Article Date: 9/1/2008

Treating the Pathophysiology of Meibomian Gland Dysfunction
cultivating compliance

Treating the Pathophysiology of Meibomian Gland Dysfunction

BY VISHAKHA THAKRAR, OD , FAAO

Lid scrubs, hot compresses, oral antibiotics and artificial tears are all effective ways to manage meibomian gland dysfunction (MGD), but how many MGD patients are truly compliant with these treatments? From a clinical perspective, lack of compliance often results in unsuccessful management of this condition. Adjunctive therapy may prove useful in treating MGD.

MGD describes inflammatory or noninflammatory changes in the meibomian glands. There is a close relationship between MGD and blepharitis, as up to 74 percent of patients who have blepharitis have MGD. When blepharitis and MGD occur together, the condition is considered inflammatory.

Early signs of MGD include elevation of the orifice and blockage of the glands. The orifice may be dilated with inspissated secretions or material such as keratin. Eyelid inflammation can lead to thickening, rounding and vascularization of the lid. More severe changes result in cicatrization, notching, trichiasis and entropion. Corneal involvement includes dry eye or infiltrates.

MGD is a common cause of contact lens-related dry eye and, in many cases, leads to contact lens dropout. Slit lamp examination often reveals lens deposits, conjunctival and lid margin staining, hyperemia and keratitis sicca (KCS).

Patients who suffer from MGD often request eye drops. Topical antibiotics, steroids and steroid/antibiotic combinations often provide rapid relief, but you must exercise caution when using corticosteroids or antibiotics for extended periods of time.

More conventional treatments are limited in their ability to attack the pathophysiology of the disease. In addition, these treatments are time consuming and often result in noncompliance.

A Different Option

Cyclosporine A 0.05% (Restasis, Allergan) may be a valuable topical therapy to add to our armamentarium. Several studies have shown that Restasis increases tear production in patients whose production was presumed suppressed by ocular inflammation associated with KCS. Cyclosporine A is an immunomodulator that inhibits T-lymphocyte activation and proliferation and subsequently interferes with cytokine induction.

Inflammation can decrease tear production in the lacrimal gland and increase evaporation in patients who have MGD and blepharitis. The mechanism of MGD is not fully understood, but is probably T-cell mediated. Researchers have shown in an animal model that experimental immune mediated blepharoconjunctivitis is dependent on an antigen recognized by T-cells. Recent preliminary studies have shown that Restasis may have the potential to treat inflammation associated with MGD. Rubin and Rao (2006) demonstrated that after three months of treatment with Restasis, subjects showed an improvement in both signs and symptoms of MGD. Perry et al (2006) demonstrated improvements in the signs of MGD after three months, but no improvement in symptoms during this period. There were limitations to these preliminary studies, but they did provide information that could expand the possible treatments of MGD.

Treatment of MGD with Restasis is an off-label use of the product, but it may be a management tool in the future. By controlling the pathophysiology of MGD, we can potentially improve patients' signs and symptoms to safely improve contact lens wear. CLS

For references, please visit www.clspectrum.com/references.asp and click on document #154.


Dr. Thakrar has a specialty contact lens practice and is a clinical optometrist at the TLC Laser Eye Center in Mississauga, Ontario. She is a graduate of The Ohio State University and completed a residency in cornea and contact Lenses at the New England College of Optometry.



Contact Lens Spectrum, Issue: September 2008