EGIDs are disorders of the gastrointestinal tract that result from abnormal accumulation of eosinophils in localized areas of the tract . According to the inflamed organs, it is classified as eosinophilic esophagitis, eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE), and eosinophilic colitis (EC). EG and EC are often included in EGE. EGE is a rare disease that is difficult to diagnose in children.
Patients with EGE are typified by abdominal pain and diarrhea symptoms, high peripheral eosinophil counts, and gastrointestinal wall thickening, identifiable on CT . Histological features of EC show numerous eosinophil counts, > 50 cells/HPF in the right colon and 30 cells/HPF in the left/transverse colon . Stamm et al. reported a high prevalence of gastrointestinal eosinophilic inflammation in a large cohort of children with intestinal failure (IF) . In this current case, eosinophilic inflammation was observed on blood and pathological examinations. Serum proinflammatory cytokines due to chronic inflammation associated with SBS were significantly higher in patients with SBS receiving PN, regardless of the duration of PN . Although there are many theories regarding the mechanism of dietary protein allergy and systemic immune dysregulation in children with IF [8, 9], one potential triggering mechanism for allergic gastrointestinal disease in IF is increased intestinal permeability . In our case, SBS after strangulated bowel obstruction operation caused the development of secondary EGIDs, similar to the mechanism. The management of patients with IF should include awareness of this typical endoscopic finding and careful screening for symptoms such as hematochezia .
Fundamentally, the treatment strategy for secondary EGIDs is to treat the primary disease; however, it was difficult to improve the digestive symptoms using only nutritional therapy in our case. Several studies have reported montelukast sodium as an effective treatment for EGIDs [11, 12]. Montelukast is a selective and competitive antagonist of the cysteinyl leukotriene receptor. Leukotrienes are lipid mediators released by eosinophils and are potent and selective chemoattractant for eosinophils [13, 14]. Montelukast sodium has become the focus of attention in the treatment of EGIDs. One study described the successful use of montelukast as a steroid-sparing agent in 63% adults patients , however its effectiveness as a treatment for EGIDs in children remains to be evaluated. In our case, sufficient effectiveness was not observed.
Glucocorticoids have been effective as an alternative treatment for EGIDs. Their efficacy stems from their ability to modulate immune responses and to inhibit the trafficking of inflammatory cells to the intestine . The choice of glucocorticoids should be individualized in children with SBS-related chronic intestinal inflammation. One study reported that some pediatric patients with significant eosinophils in their intestinal biopsy responded well to glucocorticoids . Thus systemic glucocorticoids can be useful for treating EGIDs.
Prednisolone activates glucocorticoid receptors and is clinically used to treat inflammatory and autoimmune disorders. We used prednisolone as one of the standard treatments for EGIDs. Prednisolone dose is often started at 0.5–2 mg/kg/day and tapered off after 1–2 weeks. Although most cases show temporary improvement, approximately 60% of patients experience recurrence of symptoms after treatment . Prednisolone administration was effective in combination with other EGIDs treatment approaches. Continued follow-up with attention to symptom recurrence is necessary.