Vitamin E and retrolental fibroplasia: ultrastructural mechanism of clinical efficacy.
Administration of control, oral or combined intramuscular and oral vitamin E to 418 high risk, preterm infants (1500 g or less birth weight; 32 weeks or less gestational age; 305 surviving more than 10 weeks) led to raised peak plasma levels of the vitamin of between 0.6 and 3.3 mg% in three consecutive clinical trials. This early, non-toxic, prophylactic supplementation suppressed the development of severe retrolental fibroplasia when the antioxidant was given continuously from the first day of life until retinal quiescence. Studies of 63 pairs of eyes by transmission electron microscopy revealed that spindle cells (the embryonic precursors of inner retinal capillaries) were the primary target of the vitamin E-induced suppression of severe retrolental fibroplasia. Extensive increases in the gap junctions between adjacent spindle cells in unsupplemented infants, or in supplemented infants of 27 weeks gestational age or less, triggered both neovascularization from the most nascent capillaries at the rearguard-vanguard retinal interface, and dilatation and tortuosity in the rearguard (posterior) retinal vessels. Continuous vitamin E supplementation permanently preserved the embryonic state of the spindle cells in infants of 28 weeks gestational age or more, and transiently retarded gap junction increases in infants of 27 weeks gestational age or less.
D002986:Clinical Trials as Topic; D005123:Eye / Q000098:blood supply / Q000187:drug effects / Q000648:ultrastructure; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D007365:Intercellular Junctions / Q000648:ultrastructure; D008854:Microscopy, Electron; D012178:Retinopathy of Prematurity / Q000517:prevention & control*; D014810:Vitamin E / Q000097:blood / Q000627:therapeutic use*
D014810:Vitamin E