Journal of Gastroenterology and Hepatology (2004) 19, 1338–1342 DOI: 10.1111/j.1400-1746.2004.03368.x
Blackwell Science, LtdOxford, UKJGHJournal of Gastroenterology and Hepatology0815-93192004 Blackwell Publishing Asia Pty Ltd191213381342Review Article Liver abscess in IBDM Margalit et al.
Correspondence: Dr Maya Margalit, Department of Internal Medicine A, Hadassah University Hospital POB 12000,
Jerusalem 91120, Israel. Email: email@example.com
Accepted for publication 17 October 2003.
Liver abscess in inflammatory bowel disease: Report of two cases
and review of the literature
MAYA MARGALIT, HILA ELINAV, YARON ILAN AND MEIR SHALIT
Department of Internal Medicine A, Hadassah University Hospital, Jerusalem, Israel
Hepatic abscesses are a rare complication of inflammatory bowel disease (IBD). Despite the fact that
certain hepatobiliary complications of IBD, including cholelithiasis, primary sclerosing cholangitis
(PSC) and cholangiocarcinoma predispose patients with IBD to ascending cholangitis, previously pub-
lished data does not demonstrate that biliary infection is an important mechanism underlying liver
abscess development in these patients. We describe two patients with inflammatory bowel disease, both
with PSC, who developed multiple liver abscesses, and review the literature on liver abscesses in asso-
ciation with inflammatory bowel disease.
© 2004 Blackwell Publishing Asia Pty Ltd
Key words: cholangitis, Crohn’s disease, inflammatory bowel disease, liver abscess, primary sclerosing
cholangitis, ulcerative colitis.
Hepatobiliary complications of inflammatory bowel dis-
ease (IBD) include cholelithiasis, fatty liver, primary
sclerosing cholangitis, chronic active hepatitis, granulo-
matous hepatitis, amyloidosis, biliary carcinoma and
Primary sclerosing cholangitis (PSC) is a chronic
inflammatory disease of the biliary tract characterized
by fibrotic strictures of intrahepatic and extrahepatic
bile ducts. Ascending cholangitis is an important com-
plication of PSC, usually occurring after endoscopic
procedures or in patients with bile duct stones or tight
strictures.2 Recurrent bacterial cholangitis is an
accepted indication for liver transplantation in selected
patients with PSC.
Hepatic abscesses are a rare complication of IBD.
Most cases described to date were of patients with
Crohn’s disease. Interestingly, biliary infection was not
a common mechanism underlying liver abscess devel-
opment in previously described cases.
We describe herein two patients with IBD and pri-
mary sclerosing cholangitis who developed multiple
liver abscesses. It is our belief that ascending cholangitis
related to primary sclerosing cholangitis (and an addi-
tional complication of cholangiocarcinoma in the
second patient) was the underlying mechanism for liver
abscess development in both cases.
A 58-year-old man of Ashkenazi Jewish origin was
referred to our hospital from another medical facility,
where he had been hospitalized and investigated for a 6-
week history of fever, rigors, night sweats, weakness and
fatigue; there were no other complaints. The patient was
diagnosed with ulcerative colitis 10 years earlier, mani-
fested by abdominal pain and bloody diarrhea and dem-
onstrated by colonoscopy with multiple biopsies. There
was no history of extraintestinal manifestations. Under
5-ASA treatment, disease flares were infrequent and
mild, characterized by episodes of bloody diarrhea with
no fever. Several months earlier, however, the patient
had a relatively severe exacerbation, which necessitated
a course of intravenous steroids. At the time of presen-
tation he was still receiving 30 mg prednisone per day.
Past medical history was also significant for cholelithi-
asis and colonic diverticuli, which were incidental find-
ings on imaging studies.
Liver abscess in IBD
Physical examination revealed a pale patient with a
temperature of 38.5∞C and mild hepatosplenomegaly.
There were no other abnormal physical findings.
Abnormal laboratory results included a slightly elevated
white blood cell count (11 150/mm3 with 80% neu-
trophils), normocytic anemia (hematocrit 24.5%),
hypoalbuminemia (2.4 g/dL), elevated aspartate ami-
notransferase (AST, 68 U), alkaline phosphatase
(251 U) and g-glutamyl transferase (473 U) levels and
elevated C-reactive protein (39.0 mg/dL). Blood cul-
tures yielded an undefined non-hemolytic streptococ-
cus species in one culture bottle out of six sets of two.
Colonoscopy revealed moderate pancolitis. Abdomi-
nal Doppler ultrasonography and computed tomogra-
phy (CT) scans showed gallbladder stones, a slightly
enlarged spleen, portal vein thrombosis with partial
recanalization and no cavernous transformation, and
multiple hepatic lesions consistent with abscesses. A CT-
guided biopsy was performed from the largest lesion,
with drainage of 5 mL of purulent material (Fig. 1). His-
tological examination revealed an extensive neutrophilic
exudate, a number of neutrophils within bile ducts, bile
duct proliferation and mild fibrotic changes. Cultures
yielded Streptococcus milleri. The patient underwent
(ERCP), which demonstrated beading of the intrahe-
patic bile ducts. Workup for hypercoagulability revealed
heterozygocity for the factor V Leiden mutation.
