Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydrogel keratophakia is a new form of lamellar refractive surgery which, in theory, can deal with almost all forms of refractive error. We examined the histopathological effects of several types of hydrogel materials on the cornea of non-human primates. With the exception of one type of hydrogel material, which was associated with endothelial cell degeneration, only minor histopathologic changes were seen up to a maximum of one year of observation, including thinning of the epithelium and decreased population of stromal keratocytes. These changes did not correlate with any clinical abnormalities. Additional extensive preclinical testing and eventual human clinical trials will determine the safety and efficacy of this procedure.
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PMID:Pathology of corneal hydrogel alloplastic implants. 405 90

It is known that when hyperopic or myopic defocus is imposed on chick eyes by spectacle lenses, they rapidly compensate, becoming myopic or hyperopic respectively, by altering the depth of their vitreous chamber. Changes in two components--ocular length and choroidal thickness--underlie this rapid compensation. With monocular lens treatment, hyperopic defocus imposed by negative lenses resulted in substantially increased ocular elongation and a slight thinning of the choroid, both changes resulting in myopia; myopic defocus imposed by positive lenses resulted a dramatic increase in choroidal thickness, which pushed the retina forward toward the image plane, and a slight decrease in ocular elongation, both changes resulting in hyperopia. The refractive error after 5 days of lens wear correlated well with vitreous chamber depth, which reflected the changes in both choroidal thickness and ocular length. The degree of compensation for lenses was not affected by whether the fellow eye was covered or open. Both form-deprivation myopia and lens-induced myopia declined with age in parallel, but wearing a -15 D lens produced more myopia than did form deprivation. The spectacle lenses affected the refractive error not only of the lens-wearing eye, but also, to a much lesser degree, of the untreated fellow eye. At lens removal refractive errors were opposite in sign to the lense worn, and the subsequent changes in choroidal thickness and ocular length were also opposite to those that occurred when the lenses were in place. In this situation as well, effects of the spectacle lenses on the fellow eyes were observed. Eyes with no functional afferent connection to the brain because of either prior optic nerve section or intraocular tetrodotoxin injections showed compensatory changes to imposed defocus, but these were limited to compensation for imposed myopic defocus, at least for the eyes with optic nerve section. In addition, optic nerve section, but not tetrodotoxin treatment, moved the set-point of the visual compensatory mechanism toward hyperopia. Optic nerve section prevents myopia in response to negative lenses but not to diffusers, suggesting that compensation for hyperopia requires the central nervous system.
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PMID:Choroidal and scleral mechanisms of compensation for spectacle lenses in chicks. 761 May 79

A 24-year-old man presented with narrow, linear areas of thinning situated horizontally in the upper part of both corneas. These areas were associated with progressive corneal ectasia, causing high degrees of "against the rule" astigmatism. By excising the affected areas, the refractive error was significantly improved in both eyes. Features of the disease suggested that the condition was related to the other ectatic corneal dystrophies.
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PMID:Bilateral linear corneal ectasia. An unusual case and its surgical management. 771 29

Most of the 19 cases of high myopia with esotropia fixus had the refractive error in childhood while esotropia fixus set in progressively during middle age. The eyeball was fixed in a position of marked adduction, and the forced duction test was positive. Electromyography showed normal innervation of the medial and lateral recti. Contracture of the medial rectus and thinning of the lateral rectus were observed during surgery. Histopathological examination revealed degeneration and fibrosis in the medial rectus. Etiology was not clear. Tenotomy of the medial rectus or that of the inferior rectus in addition, with fixation of the lateral rectus tendon to the lateral orbital rim produced satisfactory corrective results.
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PMID:[High myopia with esotropia fixus]. 816 91

A 33-year-old woman had progressive blurred vision 2 weeks after uneventful laser in situ keratomileusis surgery. Initial satisfactory uncorrected visual acuity (UCVA) was complicated by postoperative dry eye and drug toxicity. Slitlamp biomicroscopy revealed diffuse punctate epithelial keratitis and inferior corneal epithelial defect with rolled-up epithelium on the flaps and the inferior unoperated cornea in both eyes. Diffuse inflammatory cell infiltrates were evident in the stroma. Stromal thinning was evident on serial Orbscan (Bausch & Lomb) and pachymetry examinations, and a hyperopic shift of almost +6 diopters was observed in the refractive error in both eyes. These examinations showed a gradual recovery of stromal thickness after copious hydration with balanced salt solution. The UCVA was 1.0 in both eyes after corneal rehydration.
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PMID:Toxic keratopathy-related corneal dehydration after laser in situ keratomileusis. 1612 7

