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MINIREVIEWS

Eosinophilic gastroenteritis: An unusual type of

gastroenteritis

Sachin B Ingle, Chitra R Hinge (Ingle)

Sachin B Ingle, Department of Pathology, MIMSR Medical © 2013 Baishideng. All rights reserved.
College, Maharashtra 4132512, India
Chitra R Hinge (Ingle), Department of Physiology, MIMSR Key words: Eosinophilic gastroenteritis; Unusual type;
Medical College, Maharashtra 4132512, India Review of literature
Author contributions: Ingle SB and Hinge (Ingle) CR prepared
the manuscript; Ingle SB critically revised the intellectual content Core tip: Eosinophilic gastroenteritis is a rare disorder
and gave final approval of manuscript.
characterised by eosinophilic infiltration of the bowel
Correspondence to: Sachin B Ingle, Associate Professor,
Department of Pathology, MIMSR Medical College, Latur, Ma- wall and various gastrointestinal manifestations. Diag-
harastra 413512, India. dr.sachiningle@gmail.com nosis requires a high index of suspicion and exclusion
Telephone: +91-2382-227424 Fax: +91-2382-228939 of various disorders that are associated with peripheral
Received: April 24, 2013 Revised: June 23, 2013 eosinophilia. Corticosteroids are the mainstay of therapy
Accepted: June 28, 2013 with a 90% response rate.
Published online: August 21, 2013

Ingle SB, Hinge (Ingle) CR. Eosinophilic gastroenteritis: An

unusual type of gastroenteritis. World J Gastroenterol 2013;
19(31): 5061-5066 Available from: URL: http://www.wjgnet.
Abstract
com/1007-9327/full/v19/i31/5061.htm DOI: http://dx.doi.
Eosinophilic gastroenteritis (EGE) is a rare disorder char- org/10.3748/wjg.v19.i31.5061
acterized by eosinophilic infiltration of the bowel wall
with various gastrointestinal manifestations. Till date only
280 cases have been described in the literature. A high
index of suspicion, by excluding other causes of periph-
eral eosinophilia, is a pre requisite for accurate diagnosis. INTRODUCTION
EGE is an uncommon gastrointestinal disease affecting Eosinophilic gastroenteritis is a rare disorder that can
both children and adults. It was first described by Kaijser present with various gastrointestinal manifestations
in 1937. Presentation may vary depending on location depending on the specific site and specific layer of the
as well as depth and extent of bowel wall involvement gastrointestinal tract involved. Majority of the cases in-
and usually runs a chronic relapsing course. This condi- volve stomach and proximal small bowel. The diagnostic
tion can respond to low dose steroid therapy, thereby criteria include demonstration of eosinophilic infiltration
preventing grave complications like ascites and intestinal of bowel wall, lack of evidence of extra intestinal disease
obstruction that might need surgical intervention. The and exclusion of other causes of peripheral eosinophilia[1-4].
natural history of EGE has not been well documented. Eosinophilic gastroenteritis is characterized by the
Eosinophilic gastroenteritis is a chronic, waxing and wan-
presence of abnormal gastrointestinal (GI) symptoms,
ing condition. Mild and sporadic symptoms can be man-
most often abdominal pain, eosinophilic infiltration in
aged with reassurance and observation, whereas dis-
abling gastrointestinal (GI) symptom flare-ups can often one or more areas of the GI tract, defined as 50 or more
be controlled with oral corticosteroids. When the disease eosinophils per high-power field, the absence of an iden-
manifests in infancy and specific food sensitization can tified cause of eosinophilia and the exclusion of eosino-
be identified, the likelihood of disease remission by late philic involvement in organs other than the GI tract.
childhood is high. GI obstruction is the most common It can be classified into mucosal, muscular and se-
complication. Fatal outcomes are rare. rosal types based on the depth of involvement[5,6]. The

