Vitamin E and Retrolental Fibroplasia in 1982

Abstract

The retrolental fibroplasia (RLF) blind are an increasingly tragic shadow in the otherwise brightening picture for extremely premature infants1,2; thus, it is natural to feel eager anticipation at the report of vitamin E as an effective prophylactic.3 However, in seeking a solution to this frustrating disease, we must remain cautious about the price to be paid for prevention. I believe the time is ripe to ask "Where do we stand in our current knowledge of RLF; what is the history of vitamin E in this disorder; what is the strength of the evidence for its efficacy and safety; and finally is the risk/benefit ratio tipped in favor of treating the estimated 37,000 susceptible infants born annually in the United States, or must we await further evidence?" RLF OR RETINOPATHY OF PREMATURITY Through the combination of meticulous clinical observations4-7 and innovative studies in animal models,8,9 we have come to understand that acute, proliferative RLF occurs when the retina becomes ischemic following oxygen-related vaso-obliteration of immature, developing retinal arterioles. In the most immature infants (weight < 1 kg) this occurs as frequently as 75% of the time.7 There, however, our understanding of RLF ends inasmuch as cicatricial RLF (or retinopathy of prematurity with idiopathic fibrosis10), the scarred, occasional sequelae of acute RLF, is the output from a classic "black box." Prematurity, illness, and acute retinopathy go into one side, but we have no idea what determines healing vs cicatrix, the outputs on the far side. Animal models offer no help in this regard as none progress from acute vasculopathy to cicatricial sequelae (with perhaps one promising11).