Decay-accelerating factor in tears of contact lens wearers and patients with contact lens-associated complications

Purpose: Complement activation fragments have been detected in the anterior segment during 1) eye closure, 2) contact lens wear, and 3) in some contac t lens-associated pathologies. The decay-accelerating factor (DAF), a membr ane-associated complement regulatory protein that inhibits the central C3 a mplification convertases of the cascade, is present on both the ocular surf ace and in tears. In this study, we measured levels of tear DAF in asymptom atic contact lens patients and in patients who presented with contact lens- associated complications. Methods: Tears were collected from 55 patients us ing capillary pipettes. Subjects included normal non-contact lens wearing c ontrols (N = 14), asymptomatic soft (N = 13) and rigid gas permeable (N = 5 ) wearers, and individuals with contact lens-induced acute red eye (CLARE) (N = 4), ulcerative keratitis (N = 3), giant papillary conjunctivitis (GPC) (N = 8), contact lens peripheral ulcers (N = 3), and infiltrative keratiti s (N = 5). Levels of DAF were assessed using a two-site immunoradiometric a ssay using anti-DAF monoclonal antibodies. Results: The mean concentration of DAF in normal controls was found to be 149 +/- 78 ng/ml, 117 +/- 59 ng/m l, and 111 +/- 86 ng/ml for noncontact lens patients, and asymptomatic soft and rigid gas permeable lens wearers, respectively. In the conditions of G LARE, infiltrative keratitis, and GPC, DAF concentrations were significantl y reduced compared with normal noncontact lens controls. Compared with asym ptomatic soft lens patients, the condition of infiltrative keratitis showed a significant reduction in tear DAF. Conclusions: This study documents a t rend toward decreased levels of tear DAF in patients with the contact lens associated inflammatory conditions GLARE, GPC, and infiltrative keratitis. Tears of patients with infiltrates show the most significant reduction of t ear DAF. The reductions may be associated with enhanced complement activati on contributing to the pathogeneses of infiltrative keratitis and associate d ocular surface diseases.