Background/objectives: Psoriasis is a systemic immune-mediated disease with ocular involvement. While biologic therapies reduce cardiovascular and musculoskeletal comorbidities, their impact on ocular health is not well characterised. We aimed to assess whether biologic therapy is associated with reduced ocular disease risk in psoriasis patients.
Subjects/methods: We performed a large-scale, retrospective cohort study using the TriNetX Global Collaborative Network (>160 million patients worldwide). Adults with psoriasis initiating biologic therapy were compared with those receiving non-biologic systemic treatments. Cohorts were matched 1:1 by propensity scoring for demographic and clinical variables. Sixty-eight ocular outcomes were assessed over 6 to 120 months. Hazard ratios (HRs) were estimated using proportional hazards models.
Results: Among 30,911 biologic-treated and 35,832 non-biologic-treated patients with psoriasis, biologic therapy was consistently associated with reduced risk of ocular surface and corneal inflammation. The strongest associations were seen for dry eye disease (mean HR = 0.55, 95% confidence interval [CI; 0.42, 0.66], p = 0.0007), conjunctivitis (mean HR = 0.71, 95% CI [0.59, 0.86], p = 0.01), and keratitis (mean HR = 0.40, 95% CI [0.3, 0.56], p = 0.0007). These lower-risk associations were evident from 6 months and remained observable in the 10-year analysis window. No consistent reduction was observed for retinal or vitreous disease.
Conclusions: Biologic therapy in psoriasis was associated with a lower risk of ocular surface disease. These observational findings may inform interdisciplinary management and consideration of ocular outcomes in treatment decisions.
Neurotrophic keratopathy (NK) is an uncommon corneal disorder caused by trigeminal nerve dysfunction, leading to loss of ocular surface sensation, impaired corneal epithelial maintenance, and possible progressive stromal lysis. NK is of added potential visual significance in children on account of the risk of amblyopia resulting from stromal opacification. Unlike acquired NK in adult-onset disease, NK in childhood is frequently congenital or inherited, linked to genetic pain insensitivity syndromes, cranial dysinnervation disorders or broader developmental anomalies. Visual function can be well preserved in affected eyes in many children with supportive management or specific medical and surgical interventions directed at modulating sensory nerve function. A modification of the existing classification of NK stages is proposed to incorporate those eyes in which there is no detectable corneal sensation but otherwise normal eye examination, a phenotype not infrequently encountered in early NK in childhood.
Purpose: To evaluate hyperreflective choroidal foci (HCF) in Sattler's and Haller's layers as predictive biomarkers for treatment response and pachychoroid macular atrophy (pMA) development in chronic central serous chorioretinopathy (CSC).
Methods: Retrospective analysis of 70 treatment-naïve patients with recurrent CSC classified according to Chhablani's criteria. HCF were quantified separately in choroidal layers using spectral-domain OCT at baseline and 12-month follow-up. Patients received photodynamic therapy (n = 20), eplerenone (n = 16), or subthreshold micropulse laser (n = 34). Primary outcomes included treatment response (complete fluid resolution) and pMA development.
Results: At baseline, no significant differences in HCF counts existed between future responders (n = 36) and non-responders (n = 34). At 12 months, responders showed significant HCF reduction in Sattler's layer (-9.17 foci, p = 0.001) and Haller's layer (-3.19 foci, p = 0.039), while non-responders demonstrated increased Sattler's foci (+4.62, p = 0.041). pMA developed in 15 patients (21.4%), more frequently in non-responders (32.4% vs 11.1%, p = 0.001). Baseline total HCF count was the strongest predictor of pMA development (β = 0.465, R² = 0.324, p < 0.001), with final HCF counts showing even stronger associations (β = 0.512, R² = 0.348, p < 0.001).
Conclusions: Layer-specific HCF quantification provides valuable prognostic information for treatment response and pMA risk in chronic CSC. These biomarkers may guide therapeutic decisions and identify patients requiring closer monitoring for atrophy development.

