A patient on long-term topical steroid (prednisolone acetate 1%) for chronic anterior uveitis develops elevated IOP (32 mmHg). Which mechanism best explains steroid-induced ocular hypertension?
- A Increased outflow resistance in the trabecular meshwork due to accumulation of glycosaminoglycans and reduced phagocytic activity of trabecular cells ✓
- B Increased aqueous humour production due to ciliary body stimulation
- C Pupil dilation causing angle closure
- D Prostaglandin synthesis inhibition reducing uveoscleral outflow
Correct answer: A. Increased outflow resistance in the trabecular meshwork due to accumulation of glycosaminoglycans and reduced phagocytic activity of trabecular cells
Explanation
Topical corticosteroids induce ocular hypertension primarily by increasing aqueous outflow resistance at the trabecular meshwork. Steroids upregulate fibronectin and glycosaminoglycan deposition in the juxtacanalicular trabecular meshwork, reduce myocilin (MYOC) expression, inhibit metalloproteinase-mediated ECM remodelling, and impair phagocytic clearance by trabecular cells. This reduces aqueous drainage efficiency. Steroids do not significantly increase aqueous production or cause pupil dilation.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.