Anti‐ulcer drugs promote IgE formation toward dietary antigens in adult patients

Abstract

Recently, we have demonstrated that anti-ulcer drugs, such as H2-receptor blockers and proton pump inhibitors, promote the development of immediate type food allergy toward digestion-labile proteins in mice. The aim of this study was to examine the allergological relevance of these findings in humans. In an observational cohort study, we screened 152 adult patients from a gastroenterological outpatient clinic with negative case histories for atopy or allergy, who were medicated with H2-receptor blockers or proton pump inhibitors for 3 months. IgE reactivities to food allergens before and after 3 months of anti-acid treatment were compared serologically. Ten percent of the patients showed a boost of preexisting IgE antibodies and 15% de novo IgE formation toward numerous digestion-labile dietary compounds, like milk, potato, celery, carrots, apple, orange, wheat, and rye flour. Thus, the relative risk to develop food-specific IgE after anti-acid therapy was 10.5 (95% confidence interval: 1.44-76.48). The long-term effect was evaluated 5 months after therapy. Food-specific IgE could still be measured in 6% of the patients, as well as significantly elevated serum concentrations of ST2, a Th2-specific marker. An unspecific boost during the pollen season could be excluded, as 50 untreated control patients revealed no changes in their IgE pattern. In line with our previous animal experiments, our data strongly suggest that anti-ulcer treatment primes the development of IgE toward dietary compounds in long-term acid-suppressed patients.

Protective effects of a triple‐fermented barley extract (FBe) against HCl/EtOH‐induced gastric mucosa damage in mice

“…Various synthetic antiulcer drugs are currently available, and some of these including RA, are representative histamine H 2 receptor antagonists specifically used to cure gastric ulcers. However, each of these drugs has simple‐to‐severe side effects (Miederer, 1986) including cardiac toxicity (Jakob et al., 2005), risk of pneumonia in hospitalized patients (Mallow et al., 2004), infectious diarrhea (Neal et al., 1994; Ruddell et al., 1980), the development of food allergies (Untersmayr et al., 2005), and thrombocytopenia (Bangia et al., 2011). …”

“…Although, it is likely to decrease mucosal perfusion in patients with acute renal or cardiac failure, and thereby increases the risk of death (Jakob, Parviainen, Ruokonen, Uusaro, & Takala, 2005). Infectious diarrhea (Neal, Briji, Slack, Hawkey, & Logan, 1994; Ruddell, Axon, Findlay, Bartholomew, & Hill, 1980), developing food allergies (Untersmayr et al., 2005), and thrombocytopenia (Bangia, Kamath, & Mohan, 2011) have also been reported as common side effects of histamine H 2 receptor antagonists (Yesilada & Gurbuz, 2003). In this experiment, RA 100 mg/kg was selected as a positive reference drug to compare the gastric mucosa protective effects based on the previous report (Grover et al., 2001).…”

Dose-dependent food allergy induction against ovalbumin under acid-suppression: A murine food allergy model

“…The relevance of this mechanism was demonstrated both in the murine system [9][10][11] as well as for humans, as 25% of gastroenterological patients being treated with acid-suppression medication for a 3-month period due to dyspeptic disorders revealed formation of specific IgE antibodies and sensitization towards dietary compounds [9,13].…”

Anti‐ulcer treatment during pregnancy induces food allergy in mouse mothers and a Th2‐bias in their offspring

“…For the adult population, we could show in previous studies that the risk to develop sensitization against food allergens increases with the usage of acid-suppressing drugs (4,5), which are applied for the treatment of dyspeptic disorders such as gastric reflux, heartburn, and gastritis. We suggested that the hindered peptic digestion due to the elevated pH in the stomach leaves bigger fragments of alimentary proteins.…”