Rheumatoid arthritis (RA) is a systemic autoimmune disease that can involve the ocular surface and deeper ocular tissues, leading to a spectrum of ophthalmic manifestations ranging from dry eye disease to vision-threatening inflammation, such as scleritis and peripheral ulcerative keratitis (PUK). This paper presents the results of a narrative review conducted using PubMed and Google Scholar from database inception to March 2026. Eligible publications describing clinical features and management of RA-associated ocular disease were synthesized, and no unpublished data were included. According to the literature, dry eye disease (DED) is the most frequent ocular manifestation of RA, and it is primarily managed with lubrication and topical anti-inflammatory therapies, including cyclosporine and lifitegrast. Additional options for refractory disease include neurostimulation and evaporation-targeted therapy. Scleritis and PUK are less common but represent severe inflammatory complications that generally require systemic immunosuppression. Conventional management includes systemic corticosteroids and steroid-sparing agents such as methotrexate (MTX), azathioprine (AZA), cyclophosphamide (CYC), and mycophenolate mofetil (MMF) in aggressive cases. Escalation to biologic disease-modifying antirheumatic drugs (bDMARDs), specifically tumor necrosis factor-alpha (TNF-α) inhibitors and rituximab (RTX), is supported for refractory scleritis and corneal melt, although evidence is largely observational. Among anti-TNF agents, monoclonal antibodies, such as infliximab and adalimumab, appear more effective than etanercept for ocular inflammation. Rituximab is preferred for vasculitis-associated or refractory disease, and Janus Kinase (JAK) inhibitors represent an emerging option requiring careful safety monitoring. Evidence for DED therapies includes randomized controlled trials (RCTs), whereas data for RA-associated scleritis and PUK are largely derived from registries, case series, and case reports. Prospective studies with standardized ocular outcomes are needed to refine treatment algorithms and compare the effectiveness of biologic versus targeted synthetic agents.

Background/Objectives: Rho-associated protein kinase inhibitors reduce intraocular pressure (IOP) by enhancing aqueous humor outflow through the trabecular meshwork-Schlemm's canal pathway. However, it remains unclear whether the fixed-dose combination of ripasudil hydrochloride hydrate and brimonidine tartrate (GLAALPHA) enhances conventional aqueous outflow in vivo. Methods: This single-center randomized clinical trial included healthy adult volunteers who received GLAALPHA, a brimonidine tartrate-brinzolamide fixed-dose combination (Ailamide), or brimonidine tartrate monotherapy (Aiphagan) in a crossover sequence. The aqueous column width in the episcleral veins was assessed at baseline and at 2 h (primary outcome) and 8 h using hemoglobin video imaging. Results: Among 24 participants, analyses included 23 GLAALPHA-treated eyes, 21 Ailamide-treated eyes, and 22 Aiphagan-treated eyes. Two hours after instillation, the aqueous column width significantly increased from baseline only in the GLAALPHA group (p = 0.002). The percent increase in the aqueous column width at 2 h was significantly greater with GLAALPHA than with Ailamide (p = 0.039) and not significantly different between GLAALPHA and Aiphagan (p = 0.114). At 8 h, the aqueous column width did not differ from the baseline in any groups. Conclusions: In healthy adult eyes, GLAALPHA significantly increased the aqueous column width in the episcleral veins 2 h after instillation, indicating enhanced conventional aqueous outflow. These findings provide evidence that GLAALPHA promotes trabecular outflow beyond the effects of brimonidine tartrate-containing comparators and offer mechanistic insights into its action.

Intravitreal anti-vascular endothelial growth factor (VEGF) therapy has fundamentally transformed the management of retinal and choroidal neovascular diseases. Despite its proven efficacy, long-term reliance on repeated intravitreal injections imposes a substantial burden on patients and healthcare systems. Real-world studies consistently demonstrate reduced adherence and inferior visual outcomes compared with randomized clinical trials. These limitations have driven interest in alternative, non-intravitreal routes of anti-VEGF delivery aimed at reducing treatment burden while maintaining therapeutic efficacy. This narrative review provides a comprehensive evaluation of suprachoroidal, systemic, transscleral, episcleral, subretinal, and topical non-intravitreal delivery strategies. Emphasis is placed on ocular pharmacokinetic barriers, pharmacodynamic requirements for sustained VEGF suppression, reasons for historical failures, and the translational maturity of emerging experimental platforms. While selected approaches, particularly suprachoroidal and gene-based strategies, show encouraging early results, intravitreal anti-VEGF therapy continues to represent the standard of care for ocular neovascular diseases.

Marfan syndrome is an autosomal dominant, connective tissue disorder that affects various systems of the body including the eyes. We present a case of a 22 year old man with Marfan syndrome presented with a painful red left eye. On examination he was diagnosed to have non-necrotising scleritis and microspherophakia. Non-necrotising scleritis with microspherophakia is a rare and arduous situation. This is an interesting case where Hickam's dictum prevails over its counter argument of Occam's razor principle.

