THERE HAS BEEN debate within the literature regarding contact lenses potentially inducing low levels of inflammation and the relevance of this inflammation to contact lens discomfort (CLD) (Efron, 2017). Numerous studies have tried to link CLD to levels of biomarkers such as cytokines (Masoudi et al, 2017; Willcox et al, 2015), complement (Masoudi et al, 2017), and histamine (Liu et al, 2009), but most studies have not found a relationship between these markers of inflammation and CLD (Willcox, 2017).

 Still, anti-inflammatory therapy is often considered by practitioners to manage CLD, despite the absence of strong evidence of a correlation (Papas et al, 2013). There have been few well-designed clinical investigations of the use of anti-inflammatory therapies to manage CLD.

One study involving 76 female soft contact lens wearers examined oral supplementation with evening primrose oil, which contains high levels of gamma-linolenic acid (GLA), an omega-6 essential fatty acid (EFA) (Kokke et al, 2008). GLA is metabolized to dihomo-gamma-linolenic acid, which leads to increased production of anti-inflammatory eicosanoids.

The study participants rated significant improvements in symptoms of dryness at the three- and six-month visits and overall contact lens comfort at the six-month visit. Unfortunately, the study lacked any biochemical analysis to see whether changes in inflammatory markers occurred during treatment, whether in tears or otherwise.

One randomized, placebo-controlled clinical trial specifically investigated anti-inflammatory therapy in patients with CLD and its effect on tear film markers (Downie et al, 2018). Participants diagnosed with CLD using the Contact Lens Dry Eye Questionnaire (CLDEQ)-8 were randomized to receive a 12-week course of either an oral supplementation or topical treatment: oral placebo (olive oil), oral long-chain omega-3 EFA, oral long- and short-chain omega-3 EFA, or topical long-chain omega-3 EFA.

Long-chain omega-3 EFAs were derived from fish oil, while the short-chain forms were from flaxseed oil. Importantly, at the end of the 12-week period, the placebo group that received oral olive oil then received a two-week course of topical 0.1% fluorometholone alcohol drops three times a day, a known means to reduce ocular surface inflammation. This study design allowed for comparisons of the omega-3 EFA interventions versus a “gold-standard” corticosteroid therapy, which would typically be employed.

The authors reported that, when compared to baseline, some proinflammatory cytokines, including IL-17A and IL-6, were reduced by similar proportions after 12 weeks of long-chain omega-3 supplementation (whether oral or topical) followed by a two-week course of topical corticosteroids. This was a significant finding, as supplementation orally or topically with omega-3 EFA is obviously preferable as a long-term strategy for managing inflammation on the ocular surface, considering the potential side effects from chronic topical steroids.

From the perspective of patient symptoms, the oral long-chain omega-3 supplementation was the only intervention that resulted in significantly improved CLD symp-toms, with a clinically meaningful 7.3-unit (approximately 42%) reduction on the CLDEQ-8 questionnaire compared to the oral placebo group (–3.5 units, approximately 19%) at week 12. Although the topical corticosteroid showed notable improvements in the tear biomarkers, there was no significant change in CLDEQ-8 score after two weeks of use (Downie et al, 2018).

The authors concluded that omega-3 EFA is an effective anti-inflammatory therapy for CLD; further, data for topical omega-3 treatment suggest a localized anti-inflammatory treatment may be appropriate for mild ocular surface inflammation.

Management of CLD is critical to ensuring that patients continue to be long-term contact lens wearers. Managing low levels of inflammation, whether through pharmaceutical or oral supplementation, as a path to improving CLD should be considered by clinicians.

References

1. Efron N. Contact lens wear is intrinsically inflammatory. Clin Exp Optom. 2017 Jan;100:3-19.

2. Masoudi S, Zhao Z, Stapleton F, Willcox M. Contact Lens-Induced Discomfort and Inflammatory Mediator Changes in Tears. Eye Contact Lens. 2017 Jan;43:40-45.

3. Willcox MD, Zhao Z, Naduvilath T, Lazon de la Jara P. Cytokine changes in tears and relationship to contact lens discomfort. Mol Vis. 2015 Mar 15;21:293-305.

4. Liu Q, McDermott AM, Miller WL. Elevated nerve growth factor in dry eye associated with established contact lens wear. Eye Contact Lens. 2009 Sep;35:232-237.

5. Willcox MD. Is There a Role for Inflammation in Contact Lens Discomfort? Eye Contact Lens. 2017 Jan;43:5-16.

6. Papas EB, Ciolino JB, Jacobs D, et al; members of the TFOS International Workshop on Contact Lens Discomfort. The TFOS International Workshop on Contact Lens Discomfort: report of the management and therapy subcommittee. Invest Ophthalmol Vis Sci. 2013 Oct 18;54:TFOS183-TFOS203.

7. Kokke KH, Morris JA, Lawrenson JG. Oral omega-6 essential fatty acid treatment in contact lens associated dry eye. Cont Lens Anterior Eye. 2008 Jun;31:141-6;quiz 170.

8. Downie LE, Gad A, Wong CY, et al. Modulating Contact Lens Discomfort With Anti-Inflammatory Approaches: A Randomized Controlled Trial. Invest Ophthalmol Vis Sci. 2018 Jul 2;59:3755-3766.