Tolerance to Allergenic Foods Following Food Oral Immunotherapy (FOIT)
Poster Feb 21, 2015
AR Hague1, RL Wasserman1,2, SK Silvers1,2, RW Sugerman1,2, M Herbert3
Rationale: FOIT treatment desensitizes most food allergic individuals, but the achievement of immunologic tolerance is uncertain. We report on 21 selected patients who underwent food challenges (FC) after FOIT was withheld for at least 30 days.
Methods: Retrospective record review of FOIT patients approved by the North Texas IRB. After 453-1752 days of maintenance dosing selected patients stopped ingesting the allergenic food for 1 month and then were subjected to an open, graded FC.
Results: 19/21 patients passed the FC (FCP) (5/5 egg, 6/7 milk, 7/8 peanut, 1/1 cashew). 15/19 FCP and 0/2 who failed the FC (FCF) had a history of anaphylaxis to the allergenic food prior to starting FOIT. Median IgE (kU/L) before beginning FOIT for FCP were egg 5.04 (0.37-49.97), milk 5.23 (1.52-10.93), peanut 10.39 (2.44-61.33), cashew 4.53; and for FCF: milk 54.24, peanut >100. Median IgE values before FC for FCP were egg 0.35 (0.1-15.9), milk 0.17 (0.08-0.3), peanut 0.96 (0.08-7.38), and cashew 1.14; and milk 1.16, peanut 11.5 for FCF. There were 0.26 epinephrine treated reactions per patient (ETRpp) during FOIT escalation and 0.05 ETRpp during maintenance for FCP. There were 2 ETRs in escalation and none in maintenance for the 2 FCF patients.
Conclusions: 90% of selected FOIT patients achieved tolerance to their allergenic food. These data suggest that patients with high pre-OIT IgE values, high pre-FC values, and more ETRs during escalation are less likely to pass FC. More FOIT patients will need to undergo FC before meaningful conclusions may be drawn concerning tolerance.
Genome-wide association studies (GWAS) have identified more than 100 genetic loci associated with type 2 diabetes. The majority of these are located in the intergenic or intragenic regions suggesting that the implicated variants may alter chromatin conformation. This, in turn, is likely to influence the expression of nearby or more remotely located genes to alter beta cell function. At present, however, detailed molecular and functional analyses are still lacking for most of these variants. We recently analysed one of these loci and mapped five causal variants in an islet-specific enhancer cluster within the STARD10 gene locus. Here, we aimed to understand how these causal variants influence b-cell function by alteration of the chromatin structure of enhancer clusterREAD MORE