CASE REPORTOpen Access
Small duct autoimmune sclerosing cholangitis
and Crohn colitis in a 10-year-old child. A case
report and review of the literature
Erling Peter Larsen1, Allan Bayat1and Mogens Vyberg2*
Abstract: Autoimmune sclerosing cholangitis is an overlap syndrome characterized by features of both
autoimmune hepatitis and primary sclerosing cholangitis, the latter usually involving the large bile ducts.
Autoimmune sclerosing cholangitis occurs more often in children than in adults and is frequently associated
with inflammatory bowel disease, predominantly ulcerative colitis. We report a unique case of a 10-year-old
Danish boy with severe small duct autoimmune sclerosing cholangitis and synchronic Crohn colitis. He was
referred with a history of weight loss, abdominal pain, vomiting and diarrhea. Biochemical anomalies included
elevated alanine aminotransferase, γ-glutamyl transferase and immunoglobulin G levels and the presence of
smooth muscle antibodies and perinuclear antineutrophil cytoplasmic antibodies but normal alkaline
phosphatase. Liver biopsy specimen revealed features of both autoimmune hepatitis and sclerosing
cholangitis, the latter characterized by acute, hyperplastic and destructive inflammation – granulocytic
epithelial lesion – of the small ducts. Magnetic resonance cholangiography was normal. Colonoscopic biopsies
showed chronic inflammatory changes of the caecum and the ascending and transverse colon compatible
with Crohn disease. Ursodeoxycholic acid and immunosuppressive treatment was initiated and within four
weeks of treatment the general condition improved. Normalization of aminotransferase was seen at 21 weeks
and γ-glutamyl transferase at 72 weeks after first admittance, while immunoglobulin G remained slightly
Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.
Keywords: Autoimmune sclerosing cholangitis, Crohn colitis, Granulocytic epithelial lesion, Overlap syndrome
Immune-mediated liver diseases fall into two broad
categories, those with a hepatitic predominance: auto-
immune hepatitis (AIH), and those with a predomin-
ance of cholestatic features: primary biliary cirrhosis
(PBC) and primary sclerosing cholangitis (PSC). AIH
is characterized by elevated serum aminotransferases,
hypergammaglobulinaemia (primarily immunoglobulin
G), circulating autoantibodies (primarily antinuclear
antibodies (ANA) and smooth muscle cell antibodies
(SMA)) and interface hepatitis on liver biopsy speci-
phosphatase (ALP), circulating antimitochondrial anti-
bodies (AMA), or biliary changes on liver biopsy spe-
cimen are normally not present . In contrast, PBC
and PSC are characterized by cholestatic biochemistry,
occurrence of AMA (PBC only), and histological bil-
iary changes such as granulomatous cholangitis (PBC
only) or fibroobliterative cholangitis (mainly PSC),
leading to ductopenia and biliary cirrhosis. However,
PBC and PSC may also reveal features of AIH, which
are sufficiently pronounced to qualify for so-called
overlap syndromes, even though there are no estab-
lished definitions for these . A scoring system
established by the International Autoimmune Hepatitis
Group (IAIHG) for research purposes  has been
widely used in the clinical practise to classify patients
as having “definite AIH”, “probable AIH” or “not
* Correspondence: email@example.com
2Institute of Pathology, Aalborg hospital, Aarhus University Hospital, P.O.Box
561, Aalborg DK-9100, Denmark
Full list of author information is available at the end of the article
© 2012 Larsen et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Larsen et al. Diagnostic Pathology 2012, 7:100
AIH”. The scoring system is, however, not directly ap-
plicable for overlap syndromes.
The AIH/PSC overlap syndrome, also designated auto-
immune sclerosing cholangitis (AISC) is occasionally
seen in adults [2-4], but more often occur in children,
where up to about 50% of patients presenting with AIH
reveal radiological features of cholangiopathy . Even
among AIH patients with normal cholangiogram, histo-
logical biliary changes have been found in about 30% .
In other studies, cases have been classified as AISC even
though the cholangiopathy was limited to the small
Both PSC and AISC frequently occur in combination
with inflammatory bowel disease (IBD) , typically ul-
cerative colitis (UC) while fewer cases of indeterminate
colitis (IC) and Crohn disease (CD) has been described
[5,7,9-11]. We present a case of a 10-year-old boy, diag-
nosed as AISC with an unusual, severe small duct lesion
and concomitant Crohn colitis.
The patient, who had previously been in good health,
was admitted to the pediatric department because of
weight loss, upper abdominal pain, vomiting and diar-
rhea during 4 months. There was a family history of
immune-mediated disorders: The father of the patient
had been diagnosed with sarcoidosis and the father’s
brother had CD.
