435:
Elevated serum TSLP, IL-33, 6Ckine and MCP-3 levels in school children or older patients with eosinophilic gastroenteritis
Sunday, March 4, 2018
South Hall A2 (Convention Center)
Ichiro Nomura, MD, PhD, Hideaki Morita, MD PhD, Akio Matsuda, PhD., Miori Sato, MD, Motoko Mitsui, Yumiko Miyaji, MD, PhD, Shinichiro Inagaki, MD PhD, Tatsuki Fukuie, MD, PhD, Masami Narita, MD, PhD, Yukihiro Ohya, MD PhD, Hirohisa Saito, MD PhD FAAAAI, Kenji Matsumoto, MD PhD
RATIONALE:

Eosinophilic gastroenteritis (EGE) is characterized by abnormal accumulation of eosinophils in the GI mucosa. Non-IgE-mediated immune responses are reportedly involved in the pathogenesis of infantile EGE, but the pathogenesis of EGE remains largely unknown. One of the major difficulties in diagnosing and treating EGE is the lack of reliable serum biomarkers. We recently reported that serum TSLP, IL-33, 6Ckine and MCP-3 levels were elevated in infantile EGE (Shoda et al., JACI 2016). In the present study, we examined the serum cytokine/chemokine profiles of school age and adult patients with EGE.

METHODS:

We used a Milliplex assay system to determine the comprehensive cytokine/chemokine profiles in sera from 9 patients with moderate to severe EGE, 14 patients with ulcerative colitis (UC) and 31 patients with immediate-type food allergy (FA).

RESULTS: The EGE patients were 3 males and 6 females, with a median age of 12 years (5~35 y). Major symptoms and signs of EGE were abdominal pain (100%), vomiting (33%), diarrhea (56%), ascites (22%) and hypoproteinemia (33%). Among 66 chemokines/cytokines tested, TSLP (P=.035), IL-33 (P<.000), 6CKine (P=.003) and MCP3 (P=.008) levels were elevated in EGE when compared with UC and FA. Those elevated levels decreased after resolution of the symptoms. Serum proinflammatory cytokine levels were not elevated.

CONCLUSIONS: Serum TSLP, IL33, 6CKine, MCP3 levels are likely to be good biomarkers for diagnosing and treating school children and older patients with EGE. EGE in school children and older patients may have a similar pathogenesis with infantile EGE.