The present study is in line with the general estimates in the world. It has revealed a high case of mortality among the patients awaiting corrective surgery. These children need more facilities.

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Background The ophthalmic risk is more important in premature infants. Both frequency and severity are inversely proportional to the term of birth. Purpose To evaluate the impact of prematurity on the anatomical development of the eye and visual function in preschoolers. Patients and methods It is a descriptive and comparative study of sensory-motor assessment in 68 preschool children divided in 2 groups: - 34 preterm infants without retinopathy - 34 term infants, without any systemic or ocular pathology randomly selected from kindergartens after parental consent. Results We observed a similar rate of myopia and hyperopia respectively 8.82% and 20.76% among former preterm versus 7.35% and 25% in children born at term. However, astigmatism was statistically more frequent in the group of former premature (22.06% vs. 16.17%). There was no significant difference in the visual acuity and spherical equivalent. Amblyopia was significantly more frequent in the group of former premature (11.76% vs. 5.88%). There were shorter axial length and significantly more curved cornea with a greater refractive power in the group of former premature infant. The sensory and motor assessments were significantly altered in former preterm (19.18% vs. 11.76% for the sensory assessment and 36.76% vs. 17.65% for the motor evaluation). Conclusion The premature infant has an increased risk of refractive errors, strabismus and amblyopia. Our study showed other more frequent abnormalities. The early management of these problems may limit their impact on the development of visual function.

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Donohue syndrome (DS) is a very rare autosomal recessive disease affecting less than one in a million life births. It represents the most severe form of insulin resistance due to mutations involving the insulin receptor (IR) gene "INSR". DS is characterized by pre- and postnatal growth retardation with failure-to-thrive, lipoatrophy, acanthosis nigricans, hypertrichosis, and dysmorphic features. An exhaustive INSR gene sequencing was performed after PCR amplification of coding exons and introns boundaries. Bioinformatic tools, including ESEfinder, MFOLD and Proter software were also used to predict the impact of INSR mutation on INSR on gene expression as well as on the protein structure and function. The results have shown a novel unusual c.3003_3012delinsGGAAG (p.S1001_D1004delinsRE) insertion/deletion (indel) mutation within the exon 16 in the three patients, which represent the fourth indel mutation within the INSR gene. The mutation modifies the secondary structure of DNA and RNA, as well as the composition of exonic splicing enhancers of exon 16. Moreover, despite the conservation of the secondary structure of the IR, the p.S1001_D1004delinsRE in-frame mutation is accompanied by the loss of four amino acids replaced by two residues of different nature and hydrophobicity level in the juxtamembrane domain of the receptor. The results have confirmed the role of the juxtamembrane domain of IR involved in a crucial interaction of the IR with cellular effectors essentially the IR substrate 1 (IRS-1), the SHC and the Nck proteins that ensure the signal mediated by the insulin transduction pathway in target cells. Our findings have also proven the genotype/phenotype correlation between INSR mutation and DS phenotype severity.