615 ACCELERATED DEGRADATION OF ESSENTIAL FATTY ACIDS (EFA) IN PREMATURE INFANTS ON PHOTOTHERAPY (PT)

We have previously demonstrated, in vitro (Ped. Res. 10:429, 1976) by measuring O2 consumption and the products of lipid peroxidation(thiobarbituric acid reactants or TBA and diene

conjugates) that the oxidation of EFA (linoleic and (linolenic a.) is accelerated by exposure to light (460 nm), O2 and photosensitizing agents (bilirubin or methylene blue). This report

describes the phenomenon to also occur, in vivo, in premature infants on PT. METHODS: Seven premature infants while on PT for treatment of jaundice were serially tested during the first 3

days of PT for the concentration of linoleic acid (C18:2) and triene/tetraene ratio in the phospholipid and sterol ester fractions of the serum by gas liquid chromatography. Serum TBA and

diene conjugates were measured spectrophotometrically. RESULTS: During PT, there was a continuous fall in C18:2 concentration both in the phospholipid (−0.190±0.252 mg/dl/h) and sterol

(−0.372±0.580 mg/dl/h) fractions of their serum and the decay was greatest during the first 24 h of PT (−0.259 mg/dl/h in phospholipid and −0.543 mg/dl/h for sterol). The rate of decay of

C18:2 was doubled during PT, as compared to its spontaneous decay before PT (−0.088 mg/dl/h before, vs. −0.176 mg/dl/h during PT). There was also a simultaneous rise in triene/tetraene ratio

during PT, from 0.014 to 0.086, but none achieved critical EFA deficiency ratio level of 0.4. During PT, there was a rise in the conc. of products of lipid peroxidation: TBA= +0.005 OD/mg

C18:2 and diene conjugates= +0.075 OD/mg C18:2. None of the infants however showed clinical evidence of EFA despite chemical evidence of EFA decay. Furthermore, the decrease in conc. of

C18:2 during PT was prevented or corrected by the feeding of the infant. CONCLUSION: This study shows that chemical evidence of accelerated degradation of EFA (specifically C18:2) occurs in

premature infants on PT which is similar to what has been observed in vitro. Since the premature infant had been shown to be susceptible to the early development of EFA deficiency due to

poor nutritional intake, the possibility that the EFA deficiency can be further accelerated if PT is used should be seriously considered.

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