Food allergy is the commonest cause of anaphylaxis, but why IgE-mediated reactions cause anaphylaxis in some cases but not in others remains unknown.
We applied metabonomic profiling (NMR spectroscopy and mass spectrometry (MS)) to blood samples during peanut double-blind, placebo-controlled food challenges (DBPCFC). Metabonomic measurements were related to cardiovascular/immunological changes and symptoms using linear mixed-effect models.
27 adults and 30 children underwent DBPCFC: 12 (44%) adults and 17 (57%) children experienced anaphylaxis (respiratory symptoms).
NMR profiling demonstrated statistically significant differences between reactive and placebo days for albumin hemoconcentration (P=0.0011), concentration of triglyceride in VLDL lipoprotein (VLDL-6) particles (P=0.00031) and chemical shift in TSP (an internal control) which would be consistent with a fall in plasma pH (P=0.000033). A dose-response was seen between local and systemic reactions, but there was no significant difference between anaphylaxis and systemic but non-anaphylactic reactions. This is consistent with our previous observations relating to basophil activation, and changes in cardiac stroke volume.
With MS profiling, similar statistically significant trends were identified for a range of oxylipins including arachidonic acid, dihomo-γ-linolenic acid and eicosapentaenoic acid (the latter 2 have anti-inflammatory effects). Differences were also observed for 10 amino acids and 94 other non-identified compounds (all P<0.05, after Benjamini-Yekutieli multiple testing correction).
Current systems to rate reaction severity are unable to reliably assess the level of systemic involvement. Mild reactions are associated with similar underlying systemic events as those occurring in more severe reactions. This suggests an important role for homeostatic compensation during food-induced allergic reactions.