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DOI: 10.1148/rg.284075148
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RadioGraphics 2008;28:1115-1129
© RSNA, 2008

EDUCATION EXHIBIT

Mimics of Cholangiocarcinoma: Spectrum of Disease1

Christine O. Menias, MD, Venkateswar R. Surabhi, MD2, Srinivasa R. Prasad, MD, Hanlin L. Wang, MD, Vamsi R. Narra, MD, and Kedar N. Chintapalli, MD

1 From the Department of Radiology, Mallinckrodt Institute of Radiology, St Louis, Mo (C.O.M., V.R.N.); the Department of Radiology, University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78229 (V.R.S., S.R.P., K.N.C.); and the Department of Pathology, Washington University, St Louis, Mo (H.L.W.). Presented as an education exhibit at the 2006 RSNA Annual Meeting. Received June 28, 2007; revision requested August 2 and received September 14; accepted October 9. V.R.N. is on the medical advisory boards of Vital Images and Imaging Advantage and is cofounder of Tesla9; all other authors have no financial relationships to disclose. Address correspondence to S.R.P. (e-mail: prasads{at}uthscsa.edu).


   Abstract
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 Abstract
LEARNING OBJECTIVES FOR TEST...
 Introduction
 Inflammatory or Infectious...
 Hepatobiliary Tumors That Mimic...
 Conclusions
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Cholangiocarcinoma is the second most common primary malignant hepatobiliary neoplasm, accounting for approximately 15% of liver cancers. Diagnosis of cholangiocarcinoma is challenging and the prognosis is uniformly poor, with recurrence rates of 60%–90% after surgical resection. A wide spectrum of neoplastic and nonneoplastic conditions of the biliary tract may masquerade as cholangiocarcinoma, adding to the complexity of management in patients suspected to have cholangiocarcinoma. Mimics of cholangiocarcinoma constitute a heterogeneous group of entities that includes primary sclerosing cholangitis, recurrent pyogenic cholangitis, acquired immunodeficiency syndrome cholangiopathy, autoimmune pancreatitis, inflammatory pseudotumor, Mirizzi syndrome, xanthogranulomatous cholangitis, sarcoidosis, chemotherapy-induced sclerosis, hepatocellular carcinoma, metastases, melanoma, lymphoma, leukemia, and carcinoid tumors. These entities demonstrate characteristic histomorphology and variable clinicobiologic behaviors. The imaging findings of these disparate entities are protean and may be indistinguishable from those of cholangiocarcinoma. In most cases, a definitive diagnosis can be established only with histopathologic examination of a biopsy specimen.

© RSNA, 2008


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   Introduction
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Cholangiocarcinoma (CCA), the malignant neoplasm of the cholangiocyte, accounts for significant global morbidity and mortality, especially in endemic areas of liver fluke infestation (1). Other risk factors for CCA include congenital biliopan-creatic anomalies, cirrhosis, primary sclerosing cholangitis, and hepatitis B or C virus infection (1,2). Early diagnosis of CCA is difficult, and most patients present late with unresectable disease. Treatment options in advanced disease are limited and the prognosis is poor, with dismal 5-year disease-free survival rates (2).

Most CCAs are tubular or papillary adenocarcinomas with a characteristic profuse fibrous stroma (Fig 1). It is hypothesized that recruitment of activated myofibroblasts results in the formation of abundant fibrous stroma (3). In a detailed study of 240 resected CCAs, the Liver Cancer Study Group of Japan categorized CCAs on the basis of morphology and growth patterns into three types: mass forming, periductal-infil-trating, and intraductal growth types (4) (Figs 2–4). The classification schema is invaluable in the diagnosis and treatment of patients with CCAs (2).


Figure 1
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  		Figure 1.  Well-differentiated CCA. Photomicrograph (original magnification, x200; hematoxylineosin [H-E] stain) shows well-formed malignant glands (arrows) and an infiltrating desmoplastic stroma.

 

Figure 2
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  		Figure 2.  Mass-forming type of CCA. Axial fat-saturated two-dimensional gradient-echo T2-weighted magnetic resonance (MR) image shows a well-circumscribed liver mass (arrow) with associated biliary dilatation.

