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Drugs & Diseases > Pediatrics: General Medicine

PEDIATRIC PRIMARY SCLEROSING CHOLANGITIS

Updated: Jan 17, 2024
* Author: Henry C Lin, MD, MBA; Chief Editor: Carmen Cuffari, MD more...

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Sections
Pediatric Primary Sclerosing Cholangitis

* Sections Pediatric Primary Sclerosing Cholangitis
* Overview

* Background
* Pathophysiology
* Etiology
* Epidemiology
* Prognosis
* Show All
* Presentation
* DDx
* Workup

* Approach Considerations
* Laboratory Studies
* Imaging Studies
* Procedures
* Histologic Findings
* Staging
* Show All
* Treatment

* Approach Considerations
* Pharmacologic Therapy
* Liver Transplantation
* Diet
* Consultations
* Show All
* Guidelines
* Medication

* Medication Summary
* Gallstone Solubilizing Agents
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Overview

BACKGROUND

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease of
unknown etiology characterized by progressive inflammation of the intrahepatic
and/or extrahepatic bile ducts that is increasingly recognized in children. The
diagnosis is based on a combination of clinical features and cholestatic
biochemical profile, along with typical cholangiographic abnormalities, and
confirmed by liver histologic findings. In the absence of underlying bile duct
abnormalities, a generalized beading and stenosis of the intrahepatic and
extrahepatic biliary tree characterize primary sclerosing cholangitis. [1, 2, 3]

Primary sclerosing cholangitis is usually progressive, leading to cirrhosis,
portal hypertension, and liver failure. Effective medical treatment modalities
for childhood primary sclerosing cholangitis are undetermined. Liver
transplantation remains the only effective therapeutic option for patients with
end-stage liver disease from primary sclerosing cholangitis. [1]

For more information, see Primary Sclerosing Cholangitis and Primary Sclerosing
Cholangitis Imaging.

Next: Pathophysiology

PATHOPHYSIOLOGY

The mechanisms responsible for the development of primary sclerosing cholangitis
are unknown. It is often seen in association with inflammatory bowel disease
(IBD) but also occurs in association with other disorders or in isolation. The
relationship between primary sclerosing cholangitis and IBD offers several
clues. The biliary injury may be initiated by an immune-mediated destruction of
the hepatobiliary tract that is perhaps caused by transient infection or the
absorption of bacterial by-products in genetically predisposed individuals with
colonic disease. [4, 5]

Previous
Next: Pathophysiology

ETIOLOGY

Primary sclerosing cholangitis is a progressive disorder of unknown etiology.
Bacteria, toxins, viral infections, and immunologic and genetic factors have
been proposed as etiologic agents. [6]

The high degree of association of primary sclerosing cholangitis with
inflammatory bowel disorder (IBD) suggests a common pathogenetic mechanism;
however, no causal relationship has been established. An abnormal colonic
mucosal barrier may lead to portal bacteremia or abnormal absorption of toxic
metabolites or bile acids. [4, 6, 7, 8]

Reovirus and cytomegalovirus (CMV) are possible etiologic agents; primary
sclerosing cholangitis is analogous to a reovirus-induced cholestasis in mice.

Immunologically mediated damage to the biliary tree remains the most likely
etiology of primary sclerosing cholangitis. The presence of portal tract
infiltration with CD3+ T cells, serum autoantibodies, and abnormal expression of
human leukocyte antigen (HLA) on biliary epithelial cells all support an
immune-mediated process.

A high prevalence of the perinuclear antineutrophil cytoplasmic antibodies
(p-ANCA) is seen in primary sclerosing cholangitis and ulcerative colitis (UC).
Autoimmune disorders are more frequent in patients with primary sclerosing
cholangitis than in patients with IBD without liver disease; 25% of patients
with primary sclerosing cholangitis have at least one autoimmune disorder
outside of the liver and colon.

In children, primary sclerosing cholangitis is commonly associated with markers
suggestive of an autoimmune process. Some patients have elevated levels of
circulating immune complexes, immunoglobulins, and autoantibodies that are not
organ specific. [6, 9] Histologic and clinical overlap (ie, overlap syndrome)
with autoimmune hepatitis may be observed.

