AUTHOR=Lei Chunyan , Gu Jinyue , Liu Lili , Zhang Keren , Zhang Meixia 

TITLE=The correlation between peripheral complete blood count parameters and diabetic macular edema in proliferative diabetic retinopathy patients: a cross-sectional study

JOURNAL=Frontiers in Endocrinology

VOLUME=Volume 14 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2023.1190239

DOI=10.3389/fendo.2023.1190239

ISSN=1664-2392

ABSTRACT=Background: Numerous studies have demonstrated that retinal chronic inflammation plays a critical role in the pathogenesis of diabetic macular edema (DME). However, studies about the association between peripheral complete blood count, an inexpensive and easily measurable laboratory index, and DME are limited. 
Research Design and Methods: The current study was a hospital-based, cross-sectional study. The participants were inpatients with type 2 diabetes who underwent vitrectomy for PDR, and the contralateral eye in these PDR patients meeting the criteria were included as subjects in the study. Central macular thickness (CMT) was measured automatically and the DME was characterized as CMT ≥ 300 μm.
Results: A total of 239 PDR participants were enrolled. The average age was 55.46 ± 10.08 years old, and the average CMT was 284.23 ± 122.09 μm. In the fully adjusted model, for CMT, the results revealed a significantly negative association between CMT and both white blood cell (WBC) count and neutrophil count (β = -11.95, 95% CI: -22.08, -1.82; P = 0.0218; β = -14.96, 95% CI: -28.02, -1.90; P = 0.0259, respectively); for DME, the results showed an inverse association between DME and WBC count, monocyte count, eosinophil count (OR = 0.75, 95% CI: 0.59, 0.95; P = 0.0153; OR= 0.07, 95% CI: 0.00, 0.92; P = 0.0431, OR= 0.03, 95% CI: 0.00, 0.88; P = 0.0420, respectively). 
Conclusions: In conclusion, our results suggest that patients with PDR are in a subclinical inflammatory state and that inflammation mediated by WBC and its subtypes may play an important role in the pathogenesis of DME.