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Corneal Disorders
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Darren S. J. Ting, Rashmi Deshmukh, Daniel S. W. Ting, Marcus Ang
Keratoconus is the most common corneal ectactic disorder, with an estimated prevalence of 13.3–265 per 100,000 population.135 Traditionally, depending on the severity of the disease, keratoconus is managed with glasses, CL, intracorneal ring segments (ICRS), and corneal transplantation, if all measures fail.136 However, the innovation of corneal collagen cross-linking (CXL) in 2003 has revolutionized the management of keratoconus as it could halt the disease progression.137 That said, treatment success relies on early detection of the disease as CXL does not reverse the progression of keratoconus.138
Skin problems in infancy and old age
Published in Ronald Marks, Richard Motley, Common Skin Diseases, 2019
The condition rarely starts before 4–6 weeks of age and usually begins between the ages of 2 and 3 months. It may first show itself on the face, but spreads quite quickly to other areas, although the napkin area is conspicuously spared – presumably as a result of the area being kept moist. The ability to scratch develops after about 6 months of age and the appearance of the disorder alters accordingly, with excoriations and lichenification. At this time, the predominantly flexural distribution of the disorder begins, with thickened, red, scaly and excoriated (and sometimes crusted and infected) areas in the popliteal and antecubital fossae. The eyes are often affected, eye rubbing being the probable cause of sparseness of eyebrows and eyelashes. It may also be the cause of corneal softening (keratomalacia) and its deformity (keratoconus). For more severely affected infants topical tacrolimus (Protopic®) or pimecrolimus (Elidel®) has proved helpful. Emollients are important in management and mothers should be carefully instructed on their benefit and how to use them. Similarly, bathing should be quick ‘dunks’ in lukewarm water, with patting dry, rather than long-lasting hot scrubs with vigorous towelling afterwards. Weak topical corticosteroids only should be used – 1 per cent hydrocortisone and 0.1 per cent clobetasone butyrate are appropriate. Preparations of 1 per cent hydrocortisone containing urea are helpful.
The cornea
Published in Mary E. Shaw, Agnes Lee, Ophthalmic Nursing, 2018
Keratoconus or conical cornea is due to a congenital weakness of the cornea, manifesting itself in the early teens. It can be associated with conditions such as eczema, learning disability or blindness as sufferers of these conditions tend to rub their eyes.
Corneal ectasia associated with posterior lamellar opacification
Published in Ophthalmic Genetics, 2021
Madeline Yung, Angela C. Chen, Doug D. Chung, Alice Barrington, Junwei Zhang, Ricardo F. Frausto, Otavio A. Magalhaes, Anthony J. Aldave
Corneal ectatic disorders such as keratoconus and keratoglobus are characterized by progressive corneal thinning, steepening, and visual distortion (1,2). In keratoconus, disruption of the anterior corneal lamellae results in conical thinning greatest at the corneal apex, myopia, irregular astigmatism, Descemet membrane tears with acute hydrops, and anterior stromal scarring (3,4). Keratoconus is a complex disorder, associated with variants in over 60 genes, as well as non-ocular conditions, such as atopic disorders and environmental factors (5). Keratoglobus presents with congenital or progressive corneal thinning greatest in the periphery, associated with acute hydrops and a predisposition to corneal perforation following trauma. Similar to keratoconus, keratoglobus is associated with a variety of systemic, environmental, and hereditary risk factors, although a genetic locus has not been identified (6–10).
Long-term results of MyoRing implantation in patients with keratoconus
Published in Clinical and Experimental Optometry, 2021
Mostafa Naderi, Farshid Karimi, Khosrow Jadidi, Seyed Aliasghar Mosavi, Mohadeseh Ghobadi, Hossein Tireh, Masoud Khorrami-Nejad
Keratoconus is a progressive, non-inflammatory and asymmetric disease of the cornea. It is bilateral in approximately 96% of cases.1 This degeneration is usually seen as the thinning of the inferior-temporal or central part of the cornea and affects both corneal surfaces.2,3 The prevalence of keratoconus is approximately 0.0003% to 2.5% different depending on the study population, race, sex, and geographical area.4–6 It usually begins at a young age and stops at the fourth decade of life.7 Treatment of keratoconus, depending on the intensity of the disease, may include spectacles,8 contact lenses,9 collagen cross-linking,10 intracorneal ring segment implantation (ICRS),,11,12 deep anterior lamellar Keratoplasty (DALK), and penetrating keratoplasty (PK).13,14 However, due to long-term follow-ups as well as the complications after PK surgery (graft rejection, graft infection, wound infection, and problems with the sutures), the ophthalmologist and the patient are usually less enthusiastic to pursue surgery.15
Cascade of interactions between candidate genes reveals convergent mechanisms in keratoconus disease pathogenesis
Published in Ophthalmic Genetics, 2021
In this review, while attempting to discuss genes identified to date and reviewing the evidence put forth from studies to understand the etiology of keratoconus, some novel findings have been reported. 1) Since no target genes of miR-184 had yet been identified for keratoconus, an attempt was made to identify the likely mRNA target. Seed region analysis was performed on miR-184 leading to the identification of a seed GGACGGA essential for the predicted binding of the miRNA-184 with RAB3GAP1 mRNA which also happens to be one of the candidate genes of keratoconus. 2) Keratoconus pathway was elucidated for the first time using genes identified to date and detected the presence of direct cross-talk between known candidate genes of keratoconus and remarkably, 28 known candidate genes have a direct relationship among themselves that involves direct protein-protein binding, regulatory activities such as activation and inhibition, chaperone, transcriptional activation/co-activation, and enzyme catalysis. 3) gene-protein, protein-protein, miRNA-mRNA, expression influence, and up/downstream activations have been described for each candidate gene of keratoconus. The relationships and pathways have been described more specifically in the context of keratoconus pathogenesis by bringing about one general molecular pathway linking all these genes together.