Abstract
We thank Drs Finsterer and Zarrouk for their comments on the genetics of chronic progressive external ophthalmoplegia (CPEO), which is essentially beyond the scope of our study. 1 Karimi N Kashkouli MB Tahanian F Abdolalizadeh P Jafarpour S Ghahvehchian H. Long-term results of palpebral fissure transfer with no lower eyelid spacer in chronic progressive external ophthalmoplegia. Am J Ophthalmol. July 30, 2021; (Published online)https://doi.org/10.1016/j.ajo.2021.07.027 Google Scholar The majority of patients with CPEO have mitochondrial DNA (mtDNA) deletions or point mutations. 2 Heighton JN Brady LI Sadikovic B Bulman DE Tarnopolsky MA. Genotypes of chronic progressive external ophthalmoplegia in a large adult-onset cohort. Mitochondrion. 2019; 49: 227-231 Google Scholar We acknowledge that several nuclear DNA (nDNA) mutations can also cause CPEO. Notably, the common feature of these nDNA located genes is their role in stabilization of mtDNA replication and maintenance. 3 Fraser JA Biousse V Newman NJ. The neuro-ophthalmology of mitochondrial disease. Surv Ophthalmol. 2010; 55: 299-334 Google Scholar In this regard, CPEO can ultimately be described as a mitochondrial myopathy without contradicting its well-established genetic heterogeneity. Comment on ``Long-term results of palpebral fissure transfer with no lower eyelid spacer in chronic progressive external ophthalmoplegia''American Journal of OphthalmologyVol. 236PreviewWith interest we read the article by Karimi and associates1 about the outcome of palpebral fissure transfer (PFT) without lower eyelid spacer in 32 patients with chronic progressive external ophthalmoplegia (CPEO) by means of the margin reflex distance (MRD). It was concluded that lower eyelid retractor recession without spacer yields significant protective corneal coverage at the critical early postoperative period when the risk of keratopathy is highest.1 The study is appealing but raises comments and concerns. Full-Text PDF
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