Orthokeratology (OK) is a clinical technique that uses specially designed rigid contact lenses to reshape the cornea to temporarily reduce or eliminate refractive error. This article reviews the history of traditional daily-wear OK (1960s to 1980s) and discusses the reasons for the recent resurgence in interest in the new modality of overnight OK, using reverse-geometry lens designs (1990s to the present). The clinical efficacy of the current procedure is examined and outcomes from clinical studies in terms of refractive error change and unaided visual acuity are summarised. Onset of the effects of overnight OK lens wear is rapid, with most change after the first night of lens wear and stability of refractive change after seven to 10 days. Mean reductions in myopic refractive error of between 1.75 and 3.33 D and individual reductions of up to 5.00 D have been reported. There appear to be slight reductions or minimal changes in astigmatism with the use of reverse-geometry lenses and most patients are reported to achieve 6/6 unaided vision or better. The induction of higher order aberrations, in particular, spherical aberration, has been reported and this may affect subjective vision under conditions of low contrast and pupil dilation. Patient satisfaction with overnight OK has been reported as similar to or better than with other popular modalities of contact lens wear. Available evidence suggests that the corneal changes induced by overnight OK are fully reversible. The refractive effect in OK is achieved by central epithelial thinning and this has raised concerns about compromise of the epithelial barrier to microbial infection. Recent reports of microbial keratitis in the modality are reviewed and the overall safety of the procedure is examined critically. Recent research on stromal contributions to the OK effect, particularly relating to overnight oedema, is summarised. Emerging issues in OK, including myopic control, correction of other refractive errors and permanency of the OK effect, are discussed.
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PMID:Orthokeratology review and update. 1663 67

Keratoconus is a debilitating ocular disease characterised by progressive asymmetrical thinning of the cornea, the clear covering at the front of the eye. The resulting protrusion of the cornea results in severe refractive error, in the most severe cases requiring corneal grafting. It is a complex disease with a genetic component. Despite several reports of linked loci, major gene identification has been elusive. A genome-wide linkage scan in a large Australian pedigree with apparent autosomal dominant keratoconus was conducted using the Affymetrix 10K SNP chip and two regions of linkage identified. Functional candidate genes from within both linkage peaks were assessed for corneal expression and screened for mutations in affected family members. Equal evidence of linkage was detected to both 1p36.23-36.21 and 8q13.1-q21.11 with LOD scores of 1.9. Analysis of both loci concurrently suggests digenic linkage with two-locus LOD score of 3.4. All affected individuals carry identical haplotypes at both loci. Carriers of either linked haplotype without the other do not have keratoconus. No mutations were identified in the following candidate genes expressed in the cornea: ENO1, CTNNBIP1, PLOD1, UBIAD1, SPSB1 or TCEB1. Although the pedigree appears to demonstrate simple autosomal dominant inheritance, the disorder is actually genetically complex. This pedigree may provide a link between inherited forms of keratoconus and sporadic cases.
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PMID:Apparent autosomal dominant keratoconus in a large Australian pedigree accounted for by digenic inheritance of two novel loci. 1879 34

High-degree myopia (HM) is defined as a refractive error above -6 D (-8 diopters). An axial eyeball length above 26 mm and is also connected with excessive myopisation. Mechanical stretching and thinning of the choroids may lead to the development of irreversible degenerative changes in the eyeball and visual impairment. HM prevalence varies significantly by geographical area, ranging from 1.7-3.3%, while in highly urban regions of South-East Asia it affects up to 24% of university students. HM is not a homogenous disease. It is considered to be inherited in different patterns: dominant, autosomal recessive, and X-linked. Many genetic mutations linked to HM development have been described and the different patterns of inheritance may reflect different types of HM. Moreover, the clinical state of the HM eyeball may result from both genetic and environmental risk factors influencing the progression of the refractive error. The development and progression of HM is connected with sustained prolonged near work involving accommodation-convergence imbalance leading to retinal blur, the years spent at school, the amount of near work, especially writing and reading, which is related to slight chronic under-accommodation, and improper light stimuli in early childhood. Contemporary definitions of HM, views on etiopathogenesis, excessive axial elongation, and pathological changes within the eyeball in the course of HM leading to visual impairment are presented here. Genetic and environmental risk factors influencing the progression of HM, its significantly different prevalence in various geographical areas, and therapeutic options for the refractive error are also presented.<br />
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PMID:Etiopathogenesis and management of high-degree myopia. Part I. 1972 11

Keratoconus is a non-inflammatory, progressive thinning process of the cornea. It is a relatively common disorder of unknown etiology that can involve each layer of the cornea and often leads to high myopia and astigmatism. Computer- assisted corneal topography devices are valuable diagnostic tools for the diagnosis of subclinical keratoconus and for tracking the progression of the disease. The traditional conservative management of keratoconus begins with spectacle correction and contact lenses. Several newer, more invasive, treatments are currently available, especially for contact lens-intolerant patients. Intrastromal corneal ring segments can be used to reshape the abnormal cornea to improve the topographic abnormalities and visual acuity. Phakic intraocular lenses such as iris-fixated, angle-supported, posterior chamber implantable collamer and toric lenses are additional valuable options for the correction of refractive error. Corneal cross-linking is a relatively new method of stiffening the cornea to halt the progression of the disease. The future management of keratoconus will most likely incorporate multiple treatment modalities, both simultaneous and sequential, for the prevention and treatment of this disease.
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PMID:Keratoconus: overview and update on treatment. 2054 32

Keratoconus (KTCN) is non-inflammatory thinning and anterior protrusion of the cornea that results in steepening and distortion of the cornea, altered refractive error, and decreased vision. Keratoconus is a complex condition of multifactorial etiology. Both genetic and environmental factors are associated with KTCN. Evidence of genetic etiology includes familial inheritance, discordance between dizygotic twins, and association with other known genetic disorders. Several loci responsible for a familial form of KTCN have been mapped; however, no mutations in any genes have been identified for any of these loci. This article focuses on the genetic aspects. In addition, bioinformatics methods applied in KTCN gene identification process are discussed.
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PMID:The genetics of keratoconus. 2157 27


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