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BRIEF COMMUNICATIONS
Fulminant Amoebic Colitis following Loperamide Use
Alastair McGregor, MRCP,* Michael Brown, MRCP, PhD,* Khin Thway, MBBS,† and
Stephen G. Wright, FRCP*
*Hospital for Tropical Diseases and †Department of Histopathology, University College London Hospitals
NHS Trust, London, UK
DOI: 10.1111/j.1708-8305.2006.00096.x
Toxic megacolon is a rare consequence of infection with Entamoeba histolytica. We present such a patient in whom the
course of disease may have been influenced by heavy loperamide use. Loperamide and other anti-motility agents have
been implicated previously in the pathogenesis of toxic megacolon in patients with infectious gastroenteritis.
Case Report
A 58-year-old Colombian woman presented with a 12day history of worsening diarrhea and abdominal pain.
She had left Colombia 15 days previously and had spent 2
weeks traveling through Spain, France, and Italy. Three
days into her holiday, she developed mild diarrhea that
progressively worsened and became bloody. This was associated with loss of appetite, nausea, and, more recently,
abdominal pain and fever. A 3-day course of rifaximin
200 mg every 8 hours (a nonabsorbable antibiotic) was
given 8 days into her illness, with no effect. To control
her symptoms, she had been taking loperamide 2 mg every 6 hours for 12 days. Her medical history was unremarkable, except for an unconfirmed diagnosis of
amoebic dysentery many years before and long-standing
hypothyroidism, for which she was taking thyroxine.
On admission, her vital signs were stable, but she was
pyrexial. Examination revealed a distended and diffusely
tender abdomen, with reduced bowel sounds but no peritonism. An abdominal radiograph revealed dilated loops
of both large and small bowel; the transverse colon dilated to a diameter of up to 10 cm (Figure 1). Blood tests
on admission showed evidence of sepsis with neutropenia (0.38 × 109 cells/L), lymphopenia (0.55 × 109 cells/L),
hyponatremia (120 mmol/L) and hypoalbuminemia
Corresponding Author: Michael Brown, MRCP, PhD, Department of Infectious & Tropical Diseases, London School of
Hygiene & Tropical Medicine, Keppel Street, London WC1E
7HT, UK. E-mail: [email protected]
(19 g/L). Renal and liver function tests were otherwise
normal.
During the first 24 hours of her admission, her clinical state deteriorated and she was transferred to intensive
care unit (ICU). An abdominal computed tomography
scan showed gas in the peritoneal cavity. Urgent laparotomy revealed extensive, full-thickness, patchy necrosis of the colon and dilatation involving the entire colon
as far as the distal sigmoid. A subtotal colectomy with ileostomy was performed. Cefuroxime and metronidazole
were given at this stage for fecal peritonitis. The patient
made a slow but steady recovery, with resolution of hematological and biochemical parameters. On histological examination of the resected colon, numerous invading
trophozoites of Entamoeba histolytica were seen, indicating that amoebic colitis was the cause of the megacolon
and perforation in this case (Figure 2). Serological investigations for E histolytica on the day of admission revealed a positive cellulose acetate precipitation test and
an immunofluorescence antibody titer of 1:640. A single
stool sample from the patient on admission did not
contain cysts or trophozoites on microscopy; culture for
Salmonella, Shigella, Campylobacter, and Escherichia coli
0157 was negative, and Clostridium difficile toxin was not
detected.
Discussion
Fulminant amoebic colitis is an uncommon but recognized consequence of infection with E histolytica.1 Features of infection range from asymptomatic passage of
© 2007 International Society of Travel Medicine, 1195-1982
Journal of Travel Medicine, Volume 14, Issue 1, 2007, 61–62
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McGregor et al.
The history of frequent loperamide use in our patient,
the onset of symptoms after traveling from a high-prevalence country to a low-prevalence country (along with
her unconfirmed history of amoebic dysentery), and the
absence of prior corticosteroid use raise the possibility
that loperamide may have played a role in her clinical
course. Many reports have suggested that the use of this
drug may be associated with progression of gut infections
with invasive or toxin-producing organisms to toxic dilatation, although there have been no confirmed cases of
amoebiasis among these.5–11 Loperamide exerts its antidiarrheal effect by inhibiting smooth muscle motor function to delay passage of fluid through the intestine and
increasing capacitance.12 It may be that these effects promote the contact of invasive organisms such as E histolytica
with the mucosa, allowing more mucosal damage, necrosis of bowel wall, and dilatation.
The severe consequences observed in this case of
amoebic colitis should remind clinicians and patients that
the use of loperamide in infectious gastroenteritis is best
avoided when features suggesting mucosal involvement,
such as rectal bleeding and fever, are present.
Declaration of Interests
The authors state they have no conflicts of interest.
Figure 1 Plain abdominal radiograph from day of admission
demonstrating dilated loops of both small and large bowel; the
transverse colon is dilated to a maximum diameter of 10 cm.
cysts to colitis of varying extent to more severe complications such as amoebic liver abscess. Toxic dilatation results in a higher mortality rate.2,3 The diagnosis is often
delayed and is frequently only made histologically in operative or postmortem specimens.3,4
Figure 2 Periodic acid–Schiff stained section of ulcerated large
bowel mucosa containing trophozoites of Entamoeba histolytica,
characterized by spherical nuclei with central karyosomes and
vacuolated cytoplasm with abundant glycogen.
J Travel Med 2007; 14: 61–62
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