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Ocular Surface Reconstruction With Cultivated Limbal Epithelium in a Patient With Unilateral Stem Cell Deficiency Caused by Epidermolysis Bullosa Dystrophica Hallopeau-Siemens

Thanos, Melissa MD*; Pauklin, Mikk MD*†; Steuhl, Klaus-P MD*; Meller, Daniel MD*

doi: 10.1097/ICO.0b013e3181b442ea
Case Report

Purpose: To report a case of partial limbal stem cell deficiency (LSCD) caused by epidermolysis bullosa dystrophica mutilans Hallopeau-Siemens treated by transplantation of autologous ex vivo expanded limbal epithelium.

Methods: Review of the clinical findings of an 11.5-year-old boy with unilateral LSCD and epidermolysis bullosa dystrophica who underwent ocular surface reconstruction in the right eye with autologous on intact human amniotic membrane cultivated limbal epithelial cells.

Results: Twenty-eight months after reconstruction, the corneal surface is clear, smooth, and stable showing no signs of LSCD recurrence. Three subconjunctival bevacizumab (Avastin) injections reduced the recurrent growth of symblepharon and corneal vascularization. The visual acuity has increased from hand motion to 20/50.

Conclusion: Autologous transplantation of cultivated human limbal epithelial cells on intact human amniotic membrane can be a safe and effective method for corneal surface reconstruction in LSCD caused by recessive epidermolysis bullosa dystrophica.

From the *Department of Ophthalmology, University of Duisburg-Essen, Essen, Germany; and †Department of General and Molecular Pathology, University of Tartu, Tartu, Estonia.

Received for publication February 26, 2009; revision received June 8, 2009; accepted June 15, 2009.

Partially supported by the German Society of Ophthalmology (DOG), Munich, Germany; Grant ME 1623/3-1 from the Deutsche Forschungsgemeinschaft (DFG), Bonn, Germany; and Forschungsförderung AG Trockenes Auge, Berlin, Germany.

Reprint: Daniel Meller, MD, Department of Ophthalmology, University of Duisburg-Essen, Hufelandstr. 55, 45147 Essen, Germany (e-mail: daniel.meller@uk-essen.de.)

© 2010 Lippincott Williams & Wilkins, Inc.