Age and refraction in 46,000 patients as a potential predictor of refractive stability after refractive surgery.

PURPOSE: To analyze the process of emmetropization and determine the potential for progression of refractive error following refractive surgery. METHODS: The prevalence of refractive error was retrospectively examined in 46,384 consecutive patients (77,124 eyes) at an outpatient clinic in Amman, Jordan. Biometry was also obtained in 4240 eyes. Correlation of axial length and corneal power as a function of age was determined based on these data. RESULTS: Patients were distributed into four distinct groups: emmetropia, hyperopia, low to moderate myopia, and high (> 6.00 diopters [D]) myopia. The prevalence of myopia was found to be 23.8%. High myopia occurred in 3.8% of patients, and 17.5% of patients were hyperopic. Patients with < 1.00 D of myopia at age 10 and < 3.00 D of myopia at the time of refractive surgery had a stable refraction at age 18. In patients with high myopia, 7.4% demonstrated a progression of corneal power and axial length that does not stabilize until age 30. Finally, the refractive error of hyperopic patients tended to progress from age 30 to age 50. CONCLUSIONS: Myopes with < 1.00 D of myopia at age 10 and < 3.00 D of myopia at the time of refractive surgery are unlikely to progress. High myopes and hyperopes have potential to progress. Patients in which the axial length of the eye exceeds 26 mm in conjunction with higher corneal powers are likely in a state of decomposition and are at risk of marked progression of refractive error following refractive surgery. The likelihood of progression should be determined prior to surgery and explained to the patient.

Refractive error and ocular biometry in Jordanian adults.

The aim of this study was to establish the prevalence of refractive errors in Jordanian adults of working age, and to study the ocular biometric correlates of refractive error in this population. Refractive error and ocular biometry were measured in 1093 Jordanian adult subjects aged 17-40 years to determine the prevalence of refractive error, and explore structural correlations of ametropia. Refractive error was measured using a Grand-Seiko GR-3100K closed-view infrared autorefractor. Ocular component measurements were made using A-scan ultrasonography and autokeratometry. The prevalence of myopia [spherical equivalent refraction (SER) less than -0.50 DS] and hyperopia (SER greater than +0.50 DS) was 53.71 and 5.67% respectively; 40.62% of the sample was emmetropic (refraction between +0.50 D and -0.50 D inclusive in both principal meridians). The distribution of SER was found to show marked leptokurtosis, exhibiting a peak between plano and 1 D of myopia. Corneal radius, anterior chamber depth, crystalline lens thickness, vitreous chamber depth and axial length (AL) parameters were normally distributed in the population studied. AL to corneal curvature ratio was not normally distributed, and showed marked leptokurtosis. Linear regression analysis showed that AL correlated most closely with spherical equivalent refractive error. This study has established a database of refractive error prevalence and ocular biometric correlates of ametropia in a Middle Eastern population of working age.

A novel locus for Usher syndrome type I, USH1G, maps to chromosome 17q24-25.

Usher syndrome (USH) is an autosomal recessive disorder associated with sensorineural hearing impairment and progressive visual loss attributable to retinitis pigmentosa. This syndrome is both clinically and genetically heterogeneous. Three clinical types have been described of which type I (USH1) is the most severe. Six USH1 loci have been identified. We report a Palestinian consanguineous family from Jordan with three affected children. In view of the combination of profound hearing loss, vestibular dysfunction, and retinitis pigmentosa in the patients, we classified the disease as USH1. Linkage analysis excluded the involvement of any of the known USH1 loci. A genome-wide screening allowed us to map this novel locus, USH1G, in a 23-cM interval on chromosome 17q24-25. The USH1G interval overlaps the intervals for two dominant forms of isolated hearing loss, namely DFNA20 and DFNA26. Since several examples have been reported of syndromic and isolated forms of deafness being allelic, USH1G, DFNA20, and DFNA26 might result from alterations of the same gene. Finally, a mouse mutant, jackson shaker ( js), with deafness and circling behavior has been mapped to the murine homologous region on chromosome 11.