Although the pathogenesis of NEC is still unclear, inflammatory mediators like PAF have been implicated in this disease. Elevated plasma PAF levels and lower PAF-AH have been shown in newborns with NEC (Caplan et al., J Pediatr 116:960, 1990). Whether these alterations correlate with the severity of NEC, and the time course of these changes are unknown. In this study we measured plasma PAF and PAF-AH activity at the onset of NEC, 24 h and 48-72 h later, in neonates with moderate NEC treated medically (Group A); those with severe NEC(diffuse pneumatosis, shock or death) or treated surgically (Group B); and neonates who had bowel resection not due to NEC (Group C). Also, in neonates who had surgery (groups B and C) bowel samples were taken to determine PAF content. Results of initial plasma samples are shown in the table as median (range).

Table 1

Neonates with severe NEC had a significantly lower plasma PAF-AH activity than the other groups (Table, *p<0.05 by Kruskall-Wallis and ANCOVA, GA as covariate). No differences at subsequent times or in plasma PAF were found. PAF tissue content was higher in bowel from neonates in Group B compared to Group C (1439 ± 363 vs. 468 ± 117 fmol/mg prot., respectively, [horizontal bar over]x±SEM, p<0.001). A lower plasma PAF-AH activity during the early stages of severe NEC suggests that the decreased activity of this enzyme in plasma may be a risk factor for the development of NEC. In addition, a higher PAF content in bowel from neonates with severe NEC suggests that this mediator participates in the pathogenesis of NEC.