Systemic–retinal inflammatory crosstalk in diabetic macular edema: correlation between hematologic indices and macular OCT-features

TL;DR

This study explores how systemic inflammation and retinal changes are linked in diabetic macular edema, using blood markers and OCT imaging.

Contribution

The study identifies a potential link between platelet-driven systemic inflammation and retinal vascular leakage in diabetic macular edema.

Findings

Elevated platelet-to-lymphocyte ratio (PLR) correlates with hard exudates in diabetic macular edema.

OCT features like hyperreflective foci and subretinal fluid reflect localized retinal inflammation.

Systemic and retinal inflammatory pathways appear to interact in DME pathogenesis.

Abstract

This study investigated the relationship between systemic inflammatory indices and optical coherence tomography (OCT)–derived retinal inflammatory biomarkers in patients with diabetic macular edema (DME) associated with non-proliferative diabetic retinopathy (NPDR).

A cross-sectional study was conducted on 40 eyes from patients with clinically significant DME. OCT biomarkers, including hyperreflective foci (HRF), subretinal fluid (SRF), and hard exudates, were evaluated. Systemic inflammatory markers—neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII)—were derived from complete blood counts. Correlations between these parameters were analyzed using non-parametric tests.

A total of 40 eyes from 40 patients with NPDR with DME were analyzed. The mean central macular thickness was 396.28 ± 124.75 μm. Systemic inflammatory markers (NLR, MLR, PLR, SII) showed no significant differences between mild and severe DME groups. Among OCT biomarkers, eyes with hard exudates demonstrated significantly higher PLR values (p = 0.018), while differences in NLR, MLR, and SII were insignificantly higher in HRF > 30 and positive hard exudates.

DME pathogenesis appears to involve two interacting inflammatory pathways: systemic platelet-driven vascular inflammation and localized microglial-mediated neuroinflammation. Elevated PLR reflects systemic endothelial injury and correlates with vascular leakage, whereas OCT features, such as HRF and SRF, represent compartmentalized retinal inflammation. Integrating systemic hematologic indices with OCT inflammatory biomarkers offers a practical and translational framework for assessing inflammatory activity in DME and may guide personalized monitoring and therapeutic strategies.

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