Abstract

BackgroundTo investigate the corneal neurotropic phenomenon in patients with lattice corneal dystrophy (LCD) with in vivo laser scanning confocal microscopy (IVCM).MethodsIVCM was performed on a total of 15 patients (28 eyes) with LCD annually at a follow-up. A collection of the data was acquired to be analyzed.ResultsAs indicated by the analysis, the LCD patients’ normal corneal stromal nerves (Grade 0) presented a decline with the prolongation of the follow-ups, corresponding to a gradual increase in grade I and II involving amyloid-wrapped nerve fibers, which demonstrated that the growing amount of amyloid deposit due to the corneal nerve invasion increased slowly over time.ConclusionsThe neurotropic phenomenon could increase with its severity in the corneal lesion of the patients with LCD, and also reflect the distribution of the corneal nerves, to some extent. IVCM provides a rapid, noninvasive way to observe the corneal nerves, which can be an efficient means of better understanding the development of LCD.

Highlights

  • To investigate the corneal neurotropic phenomenon in patients with lattice corneal dystrophy (LCD) with in vivo laser scanning confocal microscopy (IVCM)

  • The aim of this study was to observe the neurotropic phenomenon in the corneas of the patients with Lattice corneal dystrophy (LCD) using IVCM, which could provide us with a new thinking of treatment to prevent the corneal lesions

  • Patients The study was conducted in compliance with informed consent regulations and the Declaration of Helsinki; the protocol was approved by the Internal Review Board (IRB) of Shenzhen Eye Hospital; and informed consents were obtained from the patients with LCD, who numbered 15 with eligible 28 eyes for the study in Shenzhen Eye Hospital in Shenzhen of China during the period from March 2009 to March 2018

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Summary

Introduction

To investigate the corneal neurotropic phenomenon in patients with lattice corneal dystrophy (LCD) with in vivo laser scanning confocal microscopy (IVCM). Corneal dystrophy (CD) is a type of bilateral non-inflammatory hereditary disease affecting the corneal central visual axis that becomes progressively opaque. Lattice corneal dystrophy (LCD) is a hereditary disease in which the LCD Type I and IC3D described variants such as Granular Corneal Dystrophy Type I (GCD1), Granular Corneal Dystrophy Type II (GCD2), a.k.a. Avellino Corneal Dystrophy, Thiel-Behnke Corneal Dystrophy (TBCD), and Reis-Bückler Corneal Dystrophy (RBCD), caused by the mutation of human transforming growth. Zhu et al BMC Ophthalmology (2021) 21:449 factor β-induced (TGFB-I) gene located on chromosome 5 (genetic locus 5q31). These are categorized as the “superfamily” which are all autosomal dominant. Mutations of TGFB-I gene encoding for TGFB-I p are associated with variable protein aggregation and deposition (amyloid and nonamyloid aggregates) in the cornea [1]

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