The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform
Richard A Thoft - One of the best experts on this subject based on the ideXlab platform.
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Surgical results of penetrating keratoplasty in essential Iris Atrophy
Journal of Refractive Surgery, 1994Co-Authors: Brian M Debroff, Richard A ThoftAbstract:BACKGROUND: Results of penetrating keratoplasty in iridocorneal endothelial syndrome have been considered favorable based on past studies; however, documented results in eyes specifically with essential Iris Atrophy are lacking. METHODS: A retrospective study was performed to evaluate all patients at the University of Pittsburgh with essential Iris Atrophy who had undergone penetrating keratoplasty for corneal decompensation over 21 years (1971-1992). RESULTS: Penetrating keratoplasty had been performed on six eyes with essential Iris Atrophy for corneal decompensation. All eyes postoperatively had evidence of persistent anterior uveitis resistant to corticosteroid treatment with one or more episodes of graft reaction. Five of the six eyes (83.3%) ultimately went on to graft failure. Two of the six eyes (33.3%) rejected grafts on two separate occasions. CONCLUSIONS: Penetrating keratoplasty in essential Iris Atrophy was frequently associated with chronic anterior uveitis and immunologic graft failure.
John R. Heckenlively - One of the best experts on this subject based on the ideXlab platform.
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Interacting loci cause severe Iris Atrophy and glaucoma in DBA/2J mice
Nature Genetics, 1999Co-Authors: Bo Chang, Richard S. Smith, Michael G. Anderson, Norman L Hawes, Adriana Zabaleta, Olga Savinova, Thomas H Roderick, John R. Heckenlively, Muriel T Davisson, Simon W M JohnAbstract:Glaucomas are a major cause of blindness^ 1 . Visual loss typically involves retinal ganglion cell death and optic nerve Atrophy subsequent to a pathologic elevation of intraocular pressure (IOP). Some human glaucomas are associated with anterior segment abnormalities such as pigment dispersion syndrome (PDS) and Iris Atrophy with associated synechiae^ 2 . The primary causes of these abnormalities are unknown, and their aetiology is poorly understood. We recently characterized a mouse strain (DBA/2J) that develops glaucoma subsequent to anterior segment changes including pigment dispersion and Iris Atrophy^ 3 . Using crosses between mouse strains DBA/2J (D2) and C57BL/6J (B6), we now show there are two chromosomal regions that contribute to the anterior segment changes and glaucoma. Progeny homozygous for the D2 allele of one locus on chromosome 6 (called ipd ) develop an Iris pigment dispersion phenotype similar to human PDS. ipd resides on a region of mouse chromosome 6 with conserved synteny to a region of human chromosome 7q that is associated with human PDS ( ref. 4 ). Progeny homozygous for the D2 allele of a different locus on chromosome 4 (called isa ) develop an Iris stromal Atrophy phenotype (ISA). The Tyrp1 gene is a candidate for isa and likely causes ISA via a mechanism involving pigment production. Progeny homozygous for the D2 alleles of both ipd and isa develop an earlier onset and more severe disease involving pigment dispersion and Iris stromal Atrophy.
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interacting loci cause severe Iris Atrophy and glaucoma in dba 2j mice
Nature Genetics, 1999Co-Authors: Bo Chang, Richard S. Smith, Michael G. Anderson, Norman L Hawes, Adriana Zabaleta, Thomas H Roderick, John R. Heckenlively, Muriel T Davisson, Olga V. Savinova, Simon W M JohnAbstract:Glaucomas are a major cause of blindness. Visual loss typically involves retinal ganglion cell death and optic nerve Atrophy subsequent to a pathologic elevation of intraocular pressure (IOP). Some human glaucomas are associated with anterior segment abnormalities such as pigment dispersion syndrome (PDS) and Iris Atrophy with associated synechiae. The primary causes of these abnormalities are unknown, and their aetiology is poorly understood. We recently characterized a mouse strain (DBA/2J) that develops glaucoma subsequent to anterior segment changes including pigment dispersion and Iris Atrophy. Using crosses between mouse strains DBA/2J (D2) and C57BL/6J (B6), we now show there are two chromosomal regions that contribute to the anterior segment changes and glaucoma. Progeny homozygous for the D2 allele of one locus on chromosome 6 (called ipd) develop an Iris pigment dispersion phenotype similar to human PDS. ipd resides on a region of mouse chromosome 6 with conserved synteny to a region of human chromosome 7q that is associated with human PDS. Progeny homozygous for the D2 allele of a different locus on chromosome 4 (called isa) develop an Iris stromal Atrophy phenotype (ISA). The Tyrpl gene is a candidate for isa and likely causes ISA via a mechanism involving pigment production. Progeny homozygous for the D2 alleles of both ipd and isa develop an earlier onset and more severe disease involving pigment dispersion and Iris stromal Atrophy.