The initial physical examination revealed an alert but
tired and pale boy. Weight was 39 kg and height
146 cm. Pulse rate and blood pressure were normal.
There was no hepatosplenomegaly or jaundice.
At the admission, the erythrocyte sedimentation rate
(ESR) was 75 mm/hr (normal 2–13); serum alanine ami-
notransferase (ALAT) 75 U/L (normal 5–35); γ-glutamyl
transferase (GGT) 239 U/L (normal 10–45); immuno-
globulin G (IgG) 48.0 g/L (normal 6.08-15.72); SMA
1:320; ANA negative; serum perinuclear antineutrophil
cytoplasmic antibodies (pANCA) 1:80; cytoplasmic (c)
ANCA negative; fecal calprotectin 1268 mg/kg (normal
0–50); ALP, bilirubin, albumin and blood platelets were
normal; tests for viral hepatitis and bacterial growth in
stools were negative; test for liver-kidney-microsomal
antigen-1 was not available. Based on the scoring system
proposed by the International Autoimmune Hepatitis
Group (IAIHG)  the patient fulfilled the criteria for
the diagnosis of “definite” AIH (aggregate score=21;
however, see discussion). Magnetic resonance cholangio-
pancreatography (MRCP) showed no cholangiographic
abnormalities. Endoscopic retrograde cholangiopancrea-
tography (ERCP) was not carried out. Colonoscopy
showed scattered reddened mucosa with small aphtoid
ulcers in the caecum and the ascending and transverse
colon. Biopsy specimens from these areas revealed active
chronic inflammation compatible with CD (Figure 1). A
liver needle biopsy specimen revealed features of both
AIH and PSC (Figure 2): Disturbed architecture with
marked enlargement of mainly small portal tracts due to
inflammation, edema and portal/periportal fibrosis. The
inflammatory infiltrates consisted of a mixture of lym-
phocytes, plasma cells, histiocytes, and eosinophilic and
neutrophilic granulocytes. Granulomas were not found.
In several fields ductular reaction with severe epithelial
hyperplasia, loss of polarity and focal cytoplasmic mucin
accumulation was seen. Some epithelial structures
appearing like reactive bile ductules were embedded in a
myxoid fibrotic tissue. Immunohistochemical analysis
revealed strong expression of keratin 19 and focal ex-
pression of MUC5AC (but not MUC2) in the reactive
ductules. The epithelium of some interlobular bile ducts
was focally necrotic with neutrophil infiltration, but bile
duct loss could not be demonstrated. Around these por-
tal tracts a severe interface inflammation was seen with
hydropic and rosetting juxtaportal hepatocytes sur-
rounded by a lymphoplasmacytic infiltrate. Other portal
tracts, particularly the larger ones, only showed minor
Figure 1 Endoscopic biopsy specimen from right colon showing changes compatible with Crohn disease. A. Colon mucosa with crypt
atrophy and irregularity, and lymphoid hyperplasia (H&E, bar=1 mm). B. Higher magnification revealing crypt destruction and in the lamina
propria severe accumulation of lymphocytes and plasma cells as well as a single small epithelioid cell granuloma (inset) (H&E, bar=200 μm).
Larsen et al. Diagnostic Pathology 2012, 7:100
Page 2 of 6
inflammation, no bile duct changes, and no interface in-
flammation. Bridging necrosis or fibrosis was not seen.
The parenchyma in zones I and II showed only slight
reactive changes. Copper binding protein and Mallory-
Denk bodies were not found. Immunohistochemical
analysis showed 1–3 IgG4 positive plasma cells in the
inflamed portal tracts. Treatment with prednisolone
1 mg/kg daily and ursodeoxycholic acid (UDCA)
10 mg/kg daily was started. Within four weeks of treat-
ment the patient’s general condition improved and he
resumed school activities. After ten weeks of treatment
ESR, ALAT and IgG still indicated disease activity
(Table 1). The patient started treatment with azathiopr-
ine 1.5 mg/ kg daily while the dosage of prednisolone
was slowly reduced to 7.5 mg every second day. This
resulted in a normalization of ALAT and ESR while
IgG was still slightly elevated around 18 g/L. The dos-
age of azathioprine was then raised to 2 mg/kg daily.
At the latest examination 72 weeks after diagnosis, the
general condition was good but IgG remained slightly
increased. A slight increase in ALAT and ESR was
ascribed to an acute viral infection. In order to rule
out progressive biliary damage an MRCP was done,
which was still normal.
