Corneal distrophy Groenow-i

Gazepov, Strahil and Velickovska, Dragana and Gorgiev, Alen (2023) Corneal distrophy Groenow-i. Knowledge - International Journal Scientific Papers, 57 (4). pp. 573-578. ISSN 1857-923X

[thumbnail of CORNEAL DISTROPHY GROENOW-I] Text (CORNEAL DISTROPHY GROENOW-I)
CORNEAL DISTROPHY GROENOW-I.pdf - Published Version

Download (1MB)
Official URL: http://www.ikm.mk

Abstract

We are talking about corneal dystrophy if there is clouding of its media without them being inflamed
beforehand. Corneal dystrophies are diseases that affect the cornea, they are genetic diseases and most of them are
autosomal dominant, bilateral and affect only one layer of the cornea. The signs of the disease appear mostly in the
first decade of life, but in some forms it can also occur at an older age. About 10% of sufferers develop recurrent
corneal erosions in the third decade, while more can spend a lifetime without any noticeable symptoms. There are a
large number of corneal dystrophies, but they are still divided into three basic groups depending on the affected
layer of the cornea. The layers involved are the epithelial and subepithelial layer, Bowman's layer, stromal,
Descemet's membrane and endothelial layer. A different form of the disease has its own physical pathology, signs
and symptoms, so their treatment is also different. The mutation of the genes on different parts of the affected
chromosomes are the reason for the appearance of corneal dystrophies. Among the most common symptoms that
appear in sufferers are blurred vision, the feeling of a foreign body in the eye, repeated erosions and increased
sensitivity during the placement of corneal lenses. When repeated erosions of the cornea occur, patients feel pain,
photophobia, increased tearing of the eye, redness, a decrease in visual acuity that can lead to people waking up
from sleep. This paper explains the signs and symptoms that appear in patients with presence of Groenow stroma
corneal dystrophy type I. Granular corneal dystrophy type 1 is an autosomal dominant hereditary disease. It occurs
as a result of a mutation of the TGFBI (transforming growth factor beta induced) gene. Heterozygotes have a milder
form of the disease than homozygotes. Histologically, accumulations outside the cells of the cornea can be seen in
the form of crystalloid orange-amorphous hyaloid. The diagnosis and therapy is variable and depends on the type of
corneal dystrophy, the mutated genes that contribute to its development, as well as the damaged layer of the cornea.
The leading symptom is the clouding of the cornea, which leads to a decrease in visual acuity, but there are also
patients who are asymptomatic and corneal changes can be detected during an ophthalmological examination with a
slit lamp. Granular corneal dystrophy is manifested by photophobia and progressive vision loss. They appear in the
first decade of life, and begin to bother the patient and become visible in puberty. Repetitive erosions occur less
often in this form of ocular dystrophy, and the sensitivity of the cornea gradually decreases. On examination, white
milky opacities in the form of grains located under Bowman's membrane can be seen, and the cornea between the
grains is transparent. The central parts of the cornea are affected and gradually over many years it spreads towards
the periphery and penetrates deeper into the cornea. This form of dystrophy is diagnosed with the help of symptoms
as well as corneal changes, histological results, and maybe with electron microscopy where intraepithelial
cytoplasmic granules in a rod or trapezoid shape can be observed. There is no medicine that could stop the
progression of the disease. Lamellar or penetrating keratoplasty is the primary therapy. Surgical treatment is
undertaken when visual acuity becomes unusable, which is usually around age 40. In other forms of corneal
dystrophy, therapy mainly consists in treating recurrent corneal erosions. Application of local ointments, hypertonic
agents, therapeutic contact lenses as non-conservative methods, while the invasive treatment includes lamellar
keratoplasty, anterior stromal puncturing, superficial keratectomy, photorefractive keratectomy, diamond polishing
("diamond burr polishing"). As a non-invasive therapy that gives good success is therapy with an autonomous serum
containing fibronectin, which prevents recurrent erosion, improves vision by gradually removing the opacity of the
cornea, as well as reducing the pain that appears during corneal erosion.
Keywords: dystrophy, cornea, genes, Groenow type I, keratoplasty.

Item Type: Article
Impact Factor Value: 1/62
Subjects: Medical and Health Sciences > Basic medicine
Divisions: Faculty of Medical Science
Depositing User: Strahil Gazepov
Date Deposited: 11 Apr 2023 10:11
Last Modified: 23 Aug 2023 09:27
URI: https://eprints.ugd.edu.mk/id/eprint/31651

Actions (login required)

View Item View Item