Ritonavir-Induced Ocular Hypertension Mimicking Late Dsaek Rejection: All That Glitters Is Not Gold

To describe a late Descemet’s stripping automated endothelial keratoplasty (DSAEK) graft oedema that clinically simulated immunological rejection but was caused by a pharmacokinetic interaction between topical dexamethasone and ritonavir, creating a management scenario in which steroid escalation led to rapid deterioration and withdrawal resulted in complete recovery.

Tertiary referral Cornea and Anterior Segment Unit, II Ophthalmology Department, Aristotle University of Thessaloniki, Greece.

A 55-year-old man presented with painless visual deterioration four years after uncomplicated DSAEK for Fuchs endothelial dystrophy. The graft had remained clear on long-term low-dose topical dexamethasone with stable intraocular pressure (IOP). Ritonavir had been introduced into his antiretroviral therapy three months earlier. Corrected distance visual acuity decreased from 0.22 to 0.46 logMAR and IOP was 28 mmHg. Slit-lamp examination demonstrated central and inferior graft oedema with a clear graft–host interface and no anterior chamber inflammation, a clinical picture highly suggestive of endothelial rejection. Intensive topical corticosteroid therapy was initiated, followed by rapid worsening with IOP elevation to 40 mmHg, increasing corneal oedema and epithelial bullae. Systemic medication review identified ritonavir, a potent cytochrome P450 3A4 inhibitor, as the trigger for a severe steroid-induced ocular hypertensive response. Corticosteroids were discontinued, antiglaucoma therapy was initiated and the antiretroviral regimen was modified in collaboration with infectious disease specialists. IOP normalised within days with progressive graft clearing. At three months, corrected distance visual acuity recovered, the graft remained compact and transparent and anterior segment optical coherence tomography confirmed complete anatomical restoration.

Not all late post-DSAEK oedema represents rejection. Systemic cytochrome P450 3A4 inhibition can transform a safe maintenance steroid regimen into an acute ocular hypertensive crisis that perfectly mimics graft failure. Recognising this entity is crucial, as the correct management is steroid withdrawal rather than escalation, leading to full visual and anatomical recovery and prevention of unnecessary graft-directed treatment.