 

Figure 3
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  		Figure 3.  CCA with intraductal polypoid growth pattern. Axial contrast-enhanced computed tomographic (CT) scan shows a polypoid soft-tissue mass (arrow) within the dilated common bile duct.

 

Figure 4
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  		Figure 4.  Periductal-infiltrating type of CCA. Axial delayed gadolinium-enhanced fat-saturated three-dimensional (3D) gradient-echo T1-weighted MR image shows a periductal, infiltrative pattern of tumor growth (black arrowheads) with associated biliary dilatation (white arrowheads).

 

CCAs display a wide spectrum of imaging findings. Most CCAs (with the exception of peripheral, intrahepatic CCAs) typically cause biliary ductal obstruction. CCAs show variable echogenicity at sonography. They appear as ill-defined, hypoattenuating or hypointense liver masses at CT and MR imaging. Dynamic contrast-enhanced CT or MR imaging findings include early rim enhancement and characteristic delayed and persistent enhancement of the tumor (5) (Fig 5). These imaging findings are thought to reflect the abundant fibrous content of the tumors and the slow diffusion of contrast material into the tumor interstitium (5). Imaging findings of intraductal and periductal-infiltrating types of CCA are protean and include biliary strictures, intraductal neoplasms, and focal or diffuse ductal thickening with or without enhancement (6,7) (Figs 3, 4).


Figure 5A
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  		Figure 5a.  Mass-forming CCA. (a) Axial contrast-enhanced CT scan obtained during the portal venous phase shows an ill-defined mass (arrow) in the left hepatic lobe with associated biliary dilatation (arrowheads). (b) Axial delayed contrast-enhanced CT scan obtained with a 10-minute delay shows progressive filling of the mass with contrast material (arrow). Arrowheads = associated biliary dilatation.

 

Figure 5B
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  		Figure 5b.  Mass-forming CCA. (a) Axial contrast-enhanced CT scan obtained during the portal venous phase shows an ill-defined mass (arrow) in the left hepatic lobe with associated biliary dilatation (arrowheads). (b) Axial delayed contrast-enhanced CT scan obtained with a 10-minute delay shows progressive filling of the mass with contrast material (arrow). Arrowheads = associated biliary dilatation.

 

However, a wide spectrum of inflammatory and neoplastic conditions of the bile ducts have imaging characteristics identical to those of CCAs. Indeed, in a large surgical series, benign disease was diagnosed in 24% of patients undergoing surgery for presumed hilar CCAs (8). Differentiation of biliary tract tumors or pseudotumors from CCAs permits optimal patient treatment. Some entities such as primary sclerosing cholangitis, autoimmune pancreatitis, recurrent pyogenic cholangitis, and Mirizzi syndrome may show characteristic imaging findings including morphology, disease distribution, and attendant systemic syndromes that permit their diagnosis. Primary sclerosing cholangitis typically manifests as multiple strictures associated with beading and peripheral pruning of biliary ducts. Recurrent pyogenic cholangitis typically demonstrates predominant involvement of the left lateral and right posterior segmental biliary ductal system. Mirizzi syndrome manifests as extrinsic narrowing of the common hepatic duct with a calculus impacted in the gallbladder neck or cystic duct.

However, imaging manifestations of other CCA mimics overlap with those of CCA, and differentiation is difficult on the basis of imaging findings alone. Correlation with clinical and demographic data may help narrow the differential diagnoses in these patients. In this review, we discuss the cross-sectional imaging findings of a wide spectrum of neoplastic and nonneoplastic biliary lesions that mimic CCAs at imaging.


   Inflammatory or Infectious Biliary Conditions That Mimic CCA
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Primary Sclerosing Cholangitis
Primary sclerosing cholangitis (PSC) is an idiopathic, chronic cholestatic disease of possible autoimmune origin that is characterized by diffuse cholangitis and progressive fibrosis of the extra- and intrahepatic bile ducts (9). PSC typically manifests in the fourth or fifth decade. There is a distinct male preponderance. Sixty percent to 80% of patients with PSC have associated inflammatory bowel disease, especially ulcerative colitis. The chronic inflammation of PSC predisposes to the development of CCA, the most dreaded complication of PSC (9). CCA develops in 10% of patients with PSC. The incidence of CCA in patients with PSC is 0.6%–1.5% per year, with the highest incidence in the first 2 years after diagnosis of PSC (10). Patients with PSC develop CCA approximately 2–3 decades earlier than patients without PSC.

