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The Turkish Journal of Gastroenterology |
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2005, Volume 16, No 4, Page(s) 236-239 |
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| A rare cause of colonic stricture: Amebiasis |
| Muhsin KAYA1, Fatih AYDIN2, Hüseyin BÜYÜKBAYRAM3 |
1Department of Gastroenterology, SSK Region Hospital, Diyarbakır
2Department of Gastroenterology, Türkiye Yüksek İhtisas Hospital, Ankara
3Department of Pathology, Dicle University School of Medicine, Diyarbakır |
| Keywords: Amebiasis, colonic stricture. |
| Summary |
A 41-year-old man presenting with lower abdominal pain, constipation,
abdominal distention, fever (37.5°C) and fatigue was
evaluated, and a mass localized to the left lower abdomen was
identified. Radiographic and colonoscopic examination revealed
a stricture 10 cm in length localized to the sigmoid-descending
colon junction. The diagnosis of amebiasis was confirmed
by histological examination of a biopsy specimen taken from the
stricture and stool examination. One month after the initiation
of metronidazole treatment, complete clinical and laboratory
improvement was observed. In the differential diagnosis of colonic
stricture, amebiasis should also be considered. |
Top
Summary
Introduction
Case Presentation
Discussion
References
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| Introduction |
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Amebiasis is an infectious disease caused by the
protozoan Entamoeba histolytica, which is common
in tropical countries and infects 10% of the
world’s population, resulting in approximately
100, 000 deaths per year. Amebiasis may involve
any part of the bowel, but it has a predilection for
the cecum and ascending colon (1). Colorectal
amebiasis may present in many different clinical
forms including the asymptomatic carrier state
(2), acute amebic colitis, toxic mega colon (1), and
fulminant necrotizing colitis with intestinal bleeding
and perforation (3, 4). While tissue necrosis
is often encountered in amebic colitis, chronic inflammatory
response with formation of a pseudotumor
or ameboma (5, 6) and colonic stricture (7) by
excessive granulation tissue on the intestinal wall
is less common. A quick diagnosis is possible by
examining the stool for trophozoites and cysts, but
it may be negative (1, 2). The classical colonoscopic
appearance is that of discrete areas of
ulceration covered by exudate with normal intervening
mucosa (1, 8). Rectal biopsy is useful and
accurate as it may reveal the presence of the parasites
and at the same time exclude the possibility
of a carcinoma (3-5). We reported a case with colonic
stricture simulating colon cancer. |
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Summary
Introduction
Case Presentation
Discussion
References
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| Case Presentation |
A 41-year-old man was referred to our hospital
with a chief complaint of lower abdominal pain,
constipation, abdominal distention, fever (37.5°C)
and fatigue for four weeks. There was no weight
loss. His family history was unremarkable except
for the death of his uncle two years ago due to colon
cancer. Physical examination revealed slight
tenderness and mass localized to the left lower abdomen.
Laboratory tests were normal except for
leukocytosis (13,000/mm3) and elevated erythrocyte
sedimentation rate (52 mm/hour). All biochemistry
parameters including tumor markers were within the normal limits. The stool was positive
for cysts of Entamoeba histolytica. Ultrasonography
showed marked bowel wall thickness in the
sigmoid-descending colon junction (Figure 1). Maximal
wall thickness was 20 mm. Computerized
abdominal tomography showed bowel wall thickness
and luminal narrowing in the sigmoid-descending
colon junction. Barium enema examination
revealed stricture 10 cm in length localized to
the defined bowel segment (Figure 2). Colonoscopy
showed stricture and markedly diffuse edematous
mucosa localized to the 50th cm of the sigmoid colon.
We could not traverse the stricture because of severe luminal narrowing. However, no notable
findings were observed below the defined lesion.
Histological examination of a biopsy specimen taken
from the edematous mucosa by colonoscopy
revealed inflammatory cell infiltration without ulceration
and numerous trophozoites of Entamoeba
histolytica, some of which contained ingested
erythrocytes (Figure 3). The patient was treated
with metronidazole (1500 mg/day) and ciprofloxacin
(1000 mg/day) for 15 days. His symptoms
completely resolved and abnormal laboratory findings
improved after completion of therapy. One
month after the initiation of therapy, abdominal ultrasonography and tomography showed significant
regression in the bowel wall thickness (maximal
bowel wall thickness was 8 mm), barium enema
study did not show any stricture (Figure 4) and
colonoscopy did not reveal any remarkable findings
from the rectum to the cecum except for minimal
mucosal edematous appearance localized to
the sigmoid-descending colon junction. During 10
months’ follow-up, the patient was asymptomatic.
