Saudi Journal of Gastroenterology
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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 13  |  Issue : 2  |  Page : 91-94
Endoscopic ultrasound and hisopathologic correlates in eosinophilic gastroenteritis


Division of Gastroenterology, Department of Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia

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   Abstract 

Eosinophilic gastroenteritis is a rare condition characterized by eosinophilic infiltration into any layer of stomach and intestine (mucosa, muscularis mucosa and serosa), usually in association with peripheral eosinophilia. In this case report, we present a patient with eosinophilic gastroenterocolitis who had a history of bronchial asthma and presented with abdominal pain. He was found to have peripheral eosinophilia, perforation and gangrenous bowel on performing surgery and tissue eosinophilia on histopathology examination. His endoscopic ultrasound (EUS) showed significant thickening of his antral and duodenal mucosal and submucosal layers which correlated well with the gross and microscopic pathology of the resected surgical specimen. This is the first case to demonstrate EUS abnormalities in this very rare disorder.

Keywords: Endoscopic ultrasound, eosinophilic gastroenteritis, ischemic bowel, perforation

How to cite this article:
Alnaser S, Aljebreen AM. Endoscopic ultrasound and hisopathologic correlates in eosinophilic gastroenteritis. Saudi J Gastroenterol 2007;13:91-4

How to cite this URL:
Alnaser S, Aljebreen AM. Endoscopic ultrasound and hisopathologic correlates in eosinophilic gastroenteritis. Saudi J Gastroenterol [serial online] 2007 [cited 2020 Oct 28];13:91-4. Available from: https://www.saudijgastro.com/text.asp?2007/13/2/91/32185


Primary eosinophilic gastrointestinal disorders (EGIDs) are defined as disorders that selectively affect the gastrointestinal tract (GIT) with eosinophil-rich inflammation in the absence of known causes for eosinophilia (e.g., drug reactions, parasitic infections and malignancy). These disorders include eosinophilic esophagitis, eosinophilic gastritis, eosinophilic gastroenteritis (EGE), eosinophilic enteritis and eosinophilic colitis. [1] In published reports, the stomach (26-81%) and small intestine (28-100%) have been described as the predominantly affected areas, but the esophagus, large intestine and rectum may also be affected. [2],[3],[4]

EGE is a rare condition characterized by eosinophilic infiltration into any layer of the stomach and intestine (mucosa, muscularis mucosa and serosa), usually in association with peripheral eosinophilia. [1],[5],[6],[7] EGE can be subcategorized into 3 types on the basis of the level of histologic involvement: mucosal, muscularis and serosal forms. [7] The mucosal form of EGE (the most common variant) is characterized by vomiting, abdominal pain (that can even mimic acute appendicitis), diarrhea, blood loss in stools, iron-deficiency anemia, malabsorption, protein-losing enteropathy and failure to thrive. [8] The muscularis form is characterized by infiltration of eosinophils predominantly in the muscularis layer, leading to thickening of the bowel wall, which might result in gastrointestinal obstructive symptoms mimicking pyloric stenosis or other causes of gastric outlet obstruction. The serosal form occurs in a minority of EGE patients and it is characterized by exudative ascites with higher peripheral eosinophil counts as compared to the other forms. [2]

A history of atopy and allergies is present in up to 75% of the cases. [6],[9] No standards for the diagnosis of eosinophilic gastritis or gastroenteritis exist, [8] but a few findings support the diagnosis. For example, the presence of increased eosinophils in biopsy specimens from the gastrointestinal tract wall, the infiltration of eosinophils within intestinal crypts and gastric glands, the lack of involvement of other organs and the exclusion of other causes of eosinophilia (e.g., infections and inflammatory bowel disorder (IBD)) are supportive of EGE.

In this case report, we present a patient with eosinophilic gastroenterocolitis who presented with abdominal pain and was found to have peripheral eosinophilia, significant thickening of his antral and duodenal mucosal and submucosal layers on endoscopic ultrasound (EUS), perforation and gangrenous bowel on performing surgery and tissue eosinophilia on performing histopathology examination.


