Background Eosinophilic gastrointestinal diseases (EGIDs) are chronic immune-mediated inflammatory disorders characterized by gastrointestinal symptoms and eosinophilic inflammation in specific regions of the gastrointestinal tract. “Eosinophilic gastritis” (EoG) refers to the condition in which the stomach is involved. In patients with EoG, approved treatment options are restricted despite the high mortality associated with the condition. Dupilumab is a human monoclonal antibody directed against the interleukin (IL)-4 receptor α subunit and inhibits the signaling pathways of both IL-4 and IL-13. The real-world data on the effectiveness of dupilumab for EoG are limited. We present the case of a patient with EoG and accompanying severe asthma who demonstrated improvement with dupilumab administration. Case presentation A 35-year-old woman who had been treated for asthma complained of worsening intermittent upper abdominal pain. Her dyspnea aggravated and she was admitted to our hospital for asthma exacerbation. Despite the improvement in her asthma symptoms with systemic corticosteroids, her abdominal pain persisted. Upper gastrointestinal endoscopic mucosal biopsy revealed eosinophilic cell infiltration; therefore, the patient was diagnosed with EoG. Dupilumab administration was initiated for asthma, while improvement of secondary EoG was expected. Following dupilumab administration, both EoG and asthma symptoms, disease control, laboratory findings, endoscopic findings, and pathological findings improved. No adverse events have been reported after the dupilumab treatment. Conclusion This case report supports that dupilumab could be an effective treatment option for EoG and accompanying severe asthma.

Asthma and autoimmune diseases apparently have little to share except for the involvement of the immune system in both types of disorder. However, epidemiological studies have shown that asthma and Type 1 diabetes, a typical autoimmune disease, are associated at the population level, and some experimental findings have suggested that autoimmune mechanisms might be operating in asthma as well. Female preponderance, increased incidence of antinuclear autoantibodies and detection of autoantibodies against either bronchial epithelial antigens or endothelial antigens in patients with nonallergic asthma suggest that the disease may have an autoimmune basis. Approximately 50% of patients with nonallergic asthma react to intradermal injection of autologous serum, indicating the presence of circulating vasoactive factors and suggesting an autoreactive mechanism. Recent findings in experimental animals support the involvement of an autoreactive mechanism in allergic asthma as well, indicating that human alpha-nascent polypeptide-associated complex, identified as an IgE-reactive autoantigen, has the potential to sensitize and induce immediate skin reactions and airway inflammation. In summary, asthma is a heterogeneous disorder characterized by chronic inflammation of the respiratory airways that can be triggered by allergen exposure or by other mechanisms, possibly autoreactive/autoimmune. The autoimmune hypothesis is further, indirectly, supported by the response to immunosuppressive drugs.

The world is trying to kill me prematurely.

"One of our hypotheses is that what's underlying this huge mortality in African-American children is the fact that the most commonly prescribed drug for asthma is albuterol," says White. "The problem is that not everyone responds to albuterol the same way. And actually, Puerto Rican and African-American children have the worst drug response. So you're looking at two populations with the worst drug response with the highest mortality. We have a feeling those things might be related."

This happened with CFC inhalers too.