Intravenous antibiotic treatment was administered
for 8 weeks and steroids were tapered, with complete
recovery. Six months later the patient remains afebrile,
with normal liver function tests, except mild g-glutamyl
transferase elevation. All lesions previously seen on a
CT scan have resolved. Repeated ERCP showed intra-
hepatic beading compatible with primary sclerosing
A 41-year-old male of Ashkenazi Jewish origin, diag-
nosed 2 years earlier with Crohn’s disease, was admitted
to hospital in a state of septic shock. Seven months prior
to his present admission the patient was hospitalized due
to ascending cholangitis. An ERCP was performed,
demonstrating numerous extrahepatic and intrahepatic
strictures consistent with PSC, and a stent was placed in
the common bile duct (CBD). Over the next months,
the patient was hospitalized three additional times for
recurrent episodes of ascending cholangitis; repeat
ERCPs performed for stent replacement demonstrated
marked progression of the biliary findings.
On admission the patient was febrile and jaun-
diced, with severe right upper quadrant tenderness.
Laboratory results included marked leukocytosis
(35 000/mm3) with 80%
(hemoglobin = 8 g/dL) and thrombocytosis (758 000/
mm3). Liver function tests were impaired (AST, 597 U;
alanine aminotransferase, 618 U; lactate dehydrogenase
(LDH), 454 U; alkaline phosphatase, 534 U; g-
glutamyl transferase, 468 U; total bilirubin, 385 mmol/
L). Abdominal ultrasound revealed a large collection in
the right lobe of the liver containing fluid and gas. Per-
cutaneous aspiration yielded 80 mL of purulent bile. A
catheter was inserted for continuous drainage and wide
spectrum intravenous antibiotics were administered.
Blood cultures and cultures from the abscess grew
Escherichia coli, Morganella morganii and Streptococcus
faecalis. Due to lack of improvement, an abdominal CT
scan was performed, revealing several liver masses. His-
tological examination of a biopsy from one of these
masses showed grade III mucinous cholangiocarci-
noma. The patient’s condition gradually deteriorated
and he died 5 months later.
Although liver abscesses are considered to be one of the
hepatobiliary complications of IBD, this entity is very
uncommon, with only 60 reported cases to date.3–42 Of
these, most were of patients with Crohn’s disease and
seven were of patients with ulcerative colitis. Conse-
quently, practically all available data concerning liver
abscesses in patients with IBD pertains to patients with
The exact incidence of liver abscesses associated with
IBD is not known. As in the general population, liver
abscesses are more common in males,6,7 but patients
with Crohn’s disease tend to develop this entity at a
younger age.7 Crohn’s disease in patients who develop
liver abscesses may involve the small bowel, the colon or
both, and there is usually evidence for disease activity.5
Most patients who develop liver abscesses have had
long-term IBD; however, cases of Crohn’s disease pre-
senting with pyogenic liver abscesses are reported
increasingly.6–10,17,25,26 Patients with IBD have an
increased tendency to
abscesses.5,7 There is almost invariable involvement of
the right lobe of the liver, with occasional additional
involvement of the left lobe.5,7
Most clinical manifestations of liver abscesses in
patients with Crohn’s disease, including fever, chills,
anorexia, weight loss, abdominal pain with right upper
quadrant tenderness5–7,19 and pulmonary findings (par-
develop multiple liver
demonstrating multiple hepatic lesions compatible with liver
abscesses. Cultures from material obtained by CT-guided
biopsy yielded Streptococcus milleri.
Abdominal computed tomography (CT) scan
M Margalit et al.
ticularly a right pleural effusion),1,23 are similar to those
in patients with liver abscesses who do not have Crohn’s
disease. Leukocytosis with an elevated neutrophil
count, anemia, disturbed cholestatic liver function tests
(particularly alkaline phosphatase) and elevated acute
phase reactants are among the laboratory findings com-
mon to both groups.5–7
The diagnosis of liver abscesses in patients with
Crohn’s disease is challenging and often delayed. As
many of the symptoms and signs related to the existence
of liver abscesses in patients with Crohn’s disease are
similar to manifestations of their IBD, they are often
incorrectly thought to have a disease exacerbation. As a
result, many are treated with increasing doses of corti-
costeroids and some even undergo surgery for resection
of diseased bowel.5 In view of this, many now advise
that liver abscesses should be actively sought (by
abdominal ultrasound or abdominal CT scan) in febrile
patients with IBD, whose clinical findings or lack of
response to conventional treatment are incompatible
with a mere exacerbation of their background illness.5,6,9
Both aerobic and anerobic cultures should be per-
formed. As abscess cultures are positive in most cases
and blood cultures are positive in 50% of patients,5,7
specific antibiotic treatment can usually be imple-
mented after initial empirical treatment with broad-
spectrum antibiotics. Interestingly, in contrast to liver
abscesses in the general population, which are usually
polymicrobial with several gram-negative strains, a sin-
gle pathogen, often Streptococcus milleri (also known as
Streptococcus MG intermedius) is isolated in a high per-
centage of cases of liver abscesses complicating
IBD.5,7,10–12 Other pathogens that have been isolated
from liver abscesses in patients with Crohn’s disease
include (in order of decreasing frequency) additional
streptococci5,9 anaerobic bacteria such as Fusobacterium
nucleatum5 and Bacteroides fragilis,5 various gram-nega-
tive bacteria and Staphylococcus aureus.7 While it is
accepted that antibiotic treatment should be prolonged,
there are no evidence-based guidelines for its duration.