PSC affects both intra- and extrahepatic ducts; the disease distribution is as follows: involvement of both small and large ducts in 75% of patients, involvement of small ducts only in 15%, and involvement of large ducts only in 10% (9). Small ducts are bile ducts that are too small to be identified with endoscopic retrograde cholangiopancreatography (ERCP). MR cholangiopancreatography is being increasingly used to diagnose PSC and is considered to be the best initial approach to diagnosis of PSC. The classic imaging findings of PSC include multifocal strictures, segmental ectasias, ductal wall thickening, and irregular beading of the intra- and extrahepatic bile ducts (11,12) (Figs 6, 7).


Figure 6
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  		Figure 6.  PSC. Oblique coronal gray-scale sonogram shows a dilated common bile duct with associated wall thickening (arrow).

 

Figure 7
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  		Figure 7.  PSC. Coronal image from color-coded 3D T2-weighted MR cholangiopancreatography shows segmental strictures (arrow) and dilatation (arrowhead) of the bile ducts.

 
In a small percentage of patients, focal segmental involvement of PSC manifesting as a focal short-segment stricture without the classic imaging findings makes it difficult to distinguish from the periductal-infiltrating type of CCA (13). Also, CCA complicating PSC occurs, adding to the complexity of management in patients with PSC (10). There are currently no known biomarkers to screen for CCA in the subset of patients with PSC, and definitive surveillance imaging protocols in these patients are lacking. Contrast-enhanced CT and MR imaging are useful in detection of CCA that complicates PSC (9). The presence of a focal mass, bile duct wall thickening greater than 4 mm, and progressive biliary obstruction at serial imaging suggest the development of CCA against the background of PSC (14,15).

Secondary Sclerosing Cholangitis
Secondary sclerosing cholangitis syndromes are a heterogeneous group of chronic cholestatic disorders that are morphologically similar to PSC but result from distinct pathologic processes (16) (Fig 8). The wide spectrum of secondary sclerosing cholangitis entities includes recurrent pyogenic cholangitis, acquired immunodeficiency syndrome (AIDS) cholangiopathy, autoimmune pancreatitis, hepatic inflammatory pseudotumor, eosinophilic cholangitis, portal biliopathy, and ischemic cholangiopathy.


Figure 8
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  		Figure 8.  Secondary sclerosing cholangitis secondary to extrahepatic biliary obstruction. Photomicrograph (original magnification, x200; trichrome stain) shows marked concentric (onion skin–like) periductal fibrosis (arrows), which is indistinguishable from that seen in PSC.

 

Recurrent Pyogenic Cholangitis. Also referred to as "oriental" cholangiohepatitis, recurrent pyogenic cholangitis (RPC) is characterized by recurrent attacks of acute pyogenic cholangitis that occur in the setting of biliary obstruction by pigmented stones or biliary strictures (17). RPC occurs between the third and fifth decades; no specific sex predilection exists. Patients present with abdominal pain, fever, and jaundice. Ascaris lumbricoides , Clonorchis sinensis , Opisthorchis viverrini, O felineus , and Fasciola hepatica have been implicated as pathogens that may lead to initial cholangiocyte injury (17). Chronic, recurrent infections predispose to development of pigmented calculi, cholangitic abscesses, and inflammatory strictures (18).

Imaging manifestations of RPC include biliary strictures, ductal wall thickening secondary to fibrosis, and intraductal pigmented stones (18) (Fig 9). RPC has a segmental distribution with a particular predilection for the lateral segment of the left lobe, the posterior segment of the right lobe, and the extrahepatic duct (19). The ductal wall thickening and enhancement may not be distinguished from CCA with imaging studies alone. In addition, patients with RPC have an increased risk (2%–6%) of development of CCA. However, the correct diagnosis may be considered by correlating imaging findings (especially the presence of hepatolithiasis) with clinical and demographic features (18,20). The management of RPC is generally based on the extent of hepatic involvement; surgical resection is considered appropriate if the disease is confined to a single segment or single hepatic lobe, whereas percutaneous radiologic procedures are useful for patients with unresectable disease (21).