The typical features of PSC (with or without concomitant
AIH) are intrahepatic and/or extrahepatic large duct in-
volvement with cholangiographically characteristic multi-
focal strictures and segmental dilatation or beading.
Figure 2 Needle biopsy specimen from liver with changes compatible with autoimmune sclerosing cholangitis. A. Marked portal
enlargement due to inflammation, edema and portal/periportal fibrosis (Alcian-Picro-Sirius, bar=1 mm). B. In the portal/periportal fields ductular
reaction with severe epithelial hyperplasia, loss of polarity and focal cytoplasmic mucin accumulation (arrow) is seen (Alcian-Picro-Sirius,
bar=200 μm). C. The most pronounced inflammation occurs in small portal tracts around which also a severe lymfo-plasmacytic interface
inflammation is seen (H&E, bar=500 μm). D. Focally, bile duct epithelium is necrotic and infiltrated with neutrophils (black arrows). Pronounced
interface hepatitis is present (red arrows) (H&E).
Table 1 Laboratory investigations in the patient at the time of diagnosis and after 2–72 weeks of treatment
LaboratoryNormalUnitsValues at time Values during treatment (weeks)
Investigation valuesof diagnosis268122172
ESR 2-13mm/hr 75 6350 46301328
ALAT 5-35U/L 106490 1701294227 43
GGT10-45 U/L 262 239NA NA NANA17
ALAT: Alanine aminotransferase; ESR: Erythocyte sedimentation rate; GGT: γ-glutamyl transferase; NA: not available.
Larsen et al. Diagnostic Pathology 2012, 7:100
Page 3 of 6
Alternatively, PSC may present as histologically charac-
teristic bile duct changes similar to long-standing large
duct obstruction and eventually ductopenia, but with
negative cholangiogram, thus designated small duct PSC
[5,12,13]. Among PSC patients with positive cholangio-
gram, an overlap with definite or probable AIH has in
adults (or mainly adults) been diagnosed in 1.4%-35%
[4,6,14-16] while in children diagnosed in 28%-49% of
the cases [5,7,9,17,18]. However, PSC in children is fre-
quently characterized serologically by florid AIH-like
features including ANA and SMA, elevated IgG and
histologically by interface hepatitis, wherefore these
children may be diagnosed as AIH in the absence of
cholangiographic studies or with an initially normal
cholangiogram, unless characteristic bile duct changes
are identified histologically. Moreover, despite bile duct
involvement, cholestatic biochemistry in children is
relatively rare, many having normal ALP and in some
cases even normal GGT at presentation . Hence,
when either AIH or PSC is diagnosed in children, it
may take years before an overlap syndrome, i.e. AISC, is
diagnosed . To further confuse the picture, “inciden-
tal” histologic biliary changes may occur in classic AIH,
which does not appear to develop features of PSC. Czaja
and Carpenter  presented 84 AIH patients (including
a small but unspecified number of children) among
which ten appeared histologically to have destructive
cholangitis or ductopenia. However, the AIH treatment
response was not dependent on bile duct injury where-
fore the authors were reluctant to consider the lesions as
PSC. They proposed that the bile duct lesions were coin-
cidental findings associated with classic disease, or weak
expressions of a variant syndrome. In the study of Gre-
gorio et al.  8/26 children (31%) with AIH (in the ab-
sence of radiologic features of cholangiopathy) showed
histologic biliary features of which one was classified as
(small duct) PSC.
The diagnostic criteria formulated by the IAIHG 
do not readily allow for a distinction between AIH (i.e.,
without PSC) and AISC, and is not directly applicable in
children. Thus, the score for our patient could be calcu-
lated to 21, based on – among others – an ALP:ALAT
ratio <1.5, but ALP is often normal in children with PSC
and should probably be substituted with GGT [9,20].
In the current case, the liver changes are those of a
chronic cholangiopathy within the spectrum of PSC. Pe-
culiar to our patient was the severe inflammatory
changes in relation to the small intrahepatic bile ducts
with heavy neutrophil infiltration and features of de-
structive injury and marked hyperplasia, resembling the
granulocytic epithelial lesion (GEL) in autoimmune pan-
creatitis (AIP) type 2 , a feature which we have pre-
viously seen published only once, in a case study of
Grammatikopoulos et al. , who described a 13-year-
old boy with concomitant Crohn colitis and AISC with
GEL, who showed long-term remission of liver disease
after steroid treatment.