The close association between primary sclerosing cholangitis and various human
leukocyte antigen (HLA) haplotypes is well established. An increased frequency
of HLA-B8 and HLA-DR3 is observed in patients with primary sclerosing
cholangitis. HLA-B8 is also associated with other autoimmune disorders. [6, 9]

In addition, other gene polymorphisms have been suggested in the
immunopathogenesis of primary sclerosing cholangitis, including TNFa, CTLA-4,
ICAM, and metalloproteinases. [10] One study also observed a high prevalence of
cystic fibrosis transmembrane receptor (CFTR)–mediated transport dysfunction in
patients with childhood primary sclerosing cholangitis, suggesting a possible
role of CFTR protein in the mechanism. [11]

Previous
Next: Pathophysiology

EPIDEMIOLOGY

Primary sclerosing cholangitis can occur at any age but primarily affects
adults. The overall incidence of pediatric primary sclerosing cholangitis is
unknown. A 2:1 male predominance is noted in primary sclerosing cholangitis but
is not observed in children. Peak incidence of primary sclerosing cholangitis
occurs in the third and fourth decades of life, but primary sclerosing
cholangitis has also been described in infancy.

Primary sclerosing cholangitis is frequently seen in association with IBD. IBD
is present in 70-80% of patients who have primary sclerosing cholangitis.
Primary sclerosing cholangitis may precede the onset of, coincide with, or
follow the diagnosis of IBD such as following proctocolectomy. Conversely,
2.5-7.5% of patients with IBD develop primary sclerosing cholangitis. [12, 13]
Pediatric series of patients with primary sclerosing cholangitis and IBD show
that the majority of patients had ulcerative colitis. [13, 14, 15, 16]

Previous
Next: Pathophysiology

PROGNOSIS

Primary sclerosing cholangitis is characterized by a slow insidious progression
to cirrhosis. In adult patients, the median period of survival from the time of
diagnosis is 9-11 years with up to 40% of patients asymptomatic at the time of
initial presentation. The median period of survival is shorter for patients who
are symptomatic at the time of diagnosis. [17]

The identification of abnormal liver function tests (LFTs) in patients with
inflammatory bowel disease (IBD) has led to earlier diagnosis of primary
sclerosing cholangitis.

Despite progress in early recognition, optimal treatment of patients with
primary sclerosing cholangitis remains a challenge, requiring a
multidisciplinary approach among hepatologists, endoscopists, surgeons, and
interventional radiologists.

The coexistence of ulcerative colitis is not predictive of an increased risk of
death in primary sclerosing cholangitis. Ulcerative colitis may be associated
with an increased posttransplantation survival.

The Pediatric PSC Consortium developed the Sclerosing Cholangitis Outcomes in
Pediatrics (SCOPE) index, which is a multivariate risk index to stratify the
risk of progression to liver transplant or death. This index comprises of total
bilirubin, albumin, platelet count, GGT, and cholangiography. [18]

COMPLICATIONS

Cholangiocarcinoma (CCA) develops in 10-15% of adult patients with primary
sclerosing cholangitis (PSC). CCA has been reported in children with primary
sclerosing cholangitis. [16, 19, 20] Early detection of CCA is limited by a lack
of reliable serologic, radiologic, and endoscopic findings. Serum CA 19-9
appears useful (75% sensitivity, 80% specificity) in discriminating which
patients with primary sclerosing cholangitis have CCA.

The risk of colorectal cancer or dysplasia is increased in patients with
ulcerative colitis (UC) and primary sclerosing cholangitis. Colorectal cancers
associated with primary sclerosing cholangitis are more likely to be proximal,
diagnosed at a more advanced stage, and fatal. Colectomy in patients with UC and
primary sclerosing cholangitis does not alter the natural history of primary
sclerosing cholangitis.

