Posters - CONTACT LENS INDUCED PAPILLARY CONJUNCTIVITIS IS ASSOCIATED WITH INCREASED ALBUMIN DEPOSITS ON EXTENDED WEAR HYDROGEL LENSES.

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Posters

March 2002

CONTACT LENS INDUCED PAPILLARY CONJUNCTIVITIS IS ASSOCIATED WITH INCREASED ALBUMIN DEPOSITS ON EXTENDED WEAR HYDROGEL LENSES.

Maxine E Tan, Damon Pearce, Gulhan Demirci, Isabelle Jalbert, Padmaja Sankaridurg, Mark DP Willcox. Cooperative Research Center for Eye Research and Technology, University of New South Wales, Sydney, Australia.

Purpose:

Contact lens papillary conjunctivitis (CLPC) is a milder form of giant papillary
conjunctivitis. In a recent prospective clinical study CLPC was the single most common reason for contact lens wear discontinuation. The purpose of this investigation was to determine the levels of human serum albumin (HSA), secretory IgA (sIgA) and lactoferrin on contact lenses of people with and without contact lens papillary conjunctivitis.

Method:

In-house developed and validated enzyme immunoassays that are surface specific for HSA, sIgA and lactoferrin were used. Levels of HSA, sIgA and lactoferrin on extended wear hydrogel lenses were determined. Lenses from subjects with and without CLPC were analysed. Results were analysed using non-parametric statistical analysis.

Results:

There was a significant difference (p<0.0001) between lenses from subjects with CLPC (median: 0.11 µ g/lens, range: 0-1.0 µ g/lens; n=32) compared to lenses from non-CLPC subjects (median: 0.01 µ g/lens, range: 0-1.0 µ g/lens; n=191). Lenses from six of the CLPC subjects were analysed for HSA prior to the event. There was no significant difference between these levels and HSA on the non-CLPC and CLPC lenses. sIgA was not significantly different between the CLPC group (median: 0.31 µ g/lens, range: 0.11-0.38 µ g/lens) and the non-CLPC group (median: 0.27 µ g/lens, range: 0.05-0.81 µ g/lens). Lactoferrin also showed no difference between the 2 groups (CLPC – median 0.11 µ g/lens, range: 0.02-0.20 µ g/lens; non-CLPC – median:0.11 µ g/lens, range: 0-3.5 µ g/lens).

Conclusions:

Extended wear contact lenses from subjects with CLPC have significantly more HSA on their surface. Deposits of sIgA and lactoferrin appear to not be increased during CLPC. Signs of CLPC include, inflammation and redness of the upper palpebral conjunctiva and enlarged papillae. Possibly resulting in more HSA leaking from conjunctival capillaries thus increasing the HSA tear concentration and leading to increased lens deposits. Thus, surface bound albuimn may not be an initiator of CLPC but rather a marker for the active condition. Further studies will examine whether increased HSA on the surface of the contact lens occurs prior to clinical signs of the condition. Acknowledgements: Subjects under clinical direction of Assoc. Prof. D Sweeney. Support: Australian Government CRC

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