title: Relationship between aqueous humor protein level and outflow facility in patients with uveitis.
abstract: OBJECTIVE
  To determine whether there is a relationship between the aqueous humor protein level and outflow facility in patients with uveitis.
  
  
  METHODS
  Aqueous humor protein levels were determined by laser flare photometry, and outflow facility was determined by Schiotz tonography.
  
  
  RESULTS
  Thirty patients with uveitis and 10 control subjects were studied. Outflow facility was lower in patients with uveitis (0.21 +/- 0.12 microl/min x mm Hg) than in control subjects (0.33 +/- 0.05 microl/min x mm Hg, P < 0.001). Patients with uveitis and laser flare photometry results (flare) more than 20 photon units/msec (n = 21) had a lower outflow facility (0.17 +/- 0.07 microl/min x mm Hg) than patients with uveitis and flare less than 20 photon units/msec (n = 9, 0.32 +/- 0.14 microl/min x mm Hg, P = 0.004). Furthermore, no difference was identified between outflow facility in patients with active uveitis (those who had anterior chamber cells) and flare less than 20 photon units/msec and outflow in control subjects. In patients with uveitis, there was a linear correlation between flare and outflow facility (r = -0.50, P = 0.005). There was no relationship between flare measurements and either intraocular pressure or aqueous humor cell levels when scored with a clinical, semiquantitative system.
  
  
  CONCLUSIONS
  Outflow facility is significantly reduced in patients with uveitis who have high aqueous humor protein levels. Outflow facility appears to be normal in patients with active uveitis whose flare levels are low, and therefore the association between flare and outflow facility does not appear to be an indirect reflection of elevated anterior chamber cells. It is possible that elevated aqueous humor protein levels contribute to the development of uveitic glaucoma in some individuals by decreasing aqueous humor outflow facility, although a causal relationship cannot be established on the basis of this study.
authors.affiliation: Ocular Inflammatory Disease Center, Jules Stein Eye Institute, University of California Los Angeles School of Medicine, CA 90095-7003, USA.
authors.forename: J G
authors.initials: JG
authors.lastname: Ladas
authors.forename: F
authors.initials: F
authors.lastname: Yu
authors.forename: R
authors.initials: R
authors.lastname: Loo
authors.forename: J L
authors.initials: JL
authors.lastname: Davis
authors.forename: A L
authors.initials: AL
authors.lastname: Coleman
authors.forename: R D
authors.initials: RD
authors.lastname: Levinson
authors.forename: G N
authors.initials: GN
authors.lastname: Holland
mesh_terms: D000328:Adult; D000867:Anterior Chamber / Q000378:metabolism*; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001082:Aqueous Humor / Q000378:metabolism*; D005136:Eye Proteins / Q000378:metabolism*; D005260:Female; D015590:Fluorophotometry; D005901:Glaucoma / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D006801:Humans; D007429:Intraocular Pressure; D008297:Male; D014605:Uveitis / Q000150:complications / Q000378:metabolism*
chemical_list: D000959:Antihypertensive Agents; D005136:Eye Proteins