Retrolental fibroplasia: further clinical evidence and ultrastructural support for efficacy of vitamin E in the preterm infant.
To further evaluate the efficacy of oral vitamin E in preventing the development of severe retrolental fibroplasia (RLF) in very low-birth-weight infants, 100 infants treated with 100 mg/kg/d of vitamin E (dl-alpha-tocopheryl acetate) were compared with 75 infants treated with 5 mg/kg/d of vitamin E (dl-alpha-tocopherol) in the same nursery during the previous year. All 175 infants weighed less than or equal to 1,500 g at birth and required supplemental oxygen. A total of 120 infants (69 treatment; 51 control) survived greater than or equal to 10 weeks. Multivariate analysis of the control population identified five risk factors (P less than or equal to .10): gestational age, level and duration of oxygen administration, intraventricular hemorrhage, sepsis, and birth weight. When multivariate analysis was applied to both control and treatment groups, the severity of RLF was found to be significantly reduced in infants given the treatment dose of vitamin E (P = .003). Ultrastructural analyses of 58 pairs of whole-eye donations from high-risk infants surviving less than 10 weeks suggest that the initial morphologic event is gap junction increases between the plasma membranes of adjacent spindle cells of the van-guard retina. Such extensively gap junction-linked spindle cells are apparently removed from the vasoformative process as early as 4 days of life, forming a barrier to further normal vascular development and triggering retinal and vitreal neovascularizations approximately 8 weeks later. These events are maximally suppressed by elevated plasma vitamin E levels in infants greater than or equal to 27 weeks gestational age.
D002462:Cell Membrane / Q000648:ultrastructure; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007234:Infant, Premature; D007365:Intercellular Junctions / Q000648:ultrastructure; D012160:Retina / Q000648:ultrastructure; D012178:Retinopathy of Prematurity / Q000473:pathology / Q000517:prevention & control*; D014810:Vitamin E / Q000627:therapeutic use*
D014810:Vitamin E