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.

Pterygium is a condition affecting the ocular surface, marked by a triangular-shaped growth of fibrotic tissue extending from the nasal conjunctiva toward the corneal center, potentially causing visual impairment. While ultraviolet (UV )light exposure is the primary risk factor for pterygium, its underlying cause remains unclear. In order to better understand the true genesis of pterygium development, we investigated pterygium tissue and compared it with healthy conjunctiva controls. Given the eye’s direct environmental exposure, we analyzed the microbiota composition using metagenomic sequencing of pterygium tissue to identify microbes potentially associated with this condition. Metagenomic sequencing revealed a higher prevalence of the fungus Malassezia restricta in five pterygium samples, confirmed by in situ hybridization. The CHIT1 gene, which plays a role in antifungal defenses, displayed the highest expression in five pterygium tissue samples compared to healthy conjunctiva controls, suggesting the potential involvement of Malassezia restricta in pterygium development. Gene expression profiling of pterygium highlighted an IL-33 and IL-4 gene expression signature, along with an increased presence of M2 macrophages, emphasizing their role in promoting fibrosis—a hallmark feature of pterygium. The detection of Malassezia restricta in the pterygium samples and associated molecular changes provides novel insights into the ocular microbiome and raises the possibility of Malassezia’s involvement in pterygium pathology.

In this paper, a review of a rare case of paramacular choriocapillaris atrophy with a foveal-sparing phenotype is carried out. The 73-year-old patient stated that they had impaired vision and photophobia in both eyes during a regular ophthalmological examination, denying visual field defects and night blindness. A complete ophthalmological examination (best-corrected visual acuity, applanation tonometry, and biomicroscopy of anterior and posterior segments) and diagnostic tests, including fundus autofluorescence, fluorescein angiography, optical coherence tomography with angiography, computerized perimetry, and electroretinography, were carried out. The underlying genetic pattern is unclear, which points to paramacular choriocapillaris atrophy. According to recent research on histology, pathologies categorized as regional choroidal dystrophies are caused by alterations at the level of the retinal pigment epithelium. Despite the unresolved etiopathogenetic mechanism of foveal sparing in central choroidal and retinal dystrophies, a highly variable disease phenotype with spared fovea and central visual acuity present in a variety of heterogeneous dystrophies supports a disease-independent mechanism that allows the survival of foveal cones. The related preservation of BCVA has implications for individual prognosis and influences how treatment trials for choroidal and retinal dystrophies are designed.