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Topical Cyclosporine Use in Meibomian Gland Dysfunction

US Sensory Disorders Review, 2006:17-9 DOI:
Received: January 11, 2011 Accepted: January 11, 2011

Dry eye syndrome is a common disorder that results from decreased tear production, excessive tear evaporation, or abnormality in mucin or lipid components of the tear film. Accepted science states that the tear film comprises three layers: a superficial thin lipid layer produced by the meibomian glands, a middle thick aqueous layer produced by the main lacrimal glands, and an innermost hydrophilic mucin layer produced by both the conjunctiva goblet cells and the ocular surface epithelium.1

The lipid layer produced by the meibomian glands acts as a surfactant. It may also act as a barrier against foreign particles and may have some antimicrobial properties. These glands contain both polar lipids and nonpolar lipids. Increased evaporative loss is predominantly due to meibomian gland dysfunction (MGD).

Dry eye syndrome affects a significant percentage of the population, especially people 40 years old and older. Estimates put the number of people affected in the US at somewhere between 10–14 million, with similar incidence rates outside the US. While the disease may be more common in women, it is not affected by race. It can be caused by decreased tear production, excessive tear production, or an abnormality in the production of mucus or lipids normally found in the tear layer.2

Some physicians report that one in four patients at eye clinics complain of symptoms of dry eye, making it one of the most common complaints seen by ophthalmologists.3 MGD is a widespread and chronic problem often associated with dry eye syndrome, and may be referred to as posterior blepharitis as well.MGD involves the obstruction and inflammation of the glands and may occasionally be caused by gland atrophy.4 The meibomian gland is an androgen target organ; androgen deficiency may promote meibomian gland dysfunction and evaporative dry eye.5

There are other sequelae of MGD that ophthalmologists often see, such as chalazia, punctuate keratoplasty, pannus, phlyctenules, and recurrent conjunctivitis. Possible symptoms of MGD include ocular burning, irritation, fleeting pain, itching, dryness, grittiness, or foreign-body sensation. Other symptoms may include sensitivity to light and excessive blinking. Symptoms of the disease can be exacerbated by smoky or dry environments, indoor heating, or by excessive reading or computer usage. Patients with MGD may also complain of redness of the eyelids and conjunctiva; symptoms tend to be worse upon awakening in the morning. Dry eye syndrome symptoms tend to be more pronounced in the evening.1

Current treatment for MGD includes lid hygiene, oraltetracycline, doxycycline or minocycline, topical erythromycin or bacitracin ointments, homogenized castor oil eye drops, and topical corticosteroids.4

Antibiotic ophthalmic ointments such as erythromycin and bacitracin are used nightly for about 7–10 days to decrease the number of bacteria that break down the lipid layer of a patient’s tear film. Oral antibiotics, most notably tetracycline and doxycycline, help decrease the number of bacteria and help make the oil more fluid so it can flow out of the oil glands more easily.2

Cyclosporine is a highly specific immunomodulator that primarily affects T-lymphocytes, and it does not inhibit the phagocytic system as much as corticosteroids. It is not an inhibitor of wound healing, nor does it produce lens changes, and it therefore has a favorable safety profile. Topical cyclosporine has been used in numerous ophthalmic indications, including post-keratoplasty allograft rejection and corticosteroidinduced glaucoma, Thygeson’s keratitis, and superior limbic keratoconjunctivitis, among others.6

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