## 3 Discussion  
Diagnosis of non-IgE-GIFAs is difficult for the following reasons: (1) non-IgE-GIFAs are mainly caused by cows' milk; however, rice, soybeans, wheat, chicken eggs, allergens in maternal diet transmitted through the consumption of breast milk, and other allergens can also cause non-IgE-GIFAs; (2) the causative food cannot be estimated from the specific IgE antibody, as non-IgE-GIFAs is not IgE-dependent; (3) 30% of non-IgE-GIFAs are also positive for specific IgE similar to IgE-dependent immediate food allergies; and (4) no clear diagnostic criteria for FPIAP and FPE exist. In the present case, the specific IgE antibodies were also positive for foods other than milk. The gastrointestinal mucosal findings obtained using EGD before and after elimination diet therapy were helpful in making the diagnosis. Non-IgE-GIFAs may not be fully diagnosed [6], and the actual diagnosis relies on the recognition of symptom patterns in FPIAP and FPIES and biopsies in FPE. No accepted diagnostic criteria are available for FPE and FPIAP. However, some elements routinely used in clinical practice support the diagnosis of these diseases according to international consensus guidelines [1]. FPE presents in young infants (<9 months) with typical symptoms of vomiting and intestinal malabsorption. In addition, a biopsy suggestive of FPE helps confirm this diagnosis [5,10]. In FPIAP, the causative association between rectal bleeding and antigenic food must be established with a resolution of symptoms upon elimination of the offending foods and, preferably, with the documented recurrence of symptoms when foods are re-introduced [11]. Furthermore, other causes of hematochezia, such as anal fissures, must be excluded [7]. FPE causes diarrhea that lasts for more than 2 weeks, leading to poor weight gain and stunted growth due to digestive and absorptive disorders. The pathologic findings for FPE are well known, and histologic findings such as atrophy of small intestinal mucosal willi, crypt hyperplasia, and lymphocyte infiltration are useful for diagnosis. These features were observed in the present case. In contrast, EGIDs are characterized by extensive eosinophilic inflammation and mast cell infiltration [12]. In the clinical setting, non-IgE-GIFAs may be misdiagnosed because this is primarily a clinical diagnosis [13], and the symptoms do not appear immediately after ingesting the causative food antigen. However, in the present case, histopathologic evaluation of the gastrointestinal mucosa helped establish her condition, and the restoration of villous structures after milk elimination diet therapy confirmed the diagnosis. The elimination diet was very helpful in distinguishing allergic diseases such as non-IgE-GIFAs and EGIDs from nonallergic diseases such as monogenic IBD and IPEX syndrome. This is because the elimination diet alone cannot be expected to improve disease findings in nonallergic diseases. Villous atrophy is often also observed in celiac disease and microscopic enterocolitis; however, in the present case, abnormal findings were not limited to the duodenum, which is characteristic of celiac disease, and in microscopic enteritis, diarrhea did not improve dramatically with only short-term steroids and an elimination diet. Thus, celiac disease and microscopic enteritis were ruled out. In allergic diseases, removal of the causative antigen facilitates both diagnosis and treatment. Elimination diet therapies have not been established for non-IgE-GIFAs; therefore, it is difficult to assess improvements in gastrointestinal symptoms with these therapies. Elimination of the offending food significantly improves emesis and diarrhea within a few hours in patients with acute FPIES and within days in those with chronic FPIES. Visible blood in the stool resolves within a few days in patients with FPIAP. However, in patients with FPE, symptoms usually resolve in 1-4 weeks [5]. The variable time to recovery makes it difficult for clinicians to assess the effectiveness of the elimination diet.