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 Ingle SB et al . Eosinophilic gastroenteritis

stomach is the organ most commonly affected, followed immunohistochemically in diseased intestinal wall[21]. In
by small intestine and colon[7,8]. The anatomical locations addition eotaxin has been shown to have an integral role
of eosinophilic infiltrates and the depth of GI involve- in regulating the homing of eosinophils into the lamina
ment determine clinical symptoms. The therapeutic role propria of stomach and small intestine[22]. Indeed, many
of steroids and antihelminthic drugs in the treatment of patients have history of food allergy and other atopic
eosinophilic gastroenteritis is not established. In a few conditions like eczema, asthma etc. In this allergic subtype
cases, steroids have produced symptomatic improvement of disease, it is thought that food allergens cross the
in controlling malabsorption syndrome[1,9]. intestinal mucosa and trigger an inflammatory response
that includes mast cell degranulation and recruitment of
eosinophils[23,24].
EPIDEMIOLOGY
Eosinophilic gastroenteritis occurs over a wide age range
from infancy through the seventh decade, but most com- CLINICAL PRESENTATIONS
monly between third to fifth decades of life[10,11]. A slight The clinical presentations of eosinophilic gastroenteritis
male preponderance has been reported[12]. vary according to the site and depth of inflammatory
Although cases have been reported worldwide, the involvement of different layers of the intestinal wall.
exact incidence of eosinophilic gastroenteritis is unclear. Approximately 80% have symptoms for several years[25].
After first described by Kaijser[10], a little less than 300 Occasionally, the disease may manifest itself as an acute
cases have been reported in the literature. Kim et al[2] abdomen or bowel obstruction[13,14]. Children and ado-
reported 31 new cases of eosinophilic gastroenteritis in lescents can present with growth retardation, failure
Seoul, Korea, between January 1970 and July 2003. to thrive, delayed puberty or amenorrhea. Adults have
Venkataraman et al[5] reported 7 cases of eosinophilic abdominal pain, diarrhea or dysphagia. Mucosal disease
gastroenteritis over a 10-year period in India[5]. Chen et is the commonest variety that presents with features of
al[3] reported 15 patients including 2 children, with eo- protein losing enteropathy, bleeding or malabsorption.
sinophilic gastroenteritis in 2003. In eosinophilic enteritis Failure to thrive and anaemia may also be present. Lower
the morbidity is mainly due to combination of chronic gastrointestinal bleeding may imply colonic involve-
nonspecific GI symptoms which include abdominal pain, ment[1,26,27]. Involvement of muscle layer may cause bowel
nausea, vomiting, diarrhea, weight loss, and abdominal wall thickening and intestinal obstruction. Cramping and
distension and more serious complications like intestinal abdominal pain associated with nausea and vomiting oc-
obstruction and perforation[13,14]. curs frequently. It can also present as an obstructing cae-
cal mass or intussusception. The subserosal form, which
is least common but can cause more morbidity, usually
PATHOPHYSIOLOGY presents as eosinophilic ascites, which is usually an exu-
Eosinophilic gastroenteritis can involve any part of date, with abundant peripheral eosinophilia. Serosal and
gastrointestinal tract from esophagus down to the rectum. visceral peritoneal inflammation leads to leakage of fluids
The stomach and duodenum are the most common sites but has a more favourable response to corticosteroids. In
of involvement[1,13-17]. The etiology and pathogenesis is literature features like cholangitis, pancreatitis[28], eosino-
not well understood. There is evidence to suggest that philic splenitis, acute appendicitis and giant refractory
a hypersensitivity reaction may play a role. The clinical duodenal ulcer are also mentioned.
presentations of eosinophilic gastroenteritis vary according
to the site and depth of eosinophilic intestinal infiltration.
The presence of peripheral eosinophilia, abundant DIAGNOSTIC EVALUATION
eosinophils in the gastrointestinal tract and dramatic Four criteria are required for the diagnosis of eosino-
response to steroids provide some support that the disease is philic gastroenteritis namely-presence of gastrointestinal
mediated by a hypersensitivity reaction[1,18]. Moreover, a study symptoms, eosinophilic infiltration of gastrointestinal
at Mayo clinic showed that 50% of patients with eosinophilic tract, exclusion of parasitic disease and absence of other
gastroenteritis give history of allergy such as asthma, rhinitis, systemic involvement. The presence of peripheral eo-
drug allergy and eczema[1]. Peripheral blood eosinophilia sinophilia is not a universal phenomenon[1,29].
and elevated serum immunoglobulin E (IgE) are usual but A thorough evaluation of the patient is necessary,
not universal. The damage to the gastrointestinal tract wall starting with laboratory evaluation.
is caused by eosinophilic infiltration and degranulation[19]. After a detailed history and physical examination, a
Eosinophils are normally present in gastrointestinal mucosa complete blood count plays an important role. Peripheral
as a part of host defense mechanism, though the finding in blood eosinophilia is found in 20%-80% of cases. Aver-
deeper tissue is almost always pathologic[20]. In eosinophilic age count is 2000 eosinophils (eos)/µL in patients with
gastroenteritis (EGE) cytokines interleukin (IL)-3, IL-5 and mucosal layer involvement, 1000 eos/µL in patients with
granulocyte macrophage colony stimulating factor may be muscle layer involvement, and 8000 eos/µL in patients
responsible for the recruitment and activation of eosinophils with serosal involvement. Iron-deficiency anemia may be
and hence the pathogenesis. They have been observed evident on mean corpuscular volume. Serum albumin may