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essential Iris Atrophy pigment dispersion and glaucoma in dba 2j mice
Investigative Ophthalmology & Visual Science, 1998Co-Authors: Simon W M John, Richard S. Smith, Bo Chang, Norman L Hawes, Thomas H Roderick, Muriel T Davisson, Olga V. Savinova, Daniel H. Turnbull, John R. HeckenlivelyAbstract:PURPOSE. To characterize ocular abnormalities associated with Iris Atrophy in DBA/2J mice and to determine whether mice of this strain develop elevated intraocular pressure (IOP) and glaucoma. METHODS. Different approaches, including slit-lamp biomicroscopy, ophthalmoscopic examination, ultrasound backscatter microscopy, and histology were used to examine the eyes of DBA/2J mice ranging from 2 to 30 months old. lOP was measured in DBA/2J mice of different ages. RESULTS. DBA/2J mice were found to develop pigment dispersion, Iris transillumination, Iris Atrophy, anterior synechias, and elevated IOP. IOP was elevated in most mice by the age of 9 months. These changes were followed by the death of retinal ganglion cells, optic nerve Atrophy, and optic nerve cupping. The prevalence and severity of these lesions increased with age. Optic nerve Atrophy and optic nerve cupping was present in the majority of mice by the age of 22 months. CONCLUSIONS. DBA/2J mice develop a progressive form of secondary angle-closure glaucoma that appears to be initiated by Iris Atrophy and the associated formation of synechias. This mouse strain represents a useful model to evaluate mechanisms of pressure-related ganglion cell death and optic nerve Atrophy, and to evaluate strategies for neuroprotection.
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Essential Iris Atrophy, pigment dispersion, and glaucoma in DBA/2J mice.
Investigative ophthalmology & visual science, 1998Co-Authors: Simon W M John, Richard S. Smith, Bo Chang, Norman L Hawes, Thomas H Roderick, Muriel T Davisson, Olga V. Savinova, Daniel H. Turnbull, John R. HeckenlivelyAbstract:PURPOSE. To characterize ocular abnormalities associated with Iris Atrophy in DBA/2J mice and to determine whether mice of this strain develop elevated intraocular pressure (IOP) and glaucoma. METHODS. Different approaches, including slit-lamp biomicroscopy, ophthalmoscopic examination, ultrasound backscatter microscopy, and histology were used to examine the eyes of DBA/2J mice ranging from 2 to 30 months old. lOP was measured in DBA/2J mice of different ages. RESULTS. DBA/2J mice were found to develop pigment dispersion, Iris transillumination, Iris Atrophy, anterior synechias, and elevated IOP. IOP was elevated in most mice by the age of 9 months. These changes were followed by the death of retinal ganglion cells, optic nerve Atrophy, and optic nerve cupping. The prevalence and severity of these lesions increased with age. Optic nerve Atrophy and optic nerve cupping was present in the majority of mice by the age of 22 months. CONCLUSIONS. DBA/2J mice develop a progressive form of secondary angle-closure glaucoma that appears to be initiated by Iris Atrophy and the associated formation of synechias. This mouse strain represents a useful model to evaluate mechanisms of pressure-related ganglion cell death and optic nerve Atrophy, and to evaluate strategies for neuroprotection.
