High prevalence of food sensitisation in young children with liver disease: A clue to food allergy pathogenesis?

Abstract

Background: The pathogenesis of food allergy is not completely understood - animal models suggest hepatic mechanisms may be important for immune tolerance to orally ingested antigens, but there is little direct evidence for this in humans. Objectives: We investigated whether there is an association between liver dysfunction or transplantation in young children and IgE sensitisation to food. Methods: We evaluated paired pre- and post- liver transplant sera from children aged 0-36 months treated at a single centre during 2001-2008. Sera were assayed for total IgE and cow's milk, egg and peanut-specific IgE. We quantified hepatic dysfunction pre-transplant using the Paediatric End-stage Liver Disease (PELD) score. We also assessed 70 children after renal transplant to establish whether any association between liver transplant and food sensitisation was organ specific. Results: Paired sera were available from 50 of 94 children who had a liver transplant during the study period. 35 of 50 (70%) had IgE sensitisation (≥0.35 kUa/l) to ≥1 food pre-transplant and 18 (36%) post-transplant (p = 0.001). Ten (20%) children had food-specific IgE levels that carry high probability of challenge-confirmed food allergy pre-transplant. Food sensitisation pre-transplant was associated with severity of liver dysfunction [mean (s.d.) pre-transplant PELD score 1.52 (0.13) in food sensitised, 0.77 (0.22) in non-sensitised children p = 0.004]. Total IgE level was raised in 34/42 (81%) pre-transplant and fell significantly post-transplant. Interview assessment of the parents of 40 children revealed that 13 (33%) had a history consistent with food allergy. These findings were not replicated in the renal transplant group. Conclusions: Young children with severe liver dysfunction appear to have a high prevalence of food sensitisation. Hepatic mechanisms may therefore be important for establishing immune tolerance to dietary antigens in humans. © 2012 John Wiley & Sons A/S.