The aim of this study was to establish whether multiple blood parameters might predict an early treatment response to intravitreal bevacizumab injections in patients with diabetic macular edema (DME). Seventy-eight patients with non-proliferative diabetic retinopathy (NPDR) and DME were included. The treatment response was evaluated with central macular thickness decrease and best corrected visual acuity increase one month after the last bevacizumab injection. Parameters of interest were the neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), vitamin D, and apolipoprotein B to A-I ratio (ApoB/ApoA-I). The NLR (2.03 ± 0.70 vs. 2.80 ± 1.08; p < 0.001), MLR (0.23 ± 0.06 vs. 0.28 ± 0.10; p = 0.011), PLR (107.4 ± 37.3 vs. 135.8 ± 58.0; p = 0.013), and SII (445.3 ± 166.3 vs. 675.3 ± 334.0; p < 0.001) were significantly different between responder and non-responder groups. Receiver operator characteristics analysis showed the NLR (AUC 0.778; 95% CI 0.669–0.864), PLR (AUC 0.628; 95% CI 0.511–0.735), MLR (AUC 0.653; 95% CI 0.536–0.757), and SII (AUC 0.709; 95% CI 0.595–0.806) could be predictors of response to bevacizumab in patients with DME and NPDR. Patients with severe NPDR had a significantly higher ApoB/ApoA-I ratio (0.70 (0.57–0.87) vs. 0.61 (0.49–0.72), p = 0.049) and lower vitamin D (52.45 (43.10–70.60) ng/mL vs. 40.05 (25.95–55.30) ng/mL, p = 0.025). Alterations in the NLR, PLR, MLR, and SII seem to provide prognostic information regarding the response to bevacizumab in patients with DME, whilst vitamin D deficiency and the ApoB/ApoA-I ratio could contribute to better staging.

Background: Diabetic retinopathy (DR) is the most common microvascular complication of type 2 diabetes mellitus (T2DM). Catestatin (CST) has been implicated in cardiovascular physiology and autonomic modulation, but its role in diabetic microvascular disease remains unclear. Methods: In this cross-sectional study, serum CST levels were compared between healthy controls (n = 59) and patients with T2DM (n = 91), and further between T2DM patients with (n = 63) and without DR (n = 28). Results: CST levels did not differ between T2DM and healthy controls (16 vs. 14 ng/mL; p = 0.693). Among normotensive individuals, healthy controls had the lowest CST levels (6 ng/mL), whereas normotensive T2DM participants showed significantly higher concentrations (11 ng/mL; p = 0.004). Participants with DR exhibited significantly higher CST than those without DR (14 vs. 10 ng/mL; p = 0.034). In the total cohort, arterial hypertension (AH) was the strongest independent predictor of CST (B = 0.562; p < 0.001). In the multivariable model restricted to T2DM patients, DR emerged as the sole independent determinant of CST (B = 0.251; p = 0.028), whereas AH was no longer significant (p = 0.581). Conclusions: Circulating catestatin levels were not associated with the presence of T2DM itself but were significantly elevated in patients with DR. These findings suggest that CST may reflect microvascular and neurovascular stress rather than metabolic status and could represent a biomarker of diabetic microangiopathy.