Article Date: 7/1/2002

discovering dry eye
A Long Look At the Lipid Layer
BY BARBARA CAFFERY, OD, MS, FAAO

Spending time at ARVO certainly puts a clinical researcher in her place. The number of papers on the tear film alone is overwhelming. The rooms just ooze with the brain power of the best scientific minds of the day. The trick is to take home the important information that applies to one's own area of research and to the clinical arena.

The Lipid Layer in Action

My favorite image of the meeting was the lipid layer being filmed, in vivo, using kinetic analysis of the interference pattern. Goto and Tseng filmed the central 8.0mm of the lipid layer during consecutive blinks and compared the dynamics with aqueous tear deficient (ATD), normal and ATD post-punctual occlusion subjects.

In normal patients, the tear film spread uniformly in a horizontal propagating pattern that stabilized in 0.36 seconds (±0.22). The lipid layer appeared thin, uniform and stable between blinks. The lipid layer of ATD subjects was very slow-spreading (1.73±0.42sec) and showed a non-uniform pattern. The inferior image was thick and displayed a horizontal pattern. The superior portion was thin and showed vertical streaks. The ATD subjects who had punctual occlusion showed a pattern more like the normals.

The Interconnected Tear Film

It appears that the aqueous layer is intimately involved with the lipid layer, so fixing the lipid layer may not be enough to fix the tear film. Researchers at the University of Kentucky used spectroscopy to analyze the molecular level of the tear film. The lipid leaves the meibomian glands, then undergoes structural change orchestrated by the underlying aqueous layer. These structural changes decrease the evaporation rate and increase tear film stability.

The aqueous provides an unknown substance that binds to the lipids, expelling water that enhances the barrier function of the lipid layer. The researchers found that younger subjects had more ordered lipids and lower triglycerides. The unknown aqueous substance may be secretory phospholipase A2 (sPLA2), an enzyme that hydrolyses phospholipids and produces free fatty acids in tears that in turn destabilize the tear film. A laboratory in Tokyo found higher concentrations of sPLA2 in patients with meibomian gland dysfunction.

Marso, Simonin and Guillon from the UK also suggest that lipid layer function is dependent on other chemicals in the tear film. They established that high cholesterol esters are associated with thin and inefficient lipid layers, that high phospholipid content is associated with stable tear films and that lipocalin is important for lipid layer stability.

This is not to say that improving the lipid layer composition will not enhance comfort for dry eye patients. Those of us who give out lid care instructions as often as spectacle prescriptions know that improving meibomian gland function does indeed help our patients. Shine, Mathers and McCully showed that a higher level of meibum non-polar lipids is associated with increased tear evaporation rate. As clinicians we believe that this translates into dry eye symptoms and that cleaning up the lids will change this composition.

The more creative research techniques are used to study the tear film, the more complex it becomes. The lipid layer must be created correctly, secreted appropriately and depend on the rest of the tear film to allow it to spread and form a useful evaporative barrier. We can encourage our patients to help our bodies function at their complicated best with plenty of fluids, good diet, exercise, no smoking and keep-ing the lid margins clean and clear.

Dr. Caffery has practiced optometry in Toronto, Canada, in a group setting dedicated to contact lens and tear film research since 1977.

 


Contact Lens Spectrum, Issue: July 2002