Discussion
Eosinophilic gastroenteritis (EG) is a chronic inflammatory disorder
that is characterized by variable degrees of infiltration of eosinophils
within the gastrointestinal tract. EG can occur at any age, and was
first described by Kaijser in 1937
[8]. The true
incidence of EG remains unclear due to its rare nature, and most of the
literature is mainly case reports. Although no accurate epidemiologic
data are available, the incidence of EG is estimated to be approximately
1-30/100,000 [3,4], and the prevalence seems to have been increasing
in the past two decades
[9].
Eosinophils are normally present in the lamina propria, except the
esophagus, and the number of eosinophils along the GI tract varies, with
the highest concentrations found in the cecum and appendix [10].
Eosinophils are involved in the mucosal immune system of the GI tract
and play a role in host defense in healthy individuals [11]. The
number of eosinophils increases during the pathogenesis of numerous
inflammatory processes, including parasitic infections and allergic
diseases. Then, the activated eosinophils produce and release highly
bioactive inflammatory mediators, which may lead to a series of problems
in the GI tract [12,13]. However, the exact mechanism of the
pathogenesis of EG is still unclear.
Although the etiology and pathogenesis of EG remain unclear, there are
studies suggesting that approximately 45–63% of patients diagnosed
with EG had a history of allergies, such as asthma, rhinitis, drug or
food allergies; eczema; and parasitic infections
[14,15], while
others have found an association with other autoimmune conditions, such
as HIV infection
[16],
influenza A virus infection
[17],
ulcerative colitis, and systemic lupus erythematosus
[14]. The
clinical manifestations of EG are not specific. The manifestations
depend on the extent and depth of eosinophilic infiltration into the
gastrointestinal tract wall. Three clinical forms are classified,
mucosa, muscularis, and serosal, which are based on the Klein
classification from 1970
[5]. The form
involving the mucosal layer is the most common type, which can manifest
as abdominal pain, hematochezia, diarrhea, hypoproteinemia and weight
loss. Patients with EG that involves the muscularis can present with
intestinal obstruction and even perforation. When the serosal layer is
affected, ascites are the main manifestation. Full layer involvement is
rare. Endoscopic findings may vary from nonspecific to mucosal erythema
and ulceration
[18].
Therefore, EG is easily misdiagnosed due to its various clinical and
endoscopic manifestations.
In our case, we diagnosed the patient with eosinophilic gastroenteritis,
and the full layer of the gastrointestinal wall was involved, mainly
based on the following clinical evidence: First, signs of
gastrointestinal whole wall involvement, such as diarrhea with blood and
mucus, hypoproteinemia, abdominal pain, and abdominal distention, were
observed. Second, endoscopic tissue biopsy revealed marked eosinophilic
infiltration in the gastric antrum and sigmoid colon mucosa layer;
eosinophils in peripheral blood and ascites increased significantly.
Abdominal CT showed signs of thickened intestinal wall and ascites.
Finally, the corresponding examination was improved to exclude
tuberculosis peritonitis, IBD, parasitic infection, malignant tumor,
intestinal Behcet’s disease, lymphoma, and eosinophilia. Unfortunately,
deep biopsies of the gastrointestinal tract were not available for
additional evidence.
Corticosteroid therapy is the mainstay of EG treatment in both adults
and children. Other therapies include dietary therapy, leukotriene
inhibitors, mast cell stabilizers, interleukin-5 inhibitors, ketotifen,
and biological agents
[13,19]. We
recommended methylprednisolone therapy to the patient, and the above
symptoms were significantly relieved and eosinophils gradually decreased
to normal. There was no recurrence after 6 months of follow-up.
Due to the lack of clinical experience, and little attention has been
paid to the eosinophilic infiltration in the process of pathological
diagnosis, doctors in primary hospitals misdiagnosed as cholelithiasis,
and even cholecystectomy has been done. In conclusion, EG is a rare
gastrointestinal disease with atypical clinical manifestations that are
easily misdiagnosed. Timely and correct diagnosis depends on the
clinician’s understanding of the disease. Besides, more attention from
the pathologists should be paid to the eosinophilic infiltration in the
process of pathologic diagnosis. For patients with increased eosinophils
in peripheral blood accompanied by gastrointestinal symptoms, EG should
be considered. However, eosinophils in peripheral blood may not increase
in some patients, which means further endoscopic multisite biopsy to
determine whether eosinophils are infiltrating is the key to diagnosis.