Figure 1. Ultrasonographic appearance
of circular wall
thickness at the sigmoid-descending colon junction
Figure 2. Radiographic appearance of
stricture at the
sigmoid-descending colon junction
Figure 3. Numerous Entamoeba
histolytica trophozoites, some
containing ingested erythrocytes (arrow) with sparse inflammatory
cells in the biopsy specimen taken from colonic stricture
(H&EX400)
Figure 4. Stricture localized to the
sigmoid-descending colon
disappeared one month after the initiation of therapy |
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Summary
Introduction
Case Presentation
Discussion
References
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| Discussion |
Entamoeba histolytica is endemic in most tropical
and subtropical countries (9). Infection usually begins
with the ingestion of the cysts in food or water
that is contaminated by human feces. Many
individual with Entamoeba histolytica infection
have no symptoms and can clear their infection
without any signs of disease. Patients with amebic
colitis present with bloody diarrhea, abdominal
pain and tenderness. Multiple small volume
mucoid stools are common, but profuse, watery diarrhea
might be noted. Fever, weight loss and
anorexia can be present. Occasionally, individuals
develop fulminant amebic colitis, with profuse bloody
diarrhea, fever, and widespread abdominal
pain often with peritoneal signs (1). In addition,
colorectal amebiasis may occasionally manifest as
an ameboma which can resemble a carcinoma (5,
10, 11), and manifest as colonic strictures (7, 12,
13). In our patient, the presence of familial history
of colon cancer, localized mass lesion, significantly
thickened colonic wall and severe narrowing in colonic
lumen and obstruction symptoms supported
the possibility of malignant stricture. But, the
presence of leukocytosis, elevated erythrocyte sedimentation
rate, fever and tenderness over left
lower abdomen were consistent with co-existence
of infection. Occurrence of amebiasis is relatively
high in the patient’s city of residence, but amebomas
and amebic strictures are rare. The patient
had no previous history of amebic colitis. Although
we identified Entamoeba histolytica trophozoite
in the patient’s stool, we did not consider
amebic stricture before exclusion of other possible
diagnoses.
Colonoscopic features of ameboma may be erosions,
ulcers (6, 8, 13), edema, and nodularity that
narrow the lumen (6), ring-like stenosis (14), or
polypoidal stricture (5) within the colorectum. Accurate
clinical diagnosis and early histological
confirmation are mandatory in order to institute
rational management. The co-existence of an underlying malignant lesion in association with
an inflammatory lesion in an endemic area should
always be considered, particularly if it fails to respond
to empirical therapy within a short period of
time (7). In our patient, colonoscopic features were
more compatible with inflammatory mass lesion
rather than neoplasm. Histological examination
of a biopsy specimen taken from the lesion revealed
severe inflammatory infiltration with numerous
trophozoites of Entamoeba histolytica,
and there were no histological findings to support
the colon cancer. In addition, complete clinical and
radiological improvement after metronidazole treatment
excluded the possibility of the co-existence
of an underlying malignant lesion in association
with amebic stricture in our case.
Non-malignant lesions accounted for strictures in
two-thirds of patients and included amebiasis, tuberculosis,
ischemic colitis, diverticulosis, radiation
colitis, nonspecific colitis, ulcerative colitis/
Crohn’s colitis and other lesions (7). The typical
mucosal alterations that are specific for ulcerative
colitis are continuous involvement from the anus
and proximal extension, diffuse cryptitis, erosions,
and loss of vascular pattern, and for Crohn’s disease
are skip lesions, cobble stoning, aphthous ulcers,
longitudinal ulceration, ileocecal involvement
and anal lesions. Benign or malignant strictures
in the colon can be seen in patients with ulcerative
colitis and Crohn’s disease. To distinguish
between malignant and benign stricture, multiple
biopsy specimens should be taken from the edges
and the lumen of the strictures (15). In our patient,
we considered Crohn’s disease and not ulcerative
colitis in the differential diagnosis because of
clinical history and the presence of localized bowel
wall thickness with stricture formation. However,
the colonoscopic features, including the presence
of diffuse mucosal inflammation without ulceration,
skip lesions, cobble stoning or perianal lesions,
were not compatible with Crohn’s disease, and the
biopsy specimen taken from the stricture contained
no histological findings such as granuloma
formation that can be considered indicative of
Crohn’s disease. Complete clinical, radiological
and endoscopic improvement without specific treatment
for inflammatory bowel disease also excluded
the possibility of Crohn’s disease.
