Persistent Inflammation After Anti-Tubercular Therapy in Tubercular Serpiginous-Like Choroiditis: A Multivariate and Network-Based Risk Analysis.

PURPOSE: Antitubercular therapy (ATT) for tubercular serpiginous-like choroiditis (TB-SLC) is well-established, but not infallible. In this study, we investigated the risk factors underlying persistent inflammation after ATT in TB-SLC patients.

METHODS

We retrospectively reviewed consecutive TB-SLC patients, who completed ≥6 months of ATT. The primary outcome measure was persistent inflammation at the completion of ATT. The risk factors for persistent inflammation were analyzed using multivariate logistic regression. Additionally, a categorical network analysis was performed to explore the relationships among key clinical variables. The anti-inflammatory therapy was quantified as total immunosuppressive load (TIL) by scoring systemic and local corticosteroid treatments.

RESULTS

Sixty-five patients, 71% (n = 46) males, with a median age of 33 ± 11.1 years, 45% (n = 29) bilateral, were included. Twelve patients (18.5%; 17 eyes [18.1%]) had ongoing inflammation at the conclusion of ATT. In multivariate regression analysis, the mean TIL at month 1 (adjusted odds ratio, 0.64; 95% confidence interval, 0.43-0.97; P = 0.04) and persistent inflammation at month 3 of ATT (adjusted odds ratio, 13.44; 95% confidence interval, 1.61-111.92; P = 0.02) were risk factors for persistent inflammation after ATT. Network analysis revealed strong mutual associations among low 1-month TIL, persistence at 3 months, paradoxical worsening, and 6-month ATT duration.

CONCLUSIONS

Initial immunosuppression offers protection, and ongoing inflammation during therapy increases the risk of persistent inflammation after ATT. Paradoxical worsening and shorter ATT duration may affect these risk factors.

TRANSLATIONAL RELEVANCE: Persistent inflammation after antitubercular therapy for tubercular serpiginous-like choroiditis is mainly determined by nonmicrobial factors, most notably the level of immunosuppression at the start of antitubercular therapy.