Managing Soft Lens-induced
Giant Papillary Conjunctivitis
BY WILLIAM L. MILLER, OD, PHD, FAAO
Not long ago, clinicians saw the demise of contact lens-induced giant papillary conjunctivitis (CLPC) as a foregone conclusion. As most were aware, protein and perhaps other deposits that coated the lens surface gave rise to CLPC, so with the advent of disposable and daily disposable lens options, we thought the end was near for this condition. However, we still observe it, much to our chagrin, usually resulting from poor patient compliance with disposable lens replacement schedules or a more rapid coating of soft contact lenses in certain patients. This is not to suggest that a more frequent replacement schedule is for naught -- most studies of shorter replacement schedules have shown a dramatic decrease in CLPC.
Signs and symptoms are relatively straightforward and consist of itching (especially after soft lens removal), mucus (inner canthus) and lens irritation from increased lens movement. Signs include palpebral conjunctival thickening and large to giant "white-capped" papillae, which sodium fluorescein stain easily highlights. Most often occurring in soft contact lens wearers (85 percent), especially those in continuous wear, it's also occurred in GP lens patients and as giant papillary conjunctivitis (GPC) in patients who have prosthetic eyes and exposed sutures. Affected soft lens wearers tend to experience more severe signs and symptoms than affected GP wearers.
The literature has reported two types of CLPC specific to either standard hydrogel soft lenses or silicone hydrogel lenses. The first type, a general CLPC, develops over the entire palpebral conjunctiva and more commonly occurs with hydrogel soft lenses.
The second is a local CLPC, confined to one or two regions of the palpebral conjunctiva, that primarily occurs in silicone hydrogel wearers. This type likely results from the higher modulus of silicone hydrogel lenses and mimics, in part, the CLPC that occurs with GP contact lenses.
How CLPC Develops
Irritative components coupled with an antigenic response set off an inflammatory cascade that includes increased levels of IgE, cytokines and chemokines. Recent work has shown that the chemokine eotaxin is a potent chemotactic agent in recruiting eosinophils. Specifically, the level of eotaxin correlates with the severity of CLPC. Ironically, this doesn't seem to occur in prosthetic eye-initiated GPC.
The time span between lens wear and observable signs and symptoms can take several weeks to months, with most cases occurring within two years of contact lens fitting. This time interval is longer in cases of GP-initiated CLPC.
The most common CLPC treatment involves discontinuing contact lens wear and, depending on severity, prescribing topical pharmaceuticals. Mast cell stabilizers are a chronic solution to CLPC, but they involve a delay in alleviating signs and symptoms.
Therefore, my current treatment of choice is a triad of antihistamine/mast cell stabilizing agents: Zaditor (CIBA Vision), Optivar (Muro Pharmaceuticals, Inc.) and Patanol (Alcon), which works well in cases of mild to moderate CLPC. For patients who don't have backup spectacles, I instruct the usual bid dosing, administering the drops 15 minutes before and after lens wear.
For severe CLPC cases, consider mild topical steroids such as Flairex (Alcon) or Lotemax (Bausch & Lomb) to ameliorate signs and symptoms before using other therapeutic measures.
Dr. Miller is on the faculty at the University of Houston College of Optometry. He is a member of the American Optometric Association and serves on its Journal Review Board. You can reach him at
Contact Lens Spectrum, Issue: January 2005