Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PBK has become an important complication of cataract surgery and a leading indication for keratoplasty. While there are many potential causative factors, erroneous concepts of IOL positioning and design appear to have led to PBK with many iris-supported and anterior chamber lens styles. Underlying host endothelial abnormalities are an important risk factor with posterior chamber lenses. Previous studies of keratoplasty for PBK have shown variable early results in terms of graft clarity and visual rehabilitation. Specular microscopy and life-table survival analysis have been infrequently used to study endothelial and graft survival after keratoplasty. This study combined these techniques to evaluate several approaches to the original IOL at PKP for PBK. Four-hundred sixty-nine patients having PKP for PBK between 1976 and 1986 were studied in five retrospective cohorts on the basis of whether their IOL was retained, removed, or exchanged. Specular microscopy was performed prospectively on 390 patients. Survival analysis showed overall failure in 20% of IOL-removed, 24% of IOL-retained, and 16% of IOL-exchanged grafts, without significant differences. Within the retained group, however, graft failure rate for posterior chamber IOLs (6%) was significantly less than for anterior chamber (34%) and iris-supported (29%) lenses. With lens exchange, the failure rate was 8% for sutured posterior chamber lenses, 5% for one-piece anterior chamber lenses, and 24% for closed-loop anterior chamber lenses. Graft failure rates exceeded rejection rates for retained iris-supported and anterior chamber lenses, and exchanges for closed-loop anterior chamber lenses, suggesting nonimmunologic causes. The survival curve for all groups combined showed cumulative survival of 93% at 1 year, decreasing to 62% by 6 years. Survival was lowest for retained anterior chamber and iris-supported lenses and exchanged closed-loop anterior chamber lenses. Visual acuity results were best for retained posterior chamber IOL eyes and exchange for one-piece anterior chamber IOLs. Exchange for one-piece anterior chamber IOLs gave significantly better visual acuity than exchange for sutured posterior chamber IOLs. There was not a significant relationship between duration of corneal edema prior to PKP and visual outcome, refuting earlier findings. Cystoid macular edema was related to poor vision in 62% of those with visual acuity of less than 20/40 and in 36% of all patients. Specular microscopy findings at 1 year were predictive of longer term survival results. The least cell loss was for retained and exchanged posterior chamber lenses and exchange for one-piece anterior chamber lenses.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An analysis of corneal endothelial and graft survival in pseudophakic bullous keratopathy. 256 32

Although cataract surgery alone carries a risk of iatrogenic endothelial damage, IOL implantation will further increase the risk of endothelial compromise and resulting bullous keratopathy. PBK is an important consideration in the differential diagnosis of corneal disease in the pseudophakic eye and with proper treatment visual loss due to PBK is usually reversible. While seen most frequently with iris clip implants, all pseudophakes are susceptible to PBK and should be carefully observed for this disease entity.
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PMID:Pseudophakic bullous keratopathy. 405 86

Corneas with edema-related diseases lose transparency, which causes significant vision loss. This study analyzed seven aquaporins (AQPs) in normal corneas, pseudophakic/aphakic bullous keratopathy (PBK/ABK) corneas, Fuchs' dystrophy corneas, keratoconus corneas, post-cataract surgery (PCS) corneas, and normal organ-cultured corneas. RNA levels for AQP1, AQP4, and beta2-microglobulin were measured by RT-PCR. AQP1 antibody localized to stromal cells of all corneas. PBK/ABK and Fuchs' dystrophy corneas had decreased endothelial cell staining compared with normal. AQP1 mRNA was found in whole corneas and cultured stromal fibroblasts but not in isolated epithelial cells. AQP3 staining was found in basal epithelial cells of the normal, Fuchs' dystrophy, and keratoconus corneas but throughout the entire epithelium of PBK/ABK corneas. AQP4 antibody localized to endothelial cells of all corneas and in stromal cells of PBK/ABK corneas. AQP4 mRNA was identified in whole human corneas. AQP5 was found in epithelial cells of all corneas. AQP0, AQP2, and AQP9 were not found in any corneas. Normal AQP distributions were found in PCS and organ-cultured corneas, although they showed signs of swelling. Our study demonstrates that AQP abnormalities are found in PBK/ABK corneas (decreased AQP1, increased AQP3 and AQP4) and Fuchs' dystrophy corneas (decreased AQP1). Although both have vision-disrupting corneal edema, the mechanisms of fluid accumulation may be different in each disease.
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PMID:Altered expression of aquaporins in bullous keratopathy and Fuchs' dystrophy corneas. 1538 80