   Case report Top


A 53 year old Sudanese gentleman presented to the emergency department of our hospital with three weeks history of gradually evolving, moderate intensity epigastric and periumblical abdominal pain with watery diarrhea (6-10 times a day). The color of his stools had changed to black in the last three days prior to his presentation. He also gave a history of anorexia and undocumented weight loss. He denied any history of fever or night sweating. He had no history of oral ulcers, arthralgia or skin rash. He is a resident in Saudi Arabia with no travel history for the last five years. He had no recent respiratory or neurological symptoms.

He had bronchial asthma which was stable over the last 10 years and he had been using a long-acting beta agonist (salmeterol) as well as montelukast to control his symptoms.

On admission, he was unwell, in pain and tachycardic with otherwise normal vital signs. He had left lower abdominal tenderness on abdominal examination but no guarding or rigidity.

His initial laboratory work-up showed a white blood cell count of 26.9 (10 9 /L) (eosinophils: 47%), hemoglobin of 15.4 g/dL and normal renal function. He had an albumin level of 11; otherwise he had normal liver enzymes. His stool microscopy was positive for occult blood but repeatedly negative for cysts, ova or parasites. He was negative for antinuclear antibody (ANA), perinuclear antineutrophil cytoplasmic antibody (p-ANCA), rheumatoid factor (RF) and anti-double stranded DNA (anti-dsDNA). His initial abdominal X-ray was normal. An abdominal CT scan showed mucosal thickening of the stomach and small bowel with no evidence of free air or any filling defects in the celiac, superior or inferior mesenteric arteries or veins.

Given this history of abdominal pain and melena, he underwent urgent gastroscopy [Figure - 1] which showed severe erythema, edema and multiple erosions and deep ulcers of his gastric antrum and first and second part of duodenum. Multiple biopsies were taken and he was started on I.V. proton pump inhibitors (Pantoprazole 40 mg twice a day). He underwent endoscopic ultrasound [Figure - 2] in the same endoscopy session which showed significant (7-10 mm) circumferential thickening (normal = 3 mm) of the mucosal and submucosal layers of the antrum and first and second parts of the duodenum with no evidence of ascites. He also underwent colonoscopy which showed patchy erythema mainly of the left side of the colon with multiple aphthus ulcers at the sigmoid. Histopathology examination showed dense eosinophilic cellular infiltrate of the lamina propria (more than 30 eosinophils per high-power field) of the stomach; duodenum and colon with no evidence of giardiasis or malignancy [Figure - 3]. Because of his peripheral eosinophilia, he underwent bone marrow biopsy which showed increased eosinophils and their precursors with no evidence of lymphoma or granuloma.

Two days after his admission, he developed sudden severe abdominal pain and was found to have severe tenderness and rigidity on abdominal exam. Hence, an urgent plain abdominal X-ray was taken which showed multiple air-fluid levels with no evidence of free air. An abdominal CT scan was also done urgently which also showed multiple air-fluid levels with significant thickening of his small bowel wall [Figure - 4].

He was taken to the operating room where he underwent laparotomy which revealed an extensive gangrenous bowel extending from the proximal jejunum up to 15 cm proximal to the terminal ileum with evidence of multiple perforations. He had extensive small bowel resection of most of his jejunum and most of his proximal ileum. The resected specimen showed a dusky outer surface with multiple black patches and perforations, significant thickening of the mucosal and submucosal layers and dense transmural infiltration with mixed inflammatory cells including eosinophils and neutrophils. Post-operatively, the patient did very well and he was started on total parenteral nutrition, large dose of I.V. steroid (methylprednisolone, 20 mg three times a day) and broad-spectrum antibiotics. The patient was discharged 10 days later in good condition. He continues to do well two years after surgery and leads a normal life on prednisolone 10 mg/day with no recurrence of his gastrointestinal symptoms, eosinophilia or duodenal ulcers.


