Retinopathy Of Prematurity In Preterm Infants Research Articles

Retinopatía del prematuro. Casuística de los años 1995–2001

Retinopathy of prematurity (ROP) is a cause of neurosensorial morbidity. To study the incidence, associated risks factors, treatment, and outcome of ROP in premature infants born at less than 32 weeks in our hospital. We performed a descriptive study of patients born between the January 1, 1995, and December 31, 2001, in Sant Joan de Déu Hospital in Barcelona (Spain) at <= 32 weeks of gestation who survived until their first month of life. An ocular evaluation was performed between weeks 4 and 6 of life and was repeated every 1-2 weeks until retinal vascularization was complete. Ocular sequelae and visual function were evaluated. Bivariate comparison of groups with and without ROP was performed. Of the 324 patients evaluated, 74 presented ROP (22.8 %), of which 63 patients (21.7 %) were classified as stage 1 or 2 and 11 (3.7 %) as stage 3. An inverse correlation between the incidence of retinopathy and weight and gestational age was found. Threshold disease (3 plus) was detected in 9 patients (16 eyes; 3.1 % of the study sample and 12.1 % of the neonates with retinopathy). All of these neonates were treated with laser therapy. Ocular sequelae were mild in 2.7 % of the patients, moderate in 0.6 % and severe in 0.6 %. The visual function (n 236) of infants with ROP (n 74) was altered in 4 patients (1.7 %). Of these, alterations were severe in 2 patients (0.8 %). Bivariate analysis revealed significant differences (p < 0.001) in low birth weight, gestational age, days of oxygen therapy, days of mechanical ventilation, days of antibiotic therapy, and number of blood transfusions. In this study the incidence of ROP was similar to that in other centers. Development of ROP was strongly associated with its various risk factors. Severe stages were not seen above 30 weeks of gestational age. The results of laser therapy were optimal, with fewer alterations in ocular examination and visual function than those estimated in patients without treatment.

Glutathione status in retinopathy of prematurity

This study examines the glutathione status of red blood cells in patients with retinopathy of prematurity (ROP) both in vivo and after an in vitro oxidative challenge. Fifty ROP patients of different ages (between 6 weeks and 6 years), born prematurely (gestational age: 28.7 ± 1.3 weeks; birth weight: 1210 ± 313 g; mean ± SD) suffering either from active ROP (<3 months old; n = 12) or from a visual handicap due to preceding ROP (3 months–6 years; n = 38) as well as control patients of similar age and maturity ( n = 56) were included. Infants with active disease have the lowest levels of reduced glutathione (GSH), the highest levels of oxidized form (GSSG), the highest GSSG/GSH ratios and the greatest fall in GSH after an in vitro oxidative challenge. After an in vitro oxidative stress, defective glutathione recycling was found in patients with preceding ROP and was suggested as a factor predisposing to oxidative hemolysis. The glutathione redox ratio was warranted as a biochemical screen for active ROP in premature infants.

Identification of missense mutations in the Norrie disease gene associated with advanced retinopathy of prematurity.

Retinopathy of prematurity (ROP) is a retinal vascular disease occurring in infants with short gestational age and low birth weight and can lead to retinal detachment (ROP stages 4 and 5). X-linked familial exudative vitreoretinopathy is phenotypically similar to ROP and has been associated with mutations in the Norrie disease (ND) gene in some cases. To determine if similar mutations in the ND gene may play a role in the development of advanced ROP. Clinical examination and molecular genetic analysis were performed on 16 children, including 2 dizygotic and 1 monozygotic twin pairs, and their parents from 13 families. Sequencing of the amplified products revealed missense mutations (R121W and L108P) in the third exon of the ND gene in 4 patients. These mutations were not present in an unaffected premature twin, 2 children with regressed stage 3 ROP, the parents, or in 50 unrelated healthy control subjects. These findings suggest that mutations in the ND gene may play a role in the development of severe ROP in premature infants.