Diverticular disease is rare in individuals younger
than 50 years, and most affected patients have
multiple diverticula. Pa rtial colonic obstruction
can occur during an attack of acute diverticulitis because of the relative luminal narrowing resulting
from pericolic inflammation or compression
by an abscess. Recurrent attacks of acute diverticulitis,
which may be sub-clinical, can initiate
progressive fibrosis and stricturing of the colonic
wall (16). We considered stricture formation caused
by diverticulitis with co-existence of amebiasis
in the differential diagnosis. However, absence
of any other diverticula outside the stricture,
the relatively younger age of the patient (when
considering development of diverticular disease)
and lack of peri-strictural abscess formation did
not support stricture formation secondary to
diverticulitis.
Ischemic colitis is generally more common among
the elderly with considerable cardiovascular morbidity.
The typical clinical presentation is acute
sudden abdominal pain and distention with bloody
diarrhea. Common early radiographic signs include
thickening with thumb-printing of the bowel
wall and late signs are ulceration and stricture.
Findings vary greatly depending on the stage at
which colonoscopy is performed. At the outset,
purplish blebs representing mucosal and submucosal
hemorrhage may be seen. As the hemorrhage
is resorbed, varying degrees of necrosis, inflammation,
ulceration and mucosal sloughing occur,
resembling ulcerative colitis or Crohn’s disease (17). Our patient had no cardiovascular disease
that can cause ischemic bowel disease. We did not
consider ischemic colitis in our patient because clinical
presentation, radiographic findings, colonoscopic
appearance of colonic mucosa and response
to antimicrobial treatment were not compatible
with ischemic colitis.
It has been reported that gray-scale ultrasonography
can demonstrate wall thickening of the cecum,
sigmoid colon and rectum of a patient with
amebic colitis. Maximum wall thickness was reported
as 29.9 mm at the cecum, 26.5 mm at the
sigmoid colon and 18.1 mm at the rectum. The layered
structure of the wall was conserved, and the
submucosal layer showed remarkable thickening
(18). In the present case, ultrasonography revealed
marked and discrete thickening of the bowel
wall (maximal wall thickness was 20 mm) which
corresponded well to the findings of barium enema
and colonoscopic examination. One month after
the initiation of therapy, there was significant regression
in the maximal bowel wall thickness (from
20 mm to 8 mm). Ultrasonography may be a useful
and noninvasive method for detection and follow-
up of bowel wall abnormality of amebic stricture.
In conclusion, in the differential diagnosis of colonic
stricture, amebiasis should also be considered.
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Top
Summary
Introduction
Case Presentation
Discussion
References
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| References |
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1. Stanley SL. Amoebiasis. Lancet 2003; 361: 1025-34.
2.Weinrach DM, Wang KM. Amebic colitis in an asymptomatic
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in unsuspected amebic colitis. Dig Dis Sci 2000; 45:
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4.Ishida H, Inokuma S, Murata N, et al. Fulminant amoebic
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mimicking a carcinoma. Tech Coloproctol 2003; 7: 51-3.
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ameboma. Gastrointest Endosc 2003; 58: 577.
7.Pillay SP, Moshal MG, Spitaels JM, et al. Etiology of colonic
strictures in South African black and Indian patients.
Dis Colon Rectum 1981; 24: 107-13.
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9. Blessmann J, M. Ali IK, Ton Nu PA, et al. Longitudinal
study of intestinal Entamoeba histolytica infections in
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12.Cain GD, Wolma FJ, Patterson M. Extensive stenosis of colon
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13.Ito Y, Toda K, Shimazaki M, et al. A case of amebic colitis
cured with multiple cicatricial strictures. Kansenshogaku
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14.Rouas L, Amrani M, Reguragui A, et al. Diagnostic problems
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15.Hommes DW, Van Deventer SJH. Endoscopy in inflammatory
bowel disease. Gastroenterology 2004; 126: 1561-73.
16.Farrell RJ, Farrell RJ, Morrin M MD.iverticular disease in
the elderly. Gastroenterol Clin North Am 2001; 30: 475-96.
17.Greenwald DA, Brandt LJ, Reinus JF. Ischemic bowel disease
in the elderly. Gastroenterol Clin North Am 2001; 30:
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18.Tsujimoto T, Kuriyama S, Yoshiji H, et al. Ultrasonographic
findings of amebic colitis. J Gastroenterol 2003; 38: 82-6.
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Top
Summary
Introduction
Case Presentation
Discussion
References
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[ Summary ]
[ PDF ]
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