Eosinophilic gastroenteritis

I wish to respond to the article “Primary eosinophilic disorders of the gastrointestinal tract” by Yan and Shaffer. In this article Yan et al wrote extensively on the physiology of the recruitment and activation of eosinophils in the gastrointestinal tract. We wish to present a case that serves to bring to light an alternative route of recruitment and activation of eosinophils. A 47-year-old man underwent laparoscopic high anterior resection for recurrent bouts of acute diverticulitis. This diagnosis was based preoperatively on CT and colonoscopic findings, and confirmed postoperatively on pathological examination of the resected specimen. He had no personal or family history of atopy, inflammatory bowel disease or connective tissue disease. He re-presented to the Accident and Emergency Department 3 weeks later with severe crampy abdominal pain and vomiting, and small bowel obstruction was diagnosed by small bowel follow-through. At laparotomy there was an inflammatory small bowel mass in the right iliac fossa related to a pinhole perforation of the ileum. The colonic anastomosis was intact. The affected small bowel was resected and a small bowel anastomosis formed. The patient suffered severe persistent pain in the postoperative period; however, vital signs remained normal and there was no clinical evidence of peritonism. Haematological and biochemical investigations including white cell count and differential were normal. CT abdomen and pelvis and gastrograffin enema revealed no cause for the ongoing symptoms. Histological examination of the resected specimen of small bowel revealed eosinophilic infiltrate of the lamina propria and evidence of perforation, leading to a diagnosis of perforated eosinophilic gastroenteritis. The gastroenterology service was consulted and the patient commenced on oral steroid treatment. The pain settled completely over 48 h and he was discharged home on a reducing dose of steroids. A review of the literature and >200 case reports of eosinophilic gastroenteritis revealed that this is the first report of eosinophilic gastroenteritis developing as a postoperative complication. It is also one of only 16 reports of perforated eosinophilic gastroenteritis. This case highlighted to us the possibility of an alternative pathway of eosinophilic recruitment and activation in certain susceptible individuals. The traditional model of eosinophil activation as a result of an antigenic response of the gastrointestinal epithelium, releasing eotaxin and interleukin-5 (IL-5) to upregulate, attract and activate eosinophils in the local area, may also co-exist with a propensity for a similar reaction from the gastrointestinal epithelium in response to local trauma, in place of the conventional inflammatory response. The patient in this case underwent surgery 3 weeks prior to developing the symptoms he presented with. We postulate that this patient was susceptible to, and exhibited an abnormal inflammatory response to the postoperative intra-abdominal inflammation associated with his abdominal surgery. Thus, in the place of a traditional inflammatory response, this patient developed a predominantly eosinophilic response of sufficient intensity to cause perforation of his small bowel, and causing him to represent to hospital. Evidence to substantiate further that he underwent a widespread gastrointestinal eosinophilic reaction is that even after resection of the affected segment, his pain did not subside. It was only once he had been treated with systemic steroids that his pain responded, and it did so dramatically, his pain being much reduced just 12 h after commencing steroid treatment and not present at all after 48 h. Thus, in conclusion, we present this case to highlight the possibility of alternative pathways of eosinophilic activation in patients susceptible to such a process and hope to advance our understanding of this complicated disease process.