Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease. Up to one-third of patients suffering from SLE have various ocular manifestations. The ocular findings may represent the initial manifestation of the systemic disease and may lead to severe ocular complications, and even loss of vision. Ocular manifestations are often associated with degree of systemic inflammation, but also can precede the occurrence of systemic symptoms. Early diagnosis and adequate management of patients with SLE are crucial and require cooperation between various specialists. Proper preparation of ophthalmologists can help to differentiate between complication of SLE and other ocular disorders. New therapies for SLE are promising for potential benefits, however, ocular side effects are still unknown.

The eyelid skin represents a unique anatomical and immunological interface between the external environment and the ocular surface. Due to its structural delicacy, dense vascularization, and continuous exposure to microbial and environmental antigens, it is a primary target of inflammatory and autoimmune processes. This review aims to synthesize current molecular insights into eyelid skin inflammation, with particular emphasis on autoimmune mechanisms. We discuss autoimmune diseases such as ocular cicatricial pemphigoid, pemphigus, discoid and systemic lupus erythematosus, and thyroid-associated orbitopathy, focusing on the roles of T helper cell subsets, pro-inflammatory cytokines (IL-1β, IL-6, IL-17, TNF-α), and autoantibody-mediated complement activation. We further address the contribution of the periocular microbiome and meibomian gland dysfunction. Diagnostic advances, including confocal microscopy, in vivo molecular imaging, and tear proteomics, are highlighted alongside emerging targeted therapies such as biologics and small molecules directed at IL-17, TNF-α, and B-cell activity. Finally, we propose future perspectives for precision medicine approaches, integrating omics technologies and microbiome-based therapies to advance personalized management of eyelid skin inflammation.

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disorder in which ocular involvement represents a clinically significant yet frequently underrec-ognized contributor to morbidity. Ocular manifestations in SLE may arise from disease activity itself, but also as adverse effects of long-term pharmacological therapy. With the advent of targeted immunomodulatory agents, the therapeutic landscape of SLE has expanded beyond conventional drugs such as hydroxychloroquine and corticosteroids toward biologics and small molecules designed to interfere with specific immunological pathways. These advances have improved systemic disease control and survival; however, their ophthalmological safety profiles remain only partially defined. This review synthesizes current evidence on ocular adverse events associated with both traditional and emerging SLE therapies. Established agents, particularly hydroxychlo-roquine and corticosteroids, are consistently linked to complications including reti-nopathy, posterior subcapsular cataracts, steroid-induced glaucoma, and central serous chorioretinopathy. In contrast, recently approved or investigational therapies—such as belimumab, anifrolumab, voclosporin, dual BAFF/APRIL inhibitors, rituximab, JAK in-hibitors, CD40/CD40L blockade, CD38 inhibition, and mesenchymal stromal cell–based strategies—have limited but evolving safety data, with potential ocular adverse events spanning inflammatory, vascular, neuro-ophthalmic, and structural domains. Although ocular complications appear infrequent in clinical trials, underdetection in real-world practice and insufficient long-term monitoring may underestimate their true incidence. These findings highlight the need for systematic ophthalmological surveil-lance in patients receiving immunomodulatory therapies for SLE. Early recognition and timely management of ocular toxicity are crucial to safeguarding visual function and optimizing long-term therapeutic outcomes in this vulnerable patient population.

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disorder in which ocular involvement represents a clinically significant yet frequently underrecognized contributor to morbidity. Ocular manifestations in SLE may arise from disease activity itself, but also as adverse effects of long-term pharmacological therapy. With the advent of targeted immunomodulatory agents, the therapeutic landscape of SLE has expanded beyond conventional drugs such as hydroxychloroquine and corticosteroids toward biologics and small molecules designed to interfere with specific immunological pathways. These advances have improved systemic disease control and survival; however, their ophthalmological safety profiles remain only partially defined. This review synthesizes current evidence on ocular adverse events associated with both traditional and emerging SLE therapies. Established agents, particularly hydroxychloroquine and corticosteroids, are consistently linked to complications including retinopathy, posterior subcapsular cataracts, steroid-induced glaucoma, and central serous chorioretinopathy. In contrast, recently approved or investigational therapies—such as belimumab, anifrolumab, voclosporin, dual BAFF/APRIL inhibitors, rituximab, JAK inhibitors, CD40/CD40L blockade, CD38 inhibition, and mesenchymal stromal cell-based strategies—have limited but evolving safety data, with potential ocular adverse events spanning inflammatory, vascular, neuro-ophthalmic, and structural domains. Although ocular complications appear infrequent in clinical trials, underdetection in real-world practice and insufficient long-term monitoring may underestimate their true incidence. These findings highlight the need for systematic ophthalmological surveillance in patients receiving immunomodulatory therapies for SLE. Early recognition and timely management of ocular toxicity are crucial to safeguarding visual function and optimizing long-term therapeutic outcomes in this vulnerable patient population.

Closed-globe blunt ocular trauma may lead to severe ophthalmic complications, including intraocular hemorrhages, traumatic cataract, and retinopathy, the management of which remains a significant clinical challenge. We report the case of a 55-year-old male who, 15 years after right-eye trauma and unsuccessful conservative therapy, underwent surgical treatment using multistage vitreoretinal procedures. Despite an initially poor functional prognosis, a marked improvement in visual acuity was achieved, from 2.0 logMAR at baseline to 0.52 logMAR after completion of treatment. Imaging (OCT, B-scan ultrasonography) confirmed complete retinal attachment and the absence of active intra- or subretinal bleeding. This case demonstrates that, even after a long interval following trauma, vitreoretinal surgical interventions may lead to partial restoration of visual function and stabilization of ocular anatomy, underscoring the importance of individualized assessment of surgical indications in chronic post-traumatic retinal disorders.

Lamellar ichthyosis is a rare congenital disorder of keratinization frequently associated with ocular complications, most commonly cicatricial ectropion and exposure keratopathy. We present a case of severe mixed exposure-related and neurotrophic keratopathy with marked corneal thinning in a 61-year-old man with genetically confirmed lamellar ichthyosis. At presentation, the best-corrected visual acuity (BCVA) in the right eye was limited to hand motion (logMAR 2.3). Slit-lamp examination revealed a large central to inferocentral corneal ulcer measuring approximately 3 × 4 mm with severe stromal thinning in the setting of marked lower eyelid ectropion, incomplete eyelid closure, and chronic ocular surface exposure, while anterior segment optical coherence tomography (AS-OCT) demonstrated a minimal corneal thickness of approximately 165 µm. Microbiological swabs obtained from the conjunctival sac were negative, and no purulent discharge, hypopyon, or anterior chamber inflammatory reaction was present, making active infectious keratitis unlikely. Corneal sensitivity measured with Cochet–Bonnet esthesiometry at presentation, centrally and in all four peripheral quadrants of both eyes, was markedly reduced, more severely in the affected right eye, supporting the presence of a severe neurotrophic component contributing to impaired corneal healing. Intensive conservative therapy including preservative-free lubricants, dexpanthenol gel, autologous serum eye drops, topical insulin, prophylactic antibiotics, and systemic doxycycline was initiated. Serial AS-OCT imaging demonstrated progressive structural recovery, with corneal thickness increasing to 438 µm after one month of treatment and complete corneal epithelialization. The BCVA improved to 0.2 Snellen (0.7 logMAR). This case highlights the diagnostic value of multimodal anterior segment imaging in monitoring severe mixed keratopathy with advanced corneal thinning and demonstrates that intensive conservative therapy may stabilize the ocular surface and prevent corneal perforation in patients with lamellar ichthyosis.