Atsushi Azumi - One of the best experts on this subject based on the ideXlab platform.
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Zoster sine herpete with bilateral ocular involvement.
American journal of ophthalmology, 2000Co-Authors: Makoto Nakamura, Masumi Tanabe, Yuko Yamada, Atsushi AzumiAbstract:Abstract PURPOSE: To report a case of zoster sine herpete with bilateral ocular involvement. METHOD: Case report. RESULTS: A 65-year-old man showed bilateral iridocyclitis with sectoral Iris Atrophy and elevated intraocular pressure unresponsive to steroid treatment. No cutaneous eruption was manifest on the forehead. A target region of varicella-zoster virus DNA sequence was amplified from the aqueous sample from the left eye by polymerase chain reaction. Bilateral iridocyclitis resolved promptly after initiation of systemic and topical acyclovir treatment. Secondary glaucoma was well controlled by bilateral trabeculectomy. CONCLUSIONS: Zoster sine herpete should be considered and polymerase chain reaction performed on an aqueous sample to detect varicella-zoster virus DNA for rapid diagnosis whenever anterior uveitis accompanies the characteristic Iris Atrophy, even in the case of bilateral involvement.
Antti Vannas - One of the best experts on this subject based on the ideXlab platform.
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CORNEAL ENDOTHELIAL CELLS IN ESSENTIAL Iris Atrophy
Acta ophthalmologica, 2009Co-Authors: Kirsi Setälä, Antti VannasAbstract:The specular microscope was used to study the corneal endothelium in three patients with essential Iris Atrophy and three patients with anterior mesodermal disorders with uncertain diagnose. Pleomorphic and enlarged endothelial cells were found to be typical for essential Iris Atrophy. The changes were also present in one eye with normal pressure. In the patients with other types of iridal disorder the endothelial cells were normal in form. In one of these patients high intraocular pressure and surgery had seemingly led to enlargement of the endothelial cells. According to our findings, the specular microscope is a useful aid in differentiating essential Iris Atrophy from other disorders of the Iris.
Ludovico Iannetti - One of the best experts on this subject based on the ideXlab platform.
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Progression of essential Iris Atrophy studied with confocal microscopy and ultrasound biomicroscopy: a 5-year case report.
Cornea, 2009Co-Authors: Paola Pivetti Pezzi, Marco Marenco, Pamela Cosimi, Giuseppe Mannino, Ludovico IannettiAbstract:PURPOSE The purpose of this study was to report the progression of the iridocorneal endothelial syndrome during a 5-year period in a patient with the essential Iris Atrophy variant using confocal microscopy and ultrabiomicroscopy (UBM). METHODS A 47-year-old woman was referred to us in January 2002 with suspected iridocorneal endothelial syndrome. Examination of both eyes included visual acuity, biomicroscopy, intraocular pressure measurement, gonioscopy, visual field test, and UBM. Afterward, she was examined yearly and confocal microscopy performed. RESULTS Visual acuity was 20/20 in both eyes. Examination of the right eye revealed endothelial degeneration, peripheral anterior synechiae, and Iris Atrophy around the pupil that appeared displaced to the temporal side. Biomicroscopy of the left eye was unremarkable. Posterior segment was normal in both eyes. UBM of the right eye showed thickening of the Iris adherent to the corneal endothelium. Diagnosis of essential Iris Atrophy was confirmed. One year later, the right eye showed increasing iridoendothelial adherences confirmed by UBM. Confocal microscopy revealed endothelial cell abnormalities and groups of endothelial "epithelium-like" cells with hyperreflective nuclei. In April 2007, the pupil appeared more temporally dislocated. UBM showed more extended synechiae. Confocal microscopy displayed hyporeflective opacities in the endothelial layer and many grouped keratocytic clusters in the posterior stroma. No alteration of the intraocular pressure and visual field was found during the follow-up. CONCLUSIONS UBM and confocal microscopy permit observation of any corneal and iridocorneal angle changes and evaluation of essential Iris Atrophy progression.
