The Turkish Journal of Gastroenterology
2008, Volume 19, No 1, Page(s) 54-56
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|Eosinophilic colitis as an unusual cause of severe bloody
|İbrahim ERTUĞRUL1, Aysel ÜLKER1, Nesrin TURHAN2, Ülkü DAĞLI1, Nurgül ŞAŞMAZ1
|Departments of 1Gastroenterology and 2Pathology, Türkiye Yüksek İhtisas Hospital, Ankara
|Keywords: Eosinophilic colitis, hypereosinophilia, bloody
Eosinophilic gastrointestinal diseases may affect the colon;
however, isolated colonic involvement is very rare. Diagnosis of
eosinophilic colitis requires clinical suspicion and it should be
differentiated from other disorders causing eosinophil accumulation
in the colon tissue. Herein we present a 46-year-old
female admitted to the hospital with the complaints of bloody
diarrhea (25-30 times a day), fever, abdominal pain and weight
loss. Eosinophilic colitis was diagnosed and she was treated
with steroid successfully.
Eosinophilic gastrointestinal disease is rare, and
isolated colonic involvement appears to be very
sporadic (1, 2). Since clinical and endoscopic features
of eosinophilic colitis (EC) are not characteristic,
it may be difficult to determine isolated colonic
involvement. The differential diagnosis of EC requires
Herein we present a new case with EC. We also
discuss the pathogenesis and therapeutic approaches
in these patients in the light of the pertinent
A 46-year-old female was admitted to the hospital
with the complaints of bloody diarrhea (25-30 times
a day), fever, abdominal pain and weight loss
(12 kg) for a month. Past medical history revealed
mitral valve replacement 12 years ago. She denied
any exposure to toxins or other drugs other than
warfarin and digoxin, and she had no asthma or
Physical examination revealed all quadrant tenderness
and rectal bleeding. Laboratory findings were
as follows: hemoglobin 10.0 g/dl, WBC 12,100/mm3,
eosinophil count 2,300/mm3 (0?700/mm3), and platelet
count 488,000/mm3. Biochemical tests were
within normal limits other than albumin 3.1 g/dl.
Stool was positive for Charcot-Leyden crystals. Serum
immunoglobulin E (IgE) concentration was
normal. The relevant serological tests (antinuclear
antibody and antibodies to extractable nuclear antigens)
Endoscopic examination of upper gastrointestinal
system revealed antral gastritis. Mucosa and lumen
of the duodenum were normal. An abdominal
sonography revealed thickening of the wall of the
rectum (7.8 mm). Colonoscopy showed mucosal ulcerations
localized to the transverse colon, splenic
flexura, and descending and sigmoid colon (Figure
1). Histology of colonic biopsy samples showed active
inflammatory reaction with focal clusters of
eosinophils in lamina propria, consistent with EC.
There was no cryptitis, cryptic abscess or atrophy.
No ischemic or vasculitic features were identified
She was treated with systemic steroids for two weeks
and became well. At a follow-up visit one
month after the discharge, colonoscopy and control
biopsy were normal.
Eosinophilic infiltration of the gastrointestinal
tract in relation with a recognizable clinical picture
is an uncommon entity. Diagnosis of EC requires
clinical suspicion and it should be differentiated
from other disorders (inflammatory bowel disease,
parasitic diseases, eosinophilic gastroenteritis,
infections, drug reactions, vasculitis) causing
eosinophil accumulation in the colon tissue (3).
The pathogenesis of EC is not clear and it is considered
to be idiopathic. Role of eotaxin-1 and eosinophils
in the pathogenesis of the disease provides
a possible hypothesis for eosinophil-induced gastrointestinal
dysfunction. Excessive accumulation
of eosinophils results in release of eosinophilic major
protein causing destruction of the intestinal
epithelium (4, 5). Recently, gastrointestinal hypereosinophilic
disorders have been classified into
three categories: IgE-mediated, partially IgE-mediated
and cell-mediated (6). In contrast to other
gastrointestinal hypereosinophilic disorders, EC
is usually a non-IgE?associated disease. Some studies
point to a T lymphocyte?mediated process,
but the exact immunologic mechanisms responsible
for this condition have not been identified (7).
Similarly, our case had normal serum IgE.
Similar to eosinophilic gastroenteritis, there are a
variety of symptoms associated with EC, depending
on the degree and location of tissue involvement.
There are three specific patterns of eosinophilic
infiltration of the gastrointestinal tract reflected
in the presentation. Mucosal disease is usually
associated with protein-losing enteropathy,
subserosal disease with eosinophilic ascites, and
transmural disease with ileus or perforation (8).
Hypoalbuminemia may have been due to proteinlosing
enteropathy or active gastrointestinal bleeding
in our case.
Three criteria were defined for EC diagnosis: the
presence of gastrointestinal symptoms, biopsies
showing eosinophilic infiltration of one or more
areas of the gastrointestinal tract from the esophagus
to colon, or characteristic radiologic findings
with peripheral eosinophilia and no evidence
of parasitic or extraintestinal disease (5). All of
these criteria were present in our case. The peripheral
eosinophilic count seems to be normal in some
patients with EC, suggesting that it is not a reliable
diagnostic criterion. Therefore, no single
test is the gold standard for diagnosis, but peripheral
blood eosinophilia or eosinophils in the stool
are suggestive of EC (5, 9, 10).
Treatment of EC varies, primarily depending on
the disease subtype. Drugs such as cromoglycate,
montelukast, and histamine receptor antagonists
are generally not successful. Anti-inflammatory
drugs, including aminosalicylates and systemic or
topical glucocorticoids, are commonly used and appear
to be efficacious. There are several forms of
topical glucocorticoids designed to deliver drugs to
the distal colon and rectum, but EC typically also involves the proximal colon, as in our case. In severe
cases, refractory or dependent on systemic
glucocorticoid therapy, intravenous alimentation
or immunosuppressive therapies such as azathioprine
or 6-mercaptopurine are alternatives (11).
In conclusion, EC may present with severe bloody
diarrhea. It should be kept in mind especially in
the differential diagnosis of inflammatory bowel
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