Patients commonly receive antibiotics for 4–8 weeks,
often intravenously for the entire period;7 patients with
multiple liver abscesses are often treated even longer.
Formerly, the existence of a liver abscess was consid-
ered an indication for surgical drainage.5,6,13,20,21 Over
the years a more conservative approach has been
adopted and percutaneous drainage, when feasible, is
usually the procedure of choice with a favorable out-
come.7,16,22,25 Several authors have pointed out that, par-
ticularly in the context of IBD, an intra-abdominal
source of infection must be sought.5,6,13,20 In one case
review, 8 of 12 patients had to undergo surgery for elim-
ination of intra-abdominal origins of liver abscesses.6
This possibility should always be kept in mind when
opting for percutaneous drainage.
Although the etiology underlying liver abscess devel-
opment remains obscure in some patients with Crohn’s
disease,7 a number of factors are thought to increase the
propensity to develop liver abscesses in these patients.
The existence of intra-abdominal abscesses, fistuliza-
tion and intestinal perforation are some of the disease
characteristics held responsible.5–7,9–11 Abdominal sur-
gery,5,7,10,11 treatment with corticosteroids5,7,10,11 and
metronidazole7,29 as well as malnutrition and various
immunological derrangements7,11 have also been impli-
cated. Portal bacteremia, which may be secondary to
disruption of the normal mucosal barrier,9 seems to be
part of the mechanism in most cases, and some patients
develop suppurative pylephlebitis5,10,12,31,32 often with
secondary portal vein thrombosis.13,14 In view of the
well-documented existence of portal bacteremia in
patients with IBD, some point out that the incidence of
liver abscesses in these patients is surprisingly low.1
Interestingly, biliary sepsis is considered an uncommon
source for the development of liver abscesses in patients
with IBD. In a review of the literature, clear-cut bilary
tract pathology that led to liver abscess formation was
identified in a single case report, in which biliary infec-
tion secondary to the development of a duodenobiliary
fistula was described.15 This is surprising for two rea-
sons: first, there is an increased incidence of cholelith-
iasis in patients with IBD compared to the general
population;1 this could be expected to result in a higher
prevalence of choledocholithiasis and ascending cholan-
gitis. Second, ascending cholangitis is one of the well-
recognized complications of primary sclerosing cholan-
gitis; the latter develops in approximately 5% of patients
with ulcerative colitis.1 Had biliary tract pathology been
significant in the pathogenesis of liver abscesses in
patients with IBD, more patients with ulcerative colitis
may have been expected to develop this complication. It
is worthwhile mentioning that although the existence of
infectious complications in patients with PSC is consid-
ered ‘textbook knowledge’, documentation of this issue
in the currently available medical literature is sparse,
and there is no data whatsoever on the coexistence of
primary sclerosing cholangitis and liver abscesses.
We have described two patients with IBD and pri-
mary sclerosing cholangitis who developed multiple
liver abscesses. The first patient described is, to the best
of our knowledge, the first reported case of PSC pre-
senting as multiple liver abscesses. Several factors may
have contributed to abscess development in this patient,
including chronic steroid treatment and cholelithiasis.
The finding of portal vein thrombosis raises the possi-
bility of pylephlebitis as a source for hepatic bacterial
seeding. Alternatively, portal vein thrombosis may have
developed secondary to the presence of hepatic
abscesses, or as a consequence of ulcerative colitis per
se. The ERCP findings and compatible histological
changes, however, suggest primary sclerosing cholang-
itis with secondary bacterial cholangitis to be the most
plausible underlying mechanism for liver abscess devel-
opment in this case. Although similar cholangiographic
findings can occasionally be observed in pseudoscleros-
ing cholangitis secondary to portal vein thrombosis,42
the setting of acute portal vein thrombosis (without col-
laterals) and the persistence of cholestasis after liver
abscess resolution make this entity less likely. Ascending
cholangitis secondary to biliary stasis in a patient with a
biliary stent, PSC and cholangiocarcinoma seems
clearly to have been the mechanism of abscess forma-
tion in the second patient.
Thus, while previously published data surprisingly
does not support biliary sepsis as an important mecha-
nism of liver abscess development in patients with IBD,
Liver abscess in IBD
our two patients exemplify what may have been
expected to be a far more common scenario.
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