Patients who have undergone liver transplantation are susceptible to a wide
array of complications secondary to chronic immunosuppression. The incidence of
acute cellular and chronic ductopenic rejection is higher in patients
transplanted for primary sclerosing cholangitis. Chronic ductopenic rejection
adversely affects patient and graft survival. Biliary strictures, both
anastomotic and nonanastomotic, can occur. [21]

Recurrent sclerosing cholangitis occurs in 10-33% of patients with primary
sclerosing cholangitis who have undergone liver transplantation. [13, 14, 22,
23, 24, 25, 21] Data from the Mayo Clinic's review of 150 consecutive patients
with primary sclerosing cholangitis who received 174 liver allografts suggests
that postoperative biliary strictures or recurrence of primary sclerosing
cholangitis does not impact patient survival.

Clinical Presentation

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Media Gallery

* Pediatric Primary Sclerosing Cholangitis. Fibro-obliterative cholangiopathy.
Image courtesy of Dr. Kay Washington.

* Pediatric Primary Sclerosing Cholangitis. Endoscopic retrograde
cholangiopancreatography performed in a patient with abnormal liver function
test results shows multiple intrahepatic bile duct strictures and beading.

* Pediatric Primary Sclerosing Cholangitis. Double-contrast barium enema (same
patient as in the previous image) shows filiform polyps and an ahaustral
colon resulting from ulcerative colitis.

* Pediatric Primary Sclerosing Cholangitis. Percutaneous transhepatic
cholangiogram shows dilatation, stricturing, and beading of the intrahepatic
bile ducts. Note the surgical clips from a previous cholecystectomy.

* Pediatric Primary Sclerosing Cholangitis. T-tube cholangiogram shows
irregularity of the common bile duct, stricturing, beading, and dilatation of
the intrahepatic bile ducts. Note a calculus in the termination of the left
hepatic duct (arrow).

* Pediatric Primary Sclerosing Cholangitis. Magnetic resonance
cholangiopancreatography shows a normal-sized common bile duct, but
strictures of both the left and right ducts are noted as well as a dilated
proximal left hepatic duct.

* Pediatric Primary Sclerosing Cholangitis. Technetium-99m iminodiacetic acid
scan shows retention of the radionuclide proximal to strictures in the
distribution of the left hepatic duct. Note the lack of filling of the
gallbladder because of a previous cholecystectomy. Isotope has entered the
small bowel.

of 7

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CONTRIBUTOR INFORMATION AND DISCLOSURES

Author

Henry C Lin, MD, MBA Professor, Department of Pediatrics, Division of
Gastroenterology, Oregon Health and Science University School of Medicine;
Division Head, Division of Gastroenterology, Doernbecher Children’s Hospital

Henry C Lin, MD, MBA is a member of the following medical societies: Alpha Omega
Alpha, American Academy of Pediatrics, American Association for the Study of
Liver Diseases, American Gastroenterological Association, American Medical
Association, International Pediatric Transplant Association, North American
Society for Pediatric Gastroenterology, Hepatology and Nutrition, Oregon Medical
Association, Oregon Pediatric Society, Society of Pediatric Liver
Transplantation

Disclosure: Received income in an amount equal to or greater than $250 from:
Albireo Pharmaceuticals; Mirum Pharmaceuticals<br/>Consultant for: Alexion;
Albireo; Mirum.

Coauthor(s)

David A Piccoli, MD Chief of Pediatric Gastroenterology, Hepatology and
Nutrition, The Children's Hospital of Philadelphia; Professor, Perelman School
of Medicine at the University of Pennsylvania

David A Piccoli, MD is a member of the following medical societies: American
Association for the Study of Liver Diseases, American Gastroenterological
Association, North American Society for Pediatric Gastroenterology, Hepatology
and Nutrition

Disclosure: Nothing to disclose.

Chief Editor

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of
Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American
College of Gastroenterology, American Gastroenterological Association, North
American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Royal
College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and
teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.
for: Abbott Nutritional, Abbvie, speakers' bureau.

Acknowledgements

Robert Baldassano, MD Director, Center for Pediatric Inflammatory Bowel Disease,
Children's Hospital of Philadelphia; Professor, Department of Pediatrics,
Division of Gastroenterology and Nutrition, University of Pennsylvania School of
Medicine

Robert Baldassano, MD is a member of the following medical societies: Alpha
Omega Alpha, American Academy of Pediatrics, American Gastroenterological
Association, and North American Society for Pediatric Gastroenterology and
Nutrition

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska
Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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