6 research outputs found

    Long-term changes in corneal endothelial morphology after discontinuation of low gas-permeable contact lens wear

    No full text
    Low gas-permeable contact lens wear of polymethyl methacrylate or hydroxyethyl methacrylate material is known to cause morphologic abnormalities in the corneal endothelial cell layer. These lenses were widely prescribed and successfully worn until their use was actively discouraged in the late 1980s and early 1990s. This study was designed to investigate whether discontinuation of low gas-permeable contact lens wear leads to an improvement of corneal endothelial cell morphology. METHODS: At the time of discontinuation and at least 5 years after discontinuation of low gas-permeable contact lens wear, noncontact specular photographs of the central corneal endothelium were made in 66 patients (14 male and 52 female, mean age 37.7 +/- 8.4, range 24.6-69.0). By computer analysis of endothelial photographs, parameters for polymegethism and pleomorphism were calculated, as well as cell density. RESULTS: Mean follow-up time between photographs was 6.8 years (SD 1.1). Sixty-one patients were refitted with rigid high gas-permeable contact lenses or high-water-content soft lenses, and 5 patients switched to spectacle wear. A small but significant recovery of the corneal endothelial cell morphology was found for the mean coefficient of variation of cell area, from 37.5 to 35.7 (P = 0.022), and for the coefficient of variation of the number of sides, from 13.1 to 12.4 (P = 0.004). The mean percentage of hexagonal cells increased from 54.2 to 56.2 (P = 0.013). Although the corneal endothelial cell morphology improved significantly on cessation of LGP contact lens wear, the values did not return to levels observed in normal, non-contact lens wearing individuals. During follow-up, the mean endothelial cell density decreased significantly (P = 0.001) from 2994 to 2890 (a 3.5% cell loss in 6.8 years), which is similar to the known normal age-related cell loss of 0.6% per year in non-contact lens wearing healthy individuals. CONCLUSION: Endothelial polymegethism and pleomorphism caused by PMMA or HEMA contact lens wear is partly reversibl

    Clinical and theoretical results of intraocular lens power calculation for cataract surgery after photorefractive keratectomy for myopia.

    No full text
    Item does not contain fulltextOBJECTIVES: To describe the refractive results of cataract surgery after photorefractive keratectomy (PRK) for patients with myopia, and to find a more accurate method to predict intraocular lens (IOL) power in these cases. DESIGN: Nonrandomized, retrospective clinical study. PATIENTS AND METHODS: Nine patients (15 eyes) who underwent cataract surgery after prior PRK to correct myopia were identified. The medical records of both the laser and cataract surgery centers were reviewed. MAIN OUTCOME MEASURES: Eight different keratometric values (K values; measured or calculated) were entered into 3 different IOL calculation formulas: SRK/T, Holladay 1, and Hoffer Q. The actual biometry and IOL parameters were used to predict postoperative refraction, which was compared with the actual refractive outcome. Also, the relative underestimation of the refractive change in corneal dioptric power by keratometry after PRK was calculated. RESULTS: In 7 of 15 eyes, IOL exchange or piggybacking was performed because of hyperopia. Retrospectively, the most accurate K value for IOL calculation was found to be the pre-PRK K value corrected by the spectacle plane change in refraction. Use of the Hoffer Q formula would have avoided postoperative hyperopia in more cases than the other formulas. The mean underestimation of the change in corneal power after PRK varied from 42% to 74%, depending on the method of calculation. CONCLUSION: The predictability of IOL calculation for cataract surgery after PRK can be improved by using a corrected, refraction-derived K value instead of the measured, preoperative K value

    Ultrastructural and molecular analysis of Bowman's layer corneal dystrophies: an epithelial origin?

    No full text
    PURPOSE: Two mutations (R555Q and R124L) in the BIGH3 gene have been described in anterior or Bowman's layer dystrophies (CDB). The clinical, molecular, and ultrastructural findings of five families with CDB was reviewed to determine whether there is a consistent genotype:phenotype correlation. METHODS: Keratoplasty tissue from each patient was examined by light and electron microscopy (LM and EM). DNA was obtained, and exons 4 and 12 of BIGH3 were analyzed by polymerase chain reaction and single-stranded conformation polymorphism/heteroduplex analysis. Abnormally migrating products were analyzed by direct sequencing. RESULTS: In two families with type I CDB (CDBI), the R124L mutation was defined. There were light and ultrastructural features of superficial granular dystrophy and atypical banding of the "rod-shaped bodies" ultrastructurally. Patients from three families with "honeycomb" dystrophy were found to carry the R555Q mutation and had characteristic features of Bowman's dystrophy type II (CDBII). CONCLUSIONS: There is a strong genotype:phenotype correlation among CBDI (R124L) and CDBII (R555Q). LM and EM findings suggest that epithelial abnormalities may underlie the pathology of both conditions. The findings clarify the confusion over classification of the Bowman's layer dystrophies
    corecore