higher in the patient group. The increase in BMI was correlated with leukocyte count and CRP levels. This finding is important for elucidating the etiopathogenesis of the disease, and we believe it may guide future research in this area.