   Discussion Top


Eosinophilic intestinal inflammation can occur secondarily in the gastrointestinal tract in inflammatory bowel disease (IBD), [10] autoimmune diseases, reactions to medications, [11] infections, hypereosinophilia syndrome (HES) [12] and after solid organ transplantation. [13],[14] Although the normal esophagus is devoid of eosinophils, the rest of the gastrointestinal tract contains readily detectable eosinophils. Thus, differentiation of EGIDs from the normal condition relies on several factors, including [1] eosinophil quantification (and comparisons with normal values at each medical center), [2] the location of eosinophils (e.g., their presence in abnormal sites such as the intraepithelial, superficial mucosal and intestinal crypt regions), [3] the presence of extracellular eosinophilic staining constituents (often free granules), [4] associated pathologic abnormalities (e.g., epithelial hyperplasia as in the case of EE) and [5] the absence of pathologic features suggestive of other primary disorders (e.g., neutrophilia associated with IBD or vasculitis associated with Churg-Strauss syndrome). [1]

The currently accepted diagnostic criteria are the presence of gastrointestinal symptoms, predominant eosinophilic infiltrate on histopathology examination and exclusion of other causes of eosinophilia. [6]

Our patient had the triad of gastrointestinal symptoms (abdominal pain, melena), peripheral eosinophilia and eosinophilic infiltrate of the gastrointestinal tissue. He had a history of bronchial asthma which is present in up to 75% of all cases [9] and showed involvement of both the mucosal and submucosal layers. His gastroscopy showed definite mucosal involvement with multiple deep small ulcers and EUS showed circumferential thickening of his mucosal and submucosal layers of his antrum and duodenum with no evidence of ascites (serosal involvement). EUS features of EGIDs were only reported in patients with eosinophilic esophagitis. [15],[16] Stevoff et al. [15] reported the first EUS findings of an adult patient with eosinophilic esophagitis which had a good correlation with the histopathological findings. To our knowledge, this is the first reported case of EUS findings of duodenal EGE.

Peripheral eosinophilia in the context of gastrointestinal symptoms, is a useful clue to EGE, but is not necessary to make the diagnosis. Parasitic infection can be detected with stool or duodenal aspirate for ova and parasites. In our patient, parasitic infection was ruled out based on 3 stool samples which were negative for ova or parasites and the absence of any parasites in the duodenal biopsies.

Another possible etiology of our patient's symptoms was hypereosinophilic syndrome (HES). The criteria required to diagnose HES are peripheral eosinophilia exceeding 1500 cells/mL for more than six consecutive months, absence of an underlying cause of hypereosinophilia despite extensive evaluation (drugs or parasites) and presence of organ damage or dysfunction related to hypereosinophilia. [12] The heart, skin and central nervous system are the major targets, with more than 50% patients presenting with complications in one or more of these sites. In our patient, apart from the gut involvement, there was no other organ involvement which makes the diagnosis of HES unlikely. Bone marrow hypereosinophilia is not a unique feature of HES and it has been reported in patients with EGE. [17],[18]

In the Churg Strauss syndrome and polyarteritis nodosa, vasculitis is characterized by an eosinophilic infiltrate involving the small vessels in the intestinal tract and extraintestinal organs, i.e., kidneys, lungs, nervous system. Skin manifestations are present and granulomas can be found in the Churg Strauss syndrome. However, diagnoses of the Churg Strauss syndrome and polyarteritis nodosa are remote possibilities in our patient given that his asthma was controlled during the time of his presentation, absence of typical vasculitis features on histopathology examination (lack of perivascular infiltration and fibrinoid necrosis) and the absence of other organ involvement.

One interesting finding in our patient was the gangrenous bowel and multiple small perforations which can be explained by the extensive involvement of his mucosal and submucosal layers as shown by the deep ulcers and EUS findings. This extensive involvement of the mucosal and submucosal layers probably complicated by obstruction and perforation led to ischemic bowel and sepsis. Other interesting points in our patient were the dramatic response to steroid despite the severe and extensive inflammatory involvement of his stomach, small and large bowel.