The sub-Tenon route for injecting triamcinolone acetonide is one of the widely practiced surgical techniques for postoperative inflammation control, but complicated conjunctival and scleral necrosis are rare occurrences. A 3-year-old boy underwent bilateral cataract surgery and an anterior sub-tendon injection of triamcinolone (AST) (20 mg). One week later, he presented with conjunctival necrosis at the injection site and thinning of the sclera in both eyes. Necroses being unresponsive to conservative management led to surgical debridement and removal of residual steroid deposits. The conjunctiva healed well without grafting, and the patient remained stable at the 6-month follow-up from the ocular point of view. This rare but serious complication of periocular steroid injection in a child demands cautious administration of steroids, prompt diagnosis of necrosis, and timely intervention to limit serious ocular morbidity.

PURPOSE: This retrospective study aims to evaluate the clinical outcomes of a customised "banana-shaped" anterior lamellar keratoplasty technique in the treatment of peripheral corneal ulcerative perforations in six patients treated at a tertiary care center in Switzerland over a one-year period.

Endoscopic cyclophotocoagulation (ECP) lowers intraocular pressure (IOP) by reducing aqueous humor production, yet the magnitude of its effect varies considerably among eyes and may occasionally lead to hypotony. Based on the Goldmann equation, in which IOP is expressed as IOP = episcleral venous pressure (EVP) + (aqueous humor production (F) - uveoscleral outflow (U)) / outflow facility (C), the pressure reduction induced by aqueous suppression can be approximated as ΔIOP (change in IOP) = dF (change in F) / C, when EVP and U are assumed to be constant. This relationship indicates that the IOP response to ECP depends not only on the degree of aqueous suppression but also strongly on the conventional outflow facility. A conceptual model assuming a fixed preoperative IOP demonstrates that eyes with low outflow facility exhibit a steeper pressure response to aqueous suppression and that eyes with low baseline aqueous production are mathematically linked to such low outflow states. These findings suggest that eyes characterized by both reduced aqueous production and impaired outflow may be particularly susceptible to excessive IOP reduction after ECP. Clinically, this includes conditions such as neovascular glaucoma with extensive angle closure, uveitic glaucoma, and glaucoma in elderly patients. The model presented is based on simplified assumptions, including constant episcleral venous pressure and uveoscleral outflow, and may not fully account for alterations in the pressure-flow relationship under pathological conditions; therefore, it should be interpreted with caution as a conceptual framework with limited physiological generalizability. However, the present conceptual framework provides a theoretical explanation for variability in ECP outcomes and suggests that securing a certain level of outflow facility prior to aqueous-suppressive procedures may be a reasonable strategy in selected cases.

We report the first documented case of chronic eosinophilic leukemia (CEL) with ETV6-SYK gene rearrangement manifesting as refractory bilateral nodular scleritis within a broader paraneoplastic autoimmune syndrome. A 25-year-old woman with pre-existing Hashimoto's thyroiditis developed progressive bilateral nodular scleritis with anterior uveitis that proved completely refractory to high-dose corticosteroids, methotrexate, and conventional disease-modifying antirheumatic drugs, along with papilledema and granulomatous rosacea, suggesting systemic inflammation. Comprehensive evaluation revealed persistent marked eosinophilia (peak 15,000/μL), prompting hematological investigation, including a bone marrow biopsy and cytogenetic analysis that confirmed CEL harboring the ETV6-SYK fusion oncogene. Recognition of this molecular target enabled precision therapy with fostamatinib, a spleen tyrosine kinase (Syk) inhibitor, combined with adalimumab, a tumor necrosis factor-alpha (TNF-α) inhibitor, resulting in complete and sustained remission of all inflammatory manifestations over 18 months of follow-up. This case underscores the critical importance of maintaining high clinical suspicion for paraneoplastic autoimmune syndromes in patients with treatment-refractory inflammatory conditions, particularly when accompanied by atypical systemic or unexplained laboratory findings, and demonstrates that molecularly targeted precision medicine approaches can transform treatment outcomes in complex paraneoplastic rheumatic disorders.

"Red eye" is one of the main reasons of urgent consultation in Primary Care and in Ophthalmologic Emergencies. In many cases, the underlying cause is a benign condition that can be managed by the Primary Care Physician. However, not every red eye is a conjunctivitis, so it is important to recognize the warning signs and symptoms associated with potentially serious conditions. Causes of red eye include diseases of the ocular surface (conjunctivitis), which are generally benign; internal eye diseases (uveitis, glaucoma, scleritis, trauma) and extraocular diseases (cavernous sinus thrombosis, orbital cellulitis), which are generally ophthalmic and systemically severe, respectively. In this expert review, we aim to provide a practical approach to the differential diagnosis of red eye in general practice, defining the criteria of severity and urgency for referral to a specialized Ophthalmology consultation.