Oxidative stress has been postulated as an underlying pathophysiologic mechanism of diabetic retinopathy (DR), the main cause of avoidable blindness in working-aged people. This review addressed the current daily clinical practice of DR and the role of antioxidants in this practice. A systematic review of the studies on antioxidant supplementation in DR patients was presented. Fifteen studies accomplished the inclusion criteria. The analysis of these studies concluded that antioxidant supplementation has a IIB level of recommendation in adult Type 1 and Type 2 diabetes mellitus subjects without retinopathy or mild-to-moderate nonproliferative DR without diabetic macular oedema as a complementary therapy together with standard medical care.

Diabetic retinopathy (DR), a leading cause of blindness in working-age adults, arises from chronic hyperglycemia-induced oxidative stress, inflammation, and vascular dysfunction. Current therapies such as laser photocoagulation, intravitreal anti-vascular endothelial growth factor (VEGF) agents, and steroids target advanced stages but fail to prevent early neuronal and microvascular damage. Emerging evidence highlights oxidative stress as a key driver of DR pathogenesis, disrupting the blood-retinal barrier (BRB), promoting neurodegeneration and angiogenesis. Advances in imaging, particularly optical coherence tomography angiography (OCTA), enable earlier detection of neurodegeneration and microvascular changes, underscoring DR as a neurovascular disorder. Polyphenols, such as resveratrol, curcumin, and pterostilbene, exhibit multitarget antioxidant, anti-inflammatory, and anti-angiogenic effects, showing promise in preclinical and limited clinical studies. However, their low bioavailability limits therapeutic efficacy. Nanotechnology-based delivery systems enhance drug stability, tissue targeting, and sustained release, offering potential for early intervention. Future strategies should integrate antioxidant therapies and precision diagnostics to prevent early irreversible retinal damage in diabetic patients.

A 36-year-old man presented complaining of bilateral painless vision loss. He was admitted with chronic ethanol abuse, as well as sporadic cocaine consumption three days before symptom onset. General medical evaluation dismissed cerebral and cardiovascular events. Blood tests revealed folic acid deficiency. Visual acuity (VA) was count fingers in both eyes (OU). Fundoscopic findings included remarkable bitemporal peripapillary hemorrhages. A diagnosis of toxic-ischemic optic neuropathy was made. The hemorrhages resolved after three weeks, with VA recovering to 20/20 OU. The sequelae included bitemporal peripapillary retinal fiber loss on optical coherence tomography, and central scotomas observed on visual field tests. This is the first report of cocaine as a triggering agent for a classical presentation of toxic optic neuropathy and the presence of peripapillary hemorrhages in its initial stages.

Chronic hyperglycemia is a major driver of neurovascular damage in diabetic retinopathy (DR), a leading cause of preventable blindness in adults. DR progression is often undetected until its advanced stages, with oxidative stress recognized as a primary contributor. In diabetes, oxidative stress disrupts retinal cellular balance, damaging proteins, DNA, and lipids, and triggering photoreceptor degeneration. Pterostilbene (Pter), a polyphenol with antioxidant properties, has demonstrated protective effects in DR animal models and was assessed in a pilot clinical study. DR patients treated with 250 mg/day of oral Pter showed a reduction in the development of retinal vascular alterations characteristic of the disease. Urinary analyses confirmed Pter’s role in reducing the lipid peroxidation of polyunsaturated fatty acids (PUFAs), including arachidonic and adrenic acids, indicators of oxidative damage in DR. Pter also improved the GSH/GSSG ratio, reflecting a restored redox balance. However, after six months without treatment, retinal damage indicators reappeared, highlighting the importance of sustained intervention. These findings suggest that Pter may help slow the progression of DR by protecting against oxidative stress and highlight the importance of implementing antioxidant therapies from the diagnosis of diabetes, although its long-term impact and the development of consistent biomarkers deserve more research to optimize DR management.

Purpose: To describe a patient with idiopathic hypereosinophilic syndrome (HES) associated with panuveitis. Methods : An interventional case report is presented. Results: A 70-year-old woman presented with intermittent cutaneous eruptions, bilateral panuveitis, and a ground-glass pattern on chest CT-scan, with isolated eosinophilia of 12.8 × 10 ⁹ /L. A complete uveitis workup was performed, and the patient was evaluated to rule out secondary causes of eosinophilia, with a thorough focus on infections, eosinophilic granulomatosis with polyangiitis, sarcoidosis, and drug-related syndromes. A bone marrow biopsy ruled out primary eosinophilia. Cytogenetics were also negative. Under steroid treatment there was no recurrence of skin rashes and panuveitis was satisfactorily resolved, but further use of mepolizumab was needed to normalize the hemogram. Conclusions: The diagnosis of HES requires a comprehensive evaluation. Ocular involvement is rare. We present the ocular findings during the acute stage for the first time, along with the current management approach.

We report a 40-year-old Caucasian male presenting sudden bilateral Choroidal Neovascularization (CNV) along with Chorioretinal Lesions (CRL). He presented previous ocular history of relapsing idiopathic bilateral anterior uveitis.