In summary, eosinophilic gastroenteritis may present with a wide spectrum of clinical characteristics, such that a high index of suspicion is needed for diagnosis. This is the first case in which EUS abnormalities were demonstrated in this very rare disorder. Small intestinal perforation and ischemic bowel due to extensive eosinophilic infiltrate of the mucosal and submucosal layers has not been previously described. Involvement of the bone marrow was only reported in 2 previous cases.

 
   References Top

1.Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol 2004;113:11-28.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Talley NJ, Shorter RG, Phillips SF, Zinsmeister AR. Eosinophilic gastroenteritis: A clinicopathological study of patients with disease of the mucosa, muscle layer and subserosal tissues. Gut 1990;31:54-8.  Back to cited text no. 2  [PUBMED]  
3.Lee CM, Changchien CS, Chen PC, Lin DY, Sheen IS, Wang CS, et al . Eosinophilic gastroenteritis: 10 years experience. Am J Gastroenterol 1993;88:70-4.  Back to cited text no. 3  [PUBMED]  
4.Orenstein SR, Shalaby TM, Di Lorenzo C, Putnam PE, Sigurdsson L, Mousa H, et al . The spectrum of pediatric eosinophilic esophagitis beyond infancy: A clinical series of 30 children. Am J Gastroenterol 2000;95:1422-30.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Khan S, Orenstein SR. Eosinophilic gastroenteritis: Epidemiology, diagnosis and management. Paediatr Drugs 2002;4:563-70.  Back to cited text no. 5  [PUBMED]  
6.Khan S. Eosinophilic gastroenteritis. Best Pract Res Clin Gastroenterol 2005;19:177-98.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Klein NC, Hargrove RL, Sleisenger MH, Jeffries GH. Eosinophilic gastroenteritis. Medicine (Baltimore) 1970;49:299-319.  Back to cited text no. 7  [PUBMED]  
8.Kelly KJ. Eosinophilic gastroenteritis. J Pediatr Gastroenterol Nutr 2000;30:S28-35.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Caldwell JH, Tennenbaum JI, Bronstein HA. Serum IgE in eosinophilic gastroenteritis. Response to intestinal challenge in two cases. N Engl J Med 1975;292:1388-90.  Back to cited text no. 9    
10.Walsh RE, Gaginella TS. The eosinophil in inflammatory bowel disease. Scand J Gastroenterol 1991;26:1217-24.  Back to cited text no. 10  [PUBMED]  
11.Barak N, Hart J, Sitrin MD. Enalapril-induced eosinophilic gastroenteritis. J Clin Gastroenterol 2001;33:157-8.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994;83:2759-79.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Dhawan A, Seemayer TA, Pinsinski C, Gross TG, Shaw BW Jr, Mack DR. Posttransplant eosinophilic gastroenteritis in children. Liver Transpl Surg 1997;3:591-3.  Back to cited text no. 13  [PUBMED]  
14.Romero R, Abramowsky CR, Pillen T, Smallwood GA, Heffron TG. Peripheral eosinophilia and eosinophilic gastroenteritis after pediatric liver transplantation. Pediatr Transplant 2003;7:484-8.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Stevoff C, Rao S, Parsons W, Kahrilas PJ, Hirano I. EUS and histopathologic correlates in eosinophilic esophagitis. Gastrointest Endosc 2001;54:373-7.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Fox VL, Nurko S, Teitelbaum JE, Badizadegan K, Furuta GT. High-resolution EUS in children with eosinophilic "allergic" esophagitis. Gastrointest Endosc 2003;57:30-6.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Lyngbaek S, Adamsen S, Aru A, Bergenfeldt M. Recurrent acute pancreatitis due to eosinophilic gastroenteritis. Case report and literature review. JOP 2006;7:211-7.  Back to cited text no. 17    
18.Steffen RM, Wyllie R, Petras RE, Caulfield ME, Michener WM, Firor HV, et al . The spectrum of eosinophilic gastroenteritis. Report of six pediatric cases and review of the literature. Clin Pediatr (Phila) 1991;30:404-11.  Back to cited text no. 18    

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Correspondence Address:
Abdulrahman M Aljebreen
Gastroenterology Division, King Khalid University Hospital, Riyadh, 11321, P.O. Box 231494
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.32185

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