Bile duct injuries in PSC and AISC may be considered
multifactorial, potentially involving immune-mediated,
chemical, genetic, ischaemic, and infectious mechanisms,
as reviewed by Krones et al. . In the above mentioned
case  as well as ours, the GELs and the remission
after steroid treatment supports an immune-mediated
disease in line with AIP type 2, which interestingly is
associated with IBD . This is in contrast to the IgG4-
associated PSC and hepatic inflammatory pseudotumour,
which may occur concomitant with AIP type 1 .
The hyperplastic bile duct lesions described in this
case bear some resemblance to the so-called hepatitis-
associated bile duct lesion type 3 , which in fact
appears to be an interface hepatitis related liver-cell le-
sion. However, in the current biopsy specimen the
cytoplasmic cytokeratin 19 as well as mucin and
MUC5AC expression in some of the lesions indicates
that the cells are more likely of bile ductular origin.
Normal small bile ducts and ductules do not secrete
mucin or express mucin core proteins (MUCs). Over-
expression in the intrahepatic biliary tree and cultured
biliary epithelial cells has been shown to be due to e.g.,
bacterial infection, presumably via lipopolysaccharide
induced synthesis of tumour necrosis factor-α and acti-
vation of protein kinase C .
Among children with AISC, almost half have concomi-
tant IBD, but CD is relatively rarely specified. In the
study of Gregorio et al.  one child with AIH and
probable small duct PSC associated with CD is men-
tioned. Feldstein et al.  described that out of 40 chil-
dren with PSC, 14 had overlap with AIH, and 8 out of
52 had CD, but did not specify how many had concomi-
tant AISC and CD. Miloh et al. described 12 children
with AISC of which 6 had concomitant IBD but it is not
clear how many had CD. In none of this cases were GEL
like changes described.
No guidelines for the treatment of AISC (isolated or
in combination with IBD) have been established, but a
combination of UDCA and immunosuppressive treat-
ment has been recommended . The present trend
is to target the treatment to one of the diseases and
then to adjust it depending on symptoms and side
effects . Patients with large duct AISC have signifi-
cantly worse prognosis than patients with AIH or large
duct PSC [2,5,9]. Small duct PSC show a more pro-
tracted course than large duct PSC [7,12], but the
number of patients with small duct AISC is too small
for a prognostic evaluation. However, one may specu-
late that the AIP type 2-like liver damage signifies a
better response to steroids compared to PSC in
Larsen et al. Diagnostic Pathology 2012, 7:100
Page 4 of 6
This report describes a rare case of AISC with concomi-
tant Crohn colitis in a child with a unique hyperplastic
and destructive cholangitis, resembling GEL in AIP type
2, limited to the small intrahepatic bile ducts.
Written informed consent was obtained from the patient
and his parents for publication of this Case Report and
any accompanying images. A copy of the written consent
is available for review by the Editor-in-Chief of this
AIH: Autoimmune hepatitis; AISC: Autoimmune sclerosing cholangitis;
ALAT: Alanine aminotransferase; ALP: Alkaline phosphatase; ANA: Antinuclear
antibody; ANCA: Antineutrophil cytoplasmic antibody; CD: Crohn disease;
ERCP: Endoscopic retrograde cholangiopancreatography; ESR: Erythrocyte
sedimentation rate; GGT: γ-glutamyl transferase; IAIHG: International
Autoimmune Hepatitis Group; IBD: Inflammatory bowel disease;
IC: Indeterminate colitis; IgG: Immunglobulin G; INR: International normalized
prothrombin ratio; LKM1: Anti-liver kidney microsomal type 1 antibody;
MRCP: Magnetic resonance cholangiopancreatography; NA: Not available;
PBC: Primary biliary cirrhosis; PSC: Primary sclerosing cholangitis;
SMA: Smooth muscle cell antibody; UC: Ulcerative colitis;
UDCA: Ursodeoxycholic acid.
The authors declare that they have no competing interests.
EPL, AB and MV equally participated in the conception of the idea and
writing of the manuscript. MV performed the histopathological interpretation
of the liver- and colon biopsies. All authors have read and approved the final
1Department of Pediatrics, Aalborg hospital, Aarhus University Hospital,
Aalborg, Denmark.2Institute of Pathology, Aalborg hospital, Aarhus University
Hospital, P.O.Box 561, Aalborg DK-9100, Denmark.
Received: 23 May 2012 Accepted: 5 August 2012
Published: 14 August 2012
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Cite this article as: Larsen et al.: Small duct autoimmune sclerosing
cholangitis and Crohn colitis in a 10-year-old child. A case report and
review of the literature. Diagnostic Pathology 2012 7:100.
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