| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6196826 | Experimental Eye Research | 2014 | 9 Pages |
â¢Time-dependent changes in the chalazion lipidome were observed.â¢They start with a fast accumulation of free cholesterol in the tissue.â¢Then, normal meibomian lipids are replaced with the lipids similar to those of macrophages.â¢Lowering cholesterol is proposed to counteract these degenerative transformations.
The aim of this prospective study was to conduct histopathologic and lipidomic analyses of chalazia, in order to evaluate time-dependent changes in the lesion. Samples of surgically excised chalazia were collected over a period of 12Â months from 10Â patients (mean age 41Â years; range, 23-58) with clinically diagnosed chalazia, who underwent scheduled surgery. The ages of chalazia varied from 2 to 28Â weeks. To confirm the clinical diagnoses, the morphology of collected tissue samples was evaluated histologically after hematoxylin and eosin staining. The lipids from individual chalazia were analyzed by high-performance liquid chromatography-mass spectrometry and compared with authentic lipid standards and with the lipids of meibum collected from normal controls. We observed gradual, lesion age-dependent transformation of the lipidome of chalazia from an almost normal meibum-like composition to a very different kind of lipidome. A rapid initial increase in the free cholesterol content was followed by a gradual replacement of extremely long chain meibomian-type lipids with a mixture of shorter-chain cholesteryl esters of the C14-C18 family, triacylglycerols, ceramides, phospholipids and sphingomyelins. In addition, a rapid disappearance of wax esters and cholesteryl esters of (1-O)-acyl-omega-hydroxy fatty acids from the lipidome of aging chalazia was observed. Our results are indicative of dramatic, time-dependent changes in the lesion that may involve cholesterol as a trigger and/or a marker of subsequent degeneration of the meibomian lipidome. We hypothesize that early inhibition of these transformations may be useful in reversing the course of the disease.
