# Eosinophilic Gastroenteritis with Appendix Involvement: Role of Intestinal Ultrasound
## 3 Discussion  
Eosinophils are pro-inflammatory leukocytes primarily present in the lamina propria of all the GI tract, except for the esophagus, with a rate of 20-30% of the cellular population [4; 9]. Their concentration in the mucosal layer varies between the different sites of the GI tract and also according to patient characteristics, such as age, climate, and diet [2]. EG is a rare disease that can affect both children and adults, with a prevalence recently reported to vary from 7/100,000 [10] to 28/100,000 people depending on the site and age of onset [11; 12]. The diagnosis is based on the presence of gastrointestinal symptoms, histologic samples demonstrating eosinophilic infiltration of the gastrointestinal tract, and absence of extra-intestinal disease (i.e., parasitic infections, food hypersensitivity, drug reactions, malignancies, inflammatory bowel disease, celiac disease, and vasculitis) [13]. Abdominal pain, nausea, weight loss, and fever are non-specific signs of the disease and are often present, although the clinical presentation depends on the gastro-intestinal wall layer involved. Three different patterns of disease have been described: mucosal (70%), muscular (20%), and serosal (10%) [3]. Frequently, more layers are involved. In the mucosal/submucosal disease, anemia from occult or manifested GI bleeding, diarrhea or protein-losing enteropathy are often observed. Intestinal obstruction and ascites are rarer complications secondary to muscular or serosal involvement, respectively [10]. The course varies from a single flare to recurring or continuous disease [14]. Peripheral eosinophil is present in about 80% of the cases [10; 15; 16], although it is not specific to EG. It does not correlate with the activity of the disease or histological healing; thus, it is not very useful for follow-up [17]. Other non-specific features include anemia, increased inflammation indices, and severe malabsorption [2; 10]. There are no specific imaging signs of EG. In most case reports, CT scan is the technique of choice [18; 19; 20; 21]. As in its clinical presentation, the CT features of EG also vary according to the different layers of the GI tract involved: ulcers and polyps in the mucosal pattern, strictures and thickening in the muscular pattern, and ascites and omental involvement in the serosal pattern [10]. Endoscopy is useful, particularly in the case of mucosal involvement. Upper and/or lower endoscopy can show mucosal damage [2], such as erosions, whitish speckles, polyps, ulcers, or stenosis, and allows tissue sample collection for histological examination, which represents the gold standard for diagnosis. Usually biopsies are recommended in all the mucosal lesions identified and in all the GI tract examined, because of the patchy involvement of the disease [10]. Biopsies of the bowel wall by means of laparotomy [22] can be performed in case of presentation of serosal patterns, and for diagnostic paracentsis [23; 24]. As for the aforementioned variations of the tissue eosinophil count, there is no consensus with regard to the histological diagnosis, except for the eosinophilic esophagitis where a cut-off value of 15 eosinophils per high-power field (HPF) is defined [25]. Recent evidence quotes the following eosinophilic tissue cut-off values as diagnostic: >30 eosinophils per high-power field in the stomach, >52 in the small intestine, >50-100 in the right colon, >35-84 in the transverse colon, and >25-65 in the left colon [26; 27; 28]. The correlation between food assumption and EG has led to the empirical food-elimination diet as the first therapeutic effort, given its good effectiveness in children with 75% remission rates [29; 30]. No data on adult populations is available because of low compliance, especially over an extended period of time. Corticosteroids remain the mainstay of medical therapy for patients who fail or do not tolerate a dietary approach [10; 31; 32], thanks to their activity as inhibitors of eosinophil growth factors, such as IL3 and IL5 [33].