Figure 9A
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  		Figure 9a.  RPC. (a) Coronal T2-weighted MR image shows segmental biliary dilatation in the left hepatic lobe with associated hepatolithiasis (arrows). (b) Axial delayed gadolinium-enhanced 3D T1-weighted MR image shows segmental biliary dilatation in the left hepatic lobe with periductal enhancement (arrow).

 

Figure 9B
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  		Figure 9b.  RPC. (a) Coronal T2-weighted MR image shows segmental biliary dilatation in the left hepatic lobe with associated hepatolithiasis (arrows). (b) Axial delayed gadolinium-enhanced 3D T1-weighted MR image shows segmental biliary dilatation in the left hepatic lobe with periductal enhancement (arrow).

 

AIDS Cholangiopathy. AIDS cholangiopathy is an uncommon form of sclerosing cholangitis that typically occurs in patients with advanced AIDS (16,22). The prevalence of AIDS cholangiopathy has decreased dramatically after widespread use of antiretroviral drugs. Several opportunistic pathogens such as cytomegalovirus, Cryptosporidium parvum , Microsporidium, Mycobacterium avium complex , and herpes simplex virus have been postulated to cause AIDS cholangiopathy (16,22). However, no definite organism is identified in up to 50% of patients. AIDS cholangiopathy typically affects patients with low CD4 counts (<135/mm3). Most patients are symptomatic and present with abdominal pain. Inflammation with edema of the biliary mucosa is the histologic hallmark of AIDS cholangiopathy. The large intrahepatic ducts are preferentially affected (16).

AIDS cholangiopathy typically manifests as biliary strictures associated with wall thickening and mural enhancement (23) (Fig 10). On the basis of ERCP findings, four distinct patterns of the disease have been described. The most common pattern is a combination of sclerosing cholangitis and papillary stenosis, which occurs in 50% of patients. Other findings include isolated papillary stenosis (15%), an isolated intrahepatic sclerosing cholangitis–like appearance (20%), and a long-segment extrahepatic duct stricture occurring in isolation or in concert with intrahepatic disease (15%) (24).


Figure 10
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  		Figure 10.  AIDS cholangiopathy. Axial delayed contrast-enhanced CT scan shows focal wall thickening and enhancement (arrowhead) of the common bile duct.

 

Autoimmune Pancreatitis-Cholangitis Syndrome. Autoimmune pancreatitis (AIP) is a rare type of chronic pancreatitis characterized by pancreatic dysfunction secondary to inflammation and fibrosis (25). The precise etiopathogenesis of AIP is not known at present. The pancreas in AIP shows prominent lymphocyte (predominantly T-lymphocyte) and immunoglobulin G4–positive plasma cell infiltration and fibrosis. Associated involvement of the gallbladder and bile ducts is seen in a subset of patients with AIP. AIP is considered a systemic disease; extrapancreatic manifestations occur in up to 49% of patients. The extrapancreatic syndromes include sclerosing cholangitis, sialadenitis, retroperitoneal fibrosis, systemic lymphadenopathy, interstitial nephritis, and chronic thyroiditis. These manifestations may be synchronous or metachronous to the onset of the pancreatic syndrome (26).

Imaging findings of AIP include diffuse or focal homogeneous enlargement of the pancreas associated with a peripheral hypoattenuating halo (25). AIP is characterized by focal or diffuse strictures of the pancreatic duct and bile ducts. Narrowing of the intrapancreatic bile duct and bile duct strictures with upstream ductal dilatation can also be seen, which may simulate the periductal-infiltrating type of CCA (25) (Fig 11). However, the presence of pancreatic abnormalities should favor the diagnosis of AIP (25). In addition, the presence of a systemic disease process such as pulmonary findings, mediastinal lymphadenopathy, and renal abnormalities may be seen (26).


Figure 11A
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  		Figure 11a.  Autoimmune pancreatitis-cholangitis syndrome. (a) Axial contrast-enhanced CT scan shows dilatation of the common bile duct (arrow). Note the associated peripancreatic inflammatory changes (arrowheads). (b) Cholangiogram from ERCP shows a long-segment stricture of the common bile duct (arrow) with upstream ductal dilatation (arrowhead).

