Introduction: Dry Eye Syndrome (DES) is a multifactorial disorder of the ocular surface, characterized by complex interactions between environmental factors, immune dysregulation, and potential genetic predispositions. Vitamin D deficiency, known for its immunomodulatory properties, has increasingly been implicated in the pathogenesis of DES; however, the underlying mechanisms remain insufficiently elucidated. Of particular interest is the vitamin D receptor (VDR) gene, whose polymorphisms may influence the bioavailability and biological activity of vitamin D. Objective: The aim of this study was to investigate the association between serum 25-hydroxyvitamin D [25(OH)D₃] levels and selected polymorphisms in the VDR gene (Taq, Fok, Apa, and Bsm) in patients with DES and to analyze their potential clinical and genetic interactions. Methods: This prospective observational study included 60 patients with a confirmed diagnosis of DES. Serum 25(OH)D₃ levels were measured, and genotyping of four VDR single-nucleotide polymorphisms (SNPs) was performed using PCR followed by restriction fragment length polymorphism analysis. Genotype distributions were assessed in relation to vitamin D status using appropriate statistical tests and Hardy–Weinberg equilibrium analysis. Results: Over 85% of patients exhibited insufficient or deficient vitamin D levels. Among the analyzed SNPs, only the ApaI polymorphism (rs7975232) showed a statistically significant association with vitamin D status (p = 0.0384), with the homozygous AA genotype being more prevalent among patients with hypovitaminosis. The remaining polymorphisms (TaqI, FokI, BsmI) did not reach statistical significance; however, potential trends were observed that may warrant further investigation in larger cohorts. Conclusion: The findings suggest a potential role for VDR gene variability in the regulation of systemic vitamin D levels in patients with DES. Identification of specific genotypes may contribute to the development of personalized diagnostic and therapeutic strategies, particularly for patients with treatment-resistant forms of the disease. These results support the integration of genetic biomarkers and nutritional parameters into modern ophthalmologic practice.

Rhegmatogenous retinal detachment (RRD) is a vision-threatening retinal disorder in which successful anatomical reattachment does not always result in satisfactory functional visual recovery. Optical coherence tomography (OCT) has become an essential non-invasive imaging modality for evaluating retinal microstructure and identifying biomarkers associated with postoperative visual outcomes. This narrative review summarizes and critically evaluates current evidence regarding the prognostic significance of OCT biomarkers following RRD repair. Available studies indicate that primary outer retinal biomarkers, particularly the integrity of the ellipsoid zone (EZ) and external limiting membrane (ELM), are the most reliable predictors of postoperative best-corrected visual acuity. Preservation of these structures reflects photoreceptor viability and is strongly associated with improved visual recovery. Secondary biomarkers, including hyperreflective foci, intraretinal cystic changes, retinal folds, persistent subretinal fluid, and preretinal hyperreflective dots, provide complementary information regarding inflammatory activity, retinal remodeling, and postoperative complications such as epiretinal membrane formation. Although these biomarkers have considerable clinical value for prognostication, patient counseling, and postoperative monitoring, their interpretation is limited by heterogeneity among studies, differences in imaging protocols, and the lack of standardized assessment criteria. Future large-scale prospective studies are needed to validate OCT biomarkers and establish standardized approaches for their integration into routine clinical practice.

Background: Penetrating keratoplasty (PK) is a technically demanding corneal transplant procedure frequently performed in elderly patients with substantial systemic comorbidities. In this population, an anesthetic strategy that ensures hemodynamic stability, cooperative sedation, adequate analgesia, and preserved spontaneous ventilation is highly desirable. Dexmedetomidine, a highly selective alpha2-adrenergic agonist, provides “cooperative” sedation with minimal risk of respiratory depression and additional sympatholytic benefits. Methods: This single-center retrospective observational case series included 50 consecutive patients (American Society of Anesthesiologists [ASA] II–III, age 50–90 years) undergoing PK under sub-Tenon block combined with continuous dexmedetomidine infusion. Dexmedetomidine was administered without a loading bolus at 0.7 mcg/kg/h for 10–15 min, then reduced to 0.5 mcg/kg/h, targeting a Ramsay Sedation Scale (RSS) score of 2–3. The sub-Tenon block was performed using a mixture of levobupivacaine 0.5% and lidocaine 2% (3–5 mL). Heart rate (HR), mean arterial pressure (MAP), oxygen saturation (SpO₂) and RSS were recorded in nine predefined perioperative phases. Data were analyzed descriptively. Results: The mean age was 72 ± 9 years; 52% of patients were ASA III. Hypertension was present in all patients; 30% had cardiovascular disease, 28% diabetes mellitus type II, and 30% chronic obstructive pulmonary disease. Progressive, controlled bradycardia was observed (mean HR decreased from 76 to 57 beats/min during graft transplantation), while MAP gradually decreased from hypertensive baseline values (150–160 mmHg) to an optimal intraoperative range of 115–130 mmHg, without episodes of clinically significant hypotension. SpO₂ remained stable at 98–99% throughout all phases, with no episodes of desaturation or need for airway intervention or supplemental oxygen. Target sedation (RSS 2–3) was achieved in all patients (median RSS 3), with preserved spontaneous breathing and cooperation. Sub-Tenon block-related bulging occurred in 6% of cases. No episodes of clinically significant bradycardia, malignant arrhythmia, respiratory compromise, or need to discontinue dexmedetomidine were recorded. No opioids or non-steroidal analgesics were required intraoperatively or in the early postoperative period. Conclusions: The combination of sub-Tenon block and continuous dexmedetomidine sedation without a loading bolus represents a hemodynamically stable and respiratory-safe anesthetic strategy for PK in elderly, high-risk patients. These preliminary, hypothesis-generating findings suggest that the protocol provides stable surgical conditions and a favorable safety profile, justifying future prospective randomized controlled trials to establish its comparative efficacy against general anesthesia or standard sedative regimens.

Diabetic retinopathy (DR) is the most frequent microvascular complication of diabetes mellitus (DM) and remains a leading cause of preventable blindness in the working-age population. Its course is notoriously variable: some patients with long-standing, poorly controlled diabetes never develop sight-threatening disease, whereas others progress rapidly despite reasonable metabolic control. This clinical heterogeneity, which the traditional risk factors cannot fully explain, has directed attention towards the inherited component of susceptibility. This review summarizes current understanding of the genetic architecture of DR, with particular emphasis on three extensively studied candidate genes: the vascular endothelial growth factor A gene (VEGFA), the angiotensin-converting enzyme gene (ACE) and the apolipoprotein E gene (APOE), specifically their most investigated polymorphisms: VEGFA rs699947, rs2010963 and rs3025039; ACE rs1799752 I/D; and APOE rs429358 and rs7412 (ε2/ε3/ε4). The evidence linking individual polymorphisms to disease is examined alongside the picture emerging from genome-wide association studies (GWAS), and the persistent inconsistency among studies is discussed in the context of ethnic differences, phenotype definition and limited statistical power. Finally, the review considers how genetic insight is beginning to inform therapy, from the established anti-VEGF paradigm to genebased approaches now in clinical trials, and outlines the main obstacles that still separate genetic findings from routine clinical use.