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 Ingle SB et al . Eosinophilic gastroenteritis

B
Figure 1 Endoscopy showing small superficial ulcers in stomach.

be low, especially in patients with mucosal involvement.

Fecal protein loss can be assessed by measuring
alpha1-antitrypsin in a 24-h feces collection. It is used
to identify the inability to digest and absorb proteins in
the GI tract. The normal value is 0-54 mg/dL. Patients
with eosinophilic gastroenteritis have elevated alpha1-
antitrypsin in their feces. Protein loss can also result in
low levels of total immunoglobulins, but serum IgE
could be elevated, which then strongly supports the diag-
nosis of eosinophilic gastroenteritis in conjunction with C
other findings. The erythrocyte sedimentation rate can be
elevated in few cases.
Stool examination should be performed to rule out
parasitic infestation. Mild-to-moderate steatorrhea is
present in approximately 30% of patients. This can be
measured by qualitative and quantitative stool tests. Skin
prick tests help to identify sensitization to specific inges-
tant and/or inhalant allergens.
Computed tomography (CT) scan may show nodular
and irregular thickening of the folds in the distal stomach
and proximal small bowel, but these findings can also
be present in other conditions like Crohn’s disease and Figure 2 Large numbers of eosinophils are often present in the muscula-
lymphoma. On ultrasonography ascitic fluid is usually de- ris and serosa. A, B: Showing dense eosinophilic infiltrates in the lamina pro-
tected in patients with serosal involvement. pria and mucosa (× 10); C: Showing dense eosinophilic infiltrates in the lamina
Radiographic changes are variable, nonspecific, and/ propria and mucosa (× 40).
or absent in at least 40% of patients. Gastric folds can
be enlarged, with or without nodular filling defects. In biopsy specimens from normal and abnormal areas of
extensive disease strictures, ulceration or polypoid lesions the bowel to exclude the possibility of sampling error. In
may occur and valvulae conniventes may be thickened patients with esophageal or colonic symptoms, additional
and flattened. In eosinophilic gastroenteritis involving biopsy specimens may be obtained from the relevant sites
the muscle layer, localized involvement of the antrum to aid the diagnosis.
and pylorus may occur, causing narrowing of the distal Patients with serosal disease present with ascites. Ab-
antrum and gastric retention. The small intestine may be dominal paracentesis demonstrates a sterile fluid with a
dilated, with an increase in the thickness of the mucosal high eosinophil count. Pleural effusion also may be present.
folds. Prominent mucosal folds may be observed in the The diagnosis can be confirmed on histopathological
colon. Other tests like exploratory laparotomy may be examination of gastric and duodenal biopsies. The gross
indicated in patients with serosal eosinophilic gastroenteritis. appearance of eosinophilic gastroenteritis upon endos-
The endoscopic appearance is nonspecific. It includes copy shows erythematous, friable, nodular, and often
erythematous, friable, nodular, and occasional ulcerative ulcerated mucosa. Microscopy demonstrates increased
changes[3] (Figure 1). Sometimes diffuse inflammation numbers of eosinophils (often > 50 eos per high-power
results in complete loss of villi, involvement of multiple field) in the lamina propria. Large numbers of eosino-
layers, submucosal oedema and fibrosis[30,31]. When per- phils are often present in the muscularis and serosa (Fig-
forming endoscopy, it is necessary to obtain at least 6 ure 2). Localized eosinophilic infiltrates may cause crypt

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 Ingle SB et al . Eosinophilic gastroenteritis

copy, ridges or furrows may be seen in the esophageal

mucosa. Presence of white exudates in esophagus is also
suggestive of the diagnosis[37,38].