 

Figure 11B
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  		Figure 11b.  Autoimmune pancreatitis-cholangitis syndrome. (a) Axial contrast-enhanced CT scan shows dilatation of the common bile duct (arrow). Note the associated peripancreatic inflammatory changes (arrowheads). (b) Cholangiogram from ERCP shows a long-segment stricture of the common bile duct (arrow) with upstream ductal dilatation (arrowhead).

 

In the presence of imaging findings suspicious for AIP, the radiologist may alert the clinician to perform appropriate laboratory tests to establish the diagnosis. The diagnosis of AIP is considered in a patient with elevated serum immunoglobulin G4 antibodies in the appropriate clinical setting. The condition may respond to steroid therapy (25).

Hepatobiliary Inflammatory Pseudotumor. Inflammatory pseudotumor (IPT) is a rare, idiopathic, nonneoplastic spindle cell proliferative disorder of uncertain histogenesis that commonly affects the lungs in young adults (27). IPT typically shows benign clinical behavior, although aggressive behavior and recurrences have been described in the literature (28). At histologic analysis, IPT is characterized predominantly by an inflammatory infiltrate consisting of lymphocytes, plasma cells, and histiocytes admixed with a variable proportion of fibroblasts and myofibroblasts (Fig 12) (28,29). The liver is the second most common target location of IPT. Although some IPTs are related to antecedent infection, others are considered to be neoplastic (29). Epstein-Barr virus has been found within the spindle cells in some IPTs, particularly in the liver and spleen (30). Hepatic IPT was described by Pack and Baker (31) in 1953.


Figure 12
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  		Figure 12.  IPT of the liver. Photomicrograph (original magnification, x400; H-E stain) shows mixed inflammatory cells (mainly lymphocytes and plasma cells) in a fibrotic background with scattered spindle-shaped myofibroblasts.

 

Imaging findings of hepatobiliary IPT are diverse and nonspecific (32,33) and indistinguishable from those of the mass-forming type of CCA (33,34) (Fig 13). Hepatobiliary IPTs appear as soft-tissue masses that may show delayed and persistent enhancement due to fibrous content, findings remarkably similar to those of CCAs (32,33). Cholangiography may show biliary strictures of intra- or extrahepatic ducts (33). In addition, IPT may be associated with RPC that leads to biliary stricture formation and thus mimic the periductal-infiltrating type of CCA (35).


Figure 13
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  		Figure 13.  Intrahepatic biliary IPT. Transverse Doppler sonogram shows an expansile soft-tissue mass (arrow) within a dilated intrahepatic bile duct.

 

Mirizzi Syndrome. In 1948, Mirizzi described a functional hepatic syndrome that consisted of a common hepatic duct obstruction secondary to compression by a gallstone impacted at the gallbladder neck or cystic duct (36). A low insertion of the cystic duct into the common hepatic duct is a predisposing factor in the development of Mirizzi syndrome. In patients with a low insertion of the cystic duct, the ducts run parallel to each other. The common hepatic duct is at increased risk of compression by impacted calculi within the cystic duct (37).

A typical ultrasonographic (US) finding of Mirizzi syndrome is a large, immobile stone in the region of the neck of a shrunken gallbladder, with dilatation of bile ducts proximal to it (38). Gallstones are not always well visualized at CT, thereby making diagnosis of Mirizzi syndrome difficult. MR cholangiopancreatography has been shown to have high sensitivity and specificity in the detection of gallstone and bile duct stenosis. MR cholangiopancreatography can show the typical features of Mirizzi syndrome, such as extrinsic narrowing of the common hepatic duct, a gallstone in the cystic duct, dilatation of the intrahepatic and common hepatic ducts, and a normal common bile duct (39) (Fig 14a). However, the imaging findings are not always specific (40) (Fig 14b). Rarely, inflammation around the common bile duct leads to stricture formation and thus resembles the periductal-infiltrating type of CCA.


Figure 14A
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  		Figure 14a.  Mirizzi syndrome. (a) Axial arterial phase gadolinium-enhanced fat-saturated 3D gradient-echo T1-weighted MR image shows concentric thickening of the wall of the common hepatic duct (arrow). (b) Coronal two-dimensional gradient-echo T2-weighted MR image shows a stricture at the confluence of the hepatic ducts (arrow), which simulates a Klatskin tumor. The gallbladder is distended with multiple calculi (arrowheads).

