A large-scale analysis of refractive errors in students attending public primary schools in Mexico.

A cross-sectional, retrospective study was conducted from September 2013 through July 2014 to determine the prevalence of refractive errors among students attending public primary schools in Mexico. Among 3,861,156 students at 14,566 public primary schools in all 32 states of Mexico, teachers identified reduced visual acuity in 1,253,589 (32.5%) using visual acuity measurement. Optometrists confirmed 391,498 [31.2%, mean (SD) age: 8.8 (1.9) years; 204,110 girls (52.9%)] had refractive errors using visual acuity measurement and noncycloplegic static retinoscopy. Among 288,537 (72.4%) of children with previous eyeglasses usage data reported, 241,505 (83.7%) had uncorrected refractive errors. Before prescription eyeglasses were provided, 281,891 students (72%) had logMAR visual acuity ≤ 0.2; eyeglasses corrected vision loss in 85.6% (n = 241,352) of them. Simple myopic astigmatism was the most frequent refractive error (25.7%, n = 100,545). Astigmatism > - 1.00 diopters was present in 54.6% of all students with ametropia. The anisometropia rate based on spherical equivalent difference between right and left eye ≥ 1.50 diopters was 3.9% (n = 15,402). Uncorrected refractive errors are an important issue in primary school students in Mexico. An updated study is needed to analyze the evolving trends over the past decade.

A new autosomal recessive syndrome consisting of posterior microphthalmos, retinitis pigmentosa, foveoschisis, and optic disc drusen is caused by a MFRP gene mutation.

PURPOSE: To describe the clinical and genetic characteristics of a new ophthalmic syndrome, which consists of posterior microphthalmos, retinitis pigmentosa, foveoschisis, and optic disc drusen, that segregates as an autosomal recessive trait in a family with four affected siblings. The membrane-type frizzled-related protein (MFRP) and CEH10 homeodomain-containing homolog (CHX10) genes, previously implicated in autosomal recessive forms of nanophthalmos/microphthalmos, were analyzed as candidate genes for this novel disease. METHODS: Complete ophthalmologic examinations were performed in four affected siblings and their parents. Ophthalmologic manifestations, fundus photographs, ultrasonographic (US) assessment, electroretinography (ERG), fluorescein retinal angiography (FA), Goldmann kinetic perimetry (GKP), and optical coherence tomography (OCT), as well as mutational status of MFRP and CHX10 genes in genomic DNA. RESULTS: In all affected siblings, ophthalmologic examination demonstrated normal horizontal corneal diameters and high hyperopia; funduscopy, ERG, and FA evidenced a progressive retinal dystrophy compatible with retinitis pigmentosa; A- and B-mode ultrasonography revealed decreased axial eye length and optic disc drusen; OCT showed localized macular retinoschisis. MFRP molecular analysis disclosed a one base pair insertion in exon 5 (c.498_499insC) in all affected individuals, a mutation that predicts a truncated protein (P165fsX198). Both parents were heterozygous for this mutation. CONCLUSIONS: A distinct autosomal recessive ophthalmic syndrome characterized by microphthalmos, retinitis pigmentosa, foveoschisis, and optic disc drusen is described. We demonstrated that this clinical association is caused by a mutation in MFRP, a gene previously implicated in isolated nanophthalmos. Our data indicate that defects in MFRP could be responsible for syndromic forms of microphthalmos/retinal degeneration and that this gene is necessary for photoreceptor maintenance.