Treatment
The role of steroids and antihelminthic drugs is not well
established. However, in a few cases, steroids have been
reported to produce symptomatic improvement in con-
trolling diarrhea and protein losing enteropathy[9].
Corticosteroids are the mainstay of therapy with a
90% response rate in some studies (Figure 3). Appropri-
ate duration of steroid treatment is unknown and relapse
often necessitates long term treatment. Various steroid
Figure 3 Post treatment (low dose steroid) biopsy showing resolution of sparing agents, e.g., sodium cromoglycate (a stabilizer of
disease.
mast cell membranes), ketotifen (an antihistamine), and
montelukast (a selective, competitive leukotriene receptor
hyperplasia, epithelial cell necrosis, and villous atrophy. antagonist) have been proposed, centering around an al-
Diffuse enteritis with complete loss of villi, submucosal lergic hypothesis, with mixed results[24,39,40].
edema, infiltration of the GI wall, and fibrosis may be
apparent. Mast cell infiltrates and hyperplastic mesenteric Corticosteroids
lymph nodes infiltrated with eosinophils may be pres- Fluticasone inhaled (Flovent): Decreases recruitment
ent[1,27,31,32]. Infiltration is often patchy, can be missed and of inflammatory cells including eosinophils and decreases
laparoscopic full thickness biopsy may be required. the release of eotaxins and other inflammatory media-
Histologic analysis of the small intestine reveals in- tors. Dosage required is higher than that used in asthma.
creased deposition of extracellular major basic proteins
and eosinophilic cationic proteins. Prednisolone (AK-Pred, Delta-Cortef): Decreases
Radio isotope scan using technetium (99mTc) exam- inflammation by suppressing migration of polymorpho-
etazime-labeled leukocyte single-photon emission CT nuclear leukocytes and reducing capillary permeability.
may be useful in assessing the extent of disease and re- Equivalent dosages of prednisone or methylprednisolone
sponse to treatment but has little value in diagnosis, as may be used.
the scan does not help differentiating EGE from other
causes of inflammation[33,34]. Budesonide (Pulmicort Respule) oral viscous sus-
When eosinophilic gastroenteritis is observed in as- pension: Decreases inflammation, reduces capillary per-
sociation with eosinophilic infiltration of other organ meability[6].
systems, the diagnosis of idiopathic hypereosinophilic
syndrome should be considered[35].
MAST CELL STABILIZERS
Differential diagnosis Cromolyn (Intal, Gastrocrom): Inhibits release of hista-
The main differential diagnoses are: (1) eosinophilic mine, leukotrienes, and other mediators from sensitized
esophagitis; (2) eosinophilic ascites; (3) coeliac disease; (4) mast cells. It also inhibits the influx of neutrophils, as
protein losing enteropathy from intolerance to cow milk well as the formation of the active form of NADPH
protein; (5) infantile formula protein intolerance; and (6) oxidase, which in turn prevents tissue damage caused by
idiopathic hypereosinophilic syndrome. oxygen radicals.
A diagnosis of idiopathic hypereosinophilic syndrome
can be ruled out when there is absence of eosinophilic Leukotriene receptor antagonists
infiltration in all other organs except the bowel[35]. Prevent or reverse some of the pathologic features as-
In celiac disease, biopsy of small bowel shows blunt- sociated with the inflammatory process mediated by
ing of villi, crypt hyperplasia, and predominantly lym- leukotrienes C4, D4 and E4. Successful treatment of eo-
phocyte infiltration of crypts. Coeliac disease is caused by sinophilic gastroenteritis has been reported in few cases,
a reaction to gliadin, a prolamin (glutenprotein) found in mainly with Montelukast (Singulair) which is a potent and
wheat, and similar proteins found in other grains[36]. selective antagonist of leukotriene D4 at the cysteinyl
In eosinophilic esophagitis only the eosophagus is leukotriene receptor, CysLT1[41].
involved and not the whole bowel. A minimum of 15 eo-
sinophils per high power field is required to make the di- Role of surgical care
agnosis. Typically, eosinophils can be found in superficial Surgery is avoided, except when it is necessary to relieve
clusters near the surface of the epithelium. An expansion persistent pyloric or small bowel obstruction. Most patients
of the basal layer is also seen in response to the inflam- respond to conservative measures and oral glucocorticoste-
matory damage to the epithelium. At the time of endos- roids. Recurrence is possible, even after surgical excision.

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 Ingle SB et al . Eosinophilic gastroenteritis

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