 

Figure 14B
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  		Figure 14b.  Mirizzi syndrome. (a) Axial arterial phase gadolinium-enhanced fat-saturated 3D gradient-echo T1-weighted MR image shows concentric thickening of the wall of the common hepatic duct (arrow). (b) Coronal two-dimensional gradient-echo T2-weighted MR image shows a stricture at the confluence of the hepatic ducts (arrow), which simulates a Klatskin tumor. The gallbladder is distended with multiple calculi (arrowheads).

 

Xanthogranulomatous Cholecystitis or Cholangitis. Xanthogranulomatous cholecystitis (XGC) is a distinctly rare form of severe, chronic infection of the gallbladder. At histopathologic analysis, XGC is characterized by an inflammatory infiltrate consisting primarily of foamy histiocytes and xanthoma cells admixed with variable acute inflammatory infiltrate and fibrosis (41,42). XGC commonly occurs in the fifth to sixth decades. Common predisposing factors include gallstones, obesity, and diabetes mellitus (41). It is hypothesized that cystic duct obstruction leads to mucosal or mural injury, leading to macrophage recruitment and activation. Phagocytosis of insoluble bile lipids and cholesterol leads to lipogranuloma formation, which subsequently results in fibrosis (41,42).

XGC appears as focal or diffuse masslike wall thickening of the gallbladder with heterogeneous contrast enhancement and extension into adjacent soft tissues (41). Shuto et al (43) found that areas of necrosis or abscess appeared markedly hyperintense on T2-weighted MR images and regions with foamy cell proliferations (xanthogranulomas) showed delayed strong enhancement. However, XGC demonstrates imaging findings similar to those of gallbladder carcinoma with local spread; accurate distinction is usually made after surgery. Xanthogranulomatous cholangitis may occur in isolation or in association with XGC (44). Xanthogranulomatous cholangitis appears as a biliary stricture with associated wall thickening and is indistinguishable from the infiltrative type of CCA (Fig 15).


Figure 15A
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  		Figure 15a.  Xanthogranulomatous cholangitis. (a) Coronal image from T2-weighted MR cholangiopancreatography shows a stricture of the intrahepatic bile duct (arrow). (b) Image from transhepatic cholangiography shows the irregular stricture of the common hepatic duct (arrow). At histopathologic analysis, the stricture was proved to be due to xanthogranulomatous inflammation.

 

Figure 15B
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  		Figure 15b.  Xanthogranulomatous cholangitis. (a) Coronal image from T2-weighted MR cholangiopancreatography shows a stricture of the intrahepatic bile duct (arrow). (b) Image from transhepatic cholangiography shows the irregular stricture of the common hepatic duct (arrow). At histopathologic analysis, the stricture was proved to be due to xanthogranulomatous inflammation.

 

Biliary Sarcoidosis. Sarcoidosis is a chronic, idiopathic, multisystem disorder that is pathologically characterized by noncaseating granulomas (Fig 16a) (45). Sarcoidosis exhibits a predilection for young women in the second to fourth decades and African-Americans. The lungs are the most common target sites in sarcoidosis, being involved in 90% of patients; other sites of involvement include the lymph nodes, eye, and skin. Extrapulmonary sarcoidosis is almost always found with concomitant pulmonary disease (46).


Figure 16A
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  		Figure 16a.  Biliary sarcoidosis. (a) Photomicrograph (original magnification, x400; H-E stain) shows a well-formed, noncaseating, nonnecrotizing granuloma that consists mainly of epithelioid histiocytes. (b) Axial contrast-enhanced CT scan shows a hypoattenuating mass in the left hepatic lobe (arrow) with associated biliary dilatation (arrowhead). (c) Cholangiogram from ERCP shows irregular strictures in the left hepatic lobe (arrow) and associated biliary dilatation (arrowhead).

