Dataset Information

Corneal Higher Order Aberrations in Granular, Lattice and Macular Corneal Dystrophies.

ABSTRACT:

Purpose

To evaluate the corneal higher-order aberrations (HOAs) in granular, lattice and macular corneal dystrophies.

Methods

This retrospective study includes consecutive patients who were diagnosed as granular corneal dystrophy type2 (GCD2; 121 eyes), lattice corneal dystrophies type 1, type 3A (LCDI; 20 eyes, LCDIIIA; 32 eyes) and macular corneal dystrophies (MCD; 13 eyes), and 18 healthy control eyes. Corneal HOAs were calculated using anterior segment optical coherence tomography, and the correlations between HOAs and visual acuity were analyzed.

Results

HOAs of the total cornea within 4 mm diameter were significantly larger in GCD2 (0.17 ± 0.35 ?m), in LCDI (0.33 ± 0.27), LCDIIIA (0.61 ± 1.56) and in MCD (0.23 ± 0.18), compared with healthy controls (0.09 ± 0.02?m, all P < 0.01). HOAs of the total cornea within 6 mm diameter were significantly larger in GCD2 (0.32 ± 0.48), in LCDI (0.60 ± 0.46), LCDIIIA (0.83 ± 2.29) and in MCD (0.44 ± 0.24), compared with healthy controls (0.19 ± 0.06, all P < 0.001). In GCD2, there was no significant correlation between logMAR and HOAs (r = 0.113, P = 0.227). In MCD, LCDI and LCDIIIA, logMAR was positively significantly correlated with HOAs (r = 0.620 and P = 0.028, r = 0.587 and P = 0.007, r = 0.614 and P < 0.001, respectively).

Conclusions

Increased HOAs occur in eyes with corneal dystrophies, especially in eye with LCD and MCD. Larger amount corneal HOAs are associated with poorer visual acuity in patients with LCD and MCD.

SUBMITTER: Yagi-Yaguchi Y

PROVIDER: S-EPMC4990250 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Publications

Corneal Higher Order Aberrations in Granular, Lattice and Macular Corneal Dystrophies.

Yagi-Yaguchi Yukari Y Yamaguchi Takefumi T Okuyama Yumi Y Satake Yoshiyuki Y Tsubota Kazuo K Shimazaki Jun J

PloS one 20160818 8

<h4>Purpose</h4>To evaluate the corneal higher-order aberrations (HOAs) in granular, lattice and macular corneal dystrophies.<h4>Methods</h4>This retrospective study includes consecutive patients who were diagnosed as granular corneal dystrophy type2 (GCD2; 121 eyes), lattice corneal dystrophies type 1, type 3A (LCDI; 20 eyes, LCDIIIA; 32 eyes) and macular corneal dystrophies (MCD; 13 eyes), and 18 healthy control eyes. Corneal HOAs were calculated using anterior segment optical coherence tomogr ...[more]

PMID: 27536778

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Project description:The term corneal dystrophy embraces a heterogenous group of bilateral genetically determined non-inflammatory corneal diseases that are restricted to the cornea. The designation is imprecise but remains in vogue because of its clinical value. Clinically, the corneal dystrophies can be divided into three groups based on the sole or predominant anatomical location of the abnormalities. Some affect primarily the corneal epithelium and its basement membrane or Bowman layer and the superficial corneal stroma (anterior corneal dystrophies), the corneal stroma (stromal corneal dystrophies), or Descemet membrane and the corneal endothelium (posterior corneal dystrophies). Most corneal dystrophies have no systemic manifestations and present with variable shaped corneal opacities in a clear or cloudy cornea and they affect visual acuity to different degrees. Corneal dystrophies may have a simple autosomal dominant, autosomal recessive or X-linked recessive Mendelian mode of inheritance. Different corneal dystrophies are caused by mutations in the CHST6, KRT3, KRT12, PIP5K3, SLC4A11, TACSTD2, TGFBI, and UBIAD1 genes. Knowledge about the responsible genetic mutations responsible for these disorders has led to a better understanding of their basic defect and to molecular tests for their precise diagnosis. Genes for other corneal dystrophies have been mapped to specific chromosomal loci, but have not yet been identified. As clinical manifestations widely vary with the different entities, corneal dystrophies should be suspected when corneal transparency is lost or corneal opacities occur spontaneously, particularly in both corneas, and especially in the presence of a positive family history or in the offspring of consanguineous parents. Main differential diagnoses include various causes of monoclonal gammopathy, lecithin-cholesterol-acyltransferase deficiency, Fabry disease, cystinosis, tyrosine transaminase deficiency, systemic lysosomal storage diseases (mucopolysaccharidoses, lipidoses, mucolipidoses), and several skin diseases (X-linked ichthyosis, keratosis follicularis spinolosa decalvans). The management of the corneal dystrophies varies with the specific disease. Some are treated medically or with methods that excise or ablate the abnormal corneal tissue, such as deep lamellar endothelial keratoplasty (DLEK) and phototherapeutic keratectomy (PTK). Other less debilitating or asymptomatic dystrophies do not warrant treatment. The prognosis varies from minimal effect on the vision to corneal blindness, with marked phenotypic variability.

Dataset Information

Corneal Higher Order Aberrations in Granular, Lattice and Macular Corneal Dystrophies.

Purpose

Methods

Results

Conclusions

Publications

Corneal Higher Order Aberrations in Granular, Lattice and Macular Corneal Dystrophies.

Similar Datasets

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