title: Outcome of raised intraocular pressure in uveitic eyes with and without a corticosteroid-induced hypertensive response.
abstract: OBJECTIVE
  To compare the management and outcome of raised intraocular pressure (IOP) in uveitis patients with a corticosteroid hypertensive response and those who are noncorticosteroid responders and to determine the impact of intraocular corticosteroid use on IOP in uveitic eyes.
  
  
  METHODS
  Retrospective study.
  
  
  METHODS
  Eight hundred and ninety-one uveitis patients were observed in a specialized clinic over 3 months. The main outcome measures were frequency, characterization, management, and outcome of uveitis-related ocular hypertension and glaucoma.
  
  
  RESULTS
  Of 891 patients with uveitis, 191 (275 eyes) had IOP elevation (21.4%). Of these, 95 (34.5%) eyes had glaucoma. IOP elevation attributed to corticosteroid-response (61.1%) was controlled more easily than that resulting from other causes (38.9%), requiring fewer eye drops (mean, 2.06 vs 2.52; P = .009) and less filtration surgery (8.9% vs 22.4%). Among eyes with uveitis and raised IOP, elevated IOP developed in 18 eyes (6.5%) after intravitreal triamcinolone, including 64.7% to 30 to 39 mm Hg and 35.3% to 40 mm Hg or more. Prostaglandin analogs were used in 49.2% of 246 eyes; no increase in inflammation was seen in these eyes.
  
  
  CONCLUSIONS
  In this tertiary center series, most instances of raised IOP were attributable to corticosteroid response. Raised IOP induced by corticosteroid response was controlled more easily and less often resulted in optic nerve or visual field changes of glaucoma. Although intravitreous triamcinolone was associated with substantial risk of corticosteroid-response IOP elevation, all cases were controlled medically without experiencing glaucomatous injury. Prostaglandin-induced uveitis was not observed despite extensive use of prostaglandin IOP-lowering agents.
authors.affiliation: Department of Clinical Ophthalmology, Institute of Ophthalmology, Moorfields Eye Hospital, London, United Kingdom.
authors.forename: Ahmed
authors.initials: A
authors.lastname: Sallam
authors.forename: Hiten G
authors.initials: HG
authors.lastname: Sheth
authors.forename: Zohar
authors.initials: Z
authors.lastname: Habot-Wilner
authors.forename: Susan
authors.initials: S
authors.lastname: Lightman
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D002908:Chronic Disease; D005260:Female; D005901:Glaucoma / Q000139:chemically induced / Q000188:drug therapy; D005938:Glucocorticoids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D007429:Intraocular Pressure / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D009798:Ocular Hypertension / Q000139:chemically induced* / Q000188:drug therapy*; D011239:Prednisolone / Q000009:adverse effects / Q000627:therapeutic use; D011461:Prostaglandins F, Synthetic / Q000627:therapeutic use; D012189:Retrospective Studies; D014065:Tonometry, Ocular; D016896:Treatment Outcome; D014222:Triamcinolone Acetonide / Q000009:adverse effects / Q000627:therapeutic use; D014605:Uveitis / Q000188:drug therapy*; D055815:Young Adult
chemical_list: D000959:Antihypertensive Agents; D005938:Glucocorticoids; D011461:Prostaglandins F, Synthetic; D011239:Prednisolone; D014222:Triamcinolone Acetonide