EEBA Program (PDF/3MB) - EEBA - Annual Meeting

TRANSPLANTATION OF AMNIOTIC MEMBRANE IN CORNEAL ULCERS AND PERSISTENTEPITHELIAL DEFECTSR. Gržetić-LenacDepartment of Ophthalmology, Clinical Hospital Center Rijeka, CroatiaIntroduction: Corneal epithelium is known for quick process of auto renewal,in the case of minorinjury or inflammation.When the normal healing of corneal epithelium is disabled, pathologicalconditions are manifested as persistent epithelium defects, corneal ulcers and reccuring erosions,which can lead to significant vision loss. The most common indications for transplantation of amnioticmembrane are persistent epithelial defects.Methods: The prospective study included 21 patients with corneal ulcer (n=18) or reccurent erosions(n=3) unresponsive to conventional treatment.We used corneal cells surrounding the defects andpart of the amniotic membrane used for transplantation. As a control group we used cells of healthydonor corneas unsuitable for transplantation.The corneal cells and rest of tranplanted amnioticmembrane were cultivated at 370 C for 24 hours, then stored at -80 oC in organ culture (Cornea Max).The concentration of IL-1α, TNF α and VEGF were measured using comercial available ELISA system.Theconcentration of IL-1ra, sTNF and VEGF-R were also measured in supernatant of amniotic membranes.Results: In corneal cell samples we have detected 3,51 +/- 1,79 pg/ml of IL-1α, 64.27+/-31.53 pg/mlTNFα and 209.07 +/- 201.82 pg/ml of VEGF. Levels of all 3 investigated cytokines were significantlyhigher as compared to controls (p≤ 0,005). Clinically all ulcers and erosions healed. Visual acuityimproved in15 patients. Amniotic membrane contained 775.69 +/- 613.98 pg/ml of IL-1ra, 0,036 +/-0,033 pg/ml of sTNF and 175.01 +/- 166.63 pg/ml of VEGF-R.Conclusions: The use of AM in patiens with corneal ulcers and persistent epithelial defects, in whomconservative treatment had failed, seams a resonable option, having in mind that IL-1α, TNFα and VEGFlevels are increased in such eyes, and AM secrets their natural antagonists IL-1ra, sTNF and VEGF-R.86