 

Figure 16B
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  		Figure 16b.  Biliary sarcoidosis. (a) Photomicrograph (original magnification, x400; H-E stain) shows a well-formed, noncaseating, nonnecrotizing granuloma that consists mainly of epithelioid histiocytes. (b) Axial contrast-enhanced CT scan shows a hypoattenuating mass in the left hepatic lobe (arrow) with associated biliary dilatation (arrowhead). (c) Cholangiogram from ERCP shows irregular strictures in the left hepatic lobe (arrow) and associated biliary dilatation (arrowhead).

 

Figure 16C
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  		Figure 16c.  Biliary sarcoidosis. (a) Photomicrograph (original magnification, x400; H-E stain) shows a well-formed, noncaseating, nonnecrotizing granuloma that consists mainly of epithelioid histiocytes. (b) Axial contrast-enhanced CT scan shows a hypoattenuating mass in the left hepatic lobe (arrow) with associated biliary dilatation (arrowhead). (c) Cholangiogram from ERCP shows irregular strictures in the left hepatic lobe (arrow) and associated biliary dilatation (arrowhead).

 

Most patients with hepatobiliary sarcoidosis are asymptomatic; only 5%–15% of patients show signs and symptoms of the disease. However, hepatobiliary involvement is found at liver biopsy in 50%–65% of patients with sarcoidosis (46). The manifestations of hepatobiliary sarcoidosis are protean and include hepatomegaly, multifocal micronodular granulomas, macronodular granulomas, granulomatous cholangitis, cirrhosis, portal hypertension, and jaundice due to periportal lymphadenopathy (46). Granulomatous cholangitis is an extremely rare disease characterized by insidious onset and chronic progression to biliary cirrhosis. It is characterized by chronic cholestasis due to formation of granulomas in bile ducts, leading to strictures and ductopenia (46,47). The imaging findings may be indistinguishable from those of CCA (47,48) (Fig 16b, 16c).

Chemotherapy-induced Biliary Sclerosis. Hepatic artery infusion of chemotherapeutic agents has been implicated as a cause of ischemic cholangitis leading to biliary stricture formation (16,49). Biliary sclerosis is a frequent and serious dose-limiting toxic effect of fluoropyrimidines (floxuridine and fluorouracil), widely used chemotherapeutic agents for the treatment of hepatic metastases from colorectal cancer (49). Intrahepatic instillation of mitomycin C, cis-diamminedichloroplatinum, or formaldehyde has also been reported to cause biliary sclerosis (16). Possible mechanisms include toxic vasculitis and drug-induced intravascular thrombosis leading to ischemic insult and stricture formation (16).


   Hepatobiliary Tumors That Mimic CCA
Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Inflammatory or Infectious...
 Hepatobiliary Tumors That Mimic...
Conclusions
 References
 
Hepatocellular Carcinoma
Hepatocellular carcinoma, the most common primary malignant hepatic neoplasm, rarely may show biliary ductal growth or invasion (50). Accurate preoperative diagnosis is difficult owing to the low prevalence of this pattern of growth and the nonspecific imaging findings. However, hepatocellular carcinoma commonly occurs in a cirrhotic liver. The presence of predisposing factors for cirrhosis such as positive serologic results for hepatitis B or C and high serum levels of {alpha}-fetoprotein may suggest the diagnosis of hepatocellular carcinoma. Hepatocellular carcinoma with an intrabiliary growth pattern appears as expansile soft-tissue masses that cause dilatation of the bile ducts (51) (Fig 17).


Figure 17
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  		Figure 17.  Hepatocellular carcinoma with an intrabiliary growth pattern. Transverse gray-scale sonogram shows a polypoid, expansile, intrabiliary soft-tissue mass (arrow) with associated biliary dilatation.

 

Intrabiliary Metastases
Intrabiliary metastases are extremely rare. Tumors that metastasize to the bile ducts include primary cancers of the lung, breast, gallbladder, colon, testicle, prostate, or pancreas; melanoma; and lymphoma. Of the listed cancers, colonic adenocarcinoma, on account of its proclivity to spread along epithelial surfaces, shows an increased predilection to involve the biliary ducts (52) (Fig 18).


Figure 18A
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  		Figure 18a.  Intrabiliary metastases from colonic adenocarcinoma. (a) Coronal delayed gadolinium-enhanced T1-weighted MR image (minimum intensity projection) shows longitudinal tumor growth within the bile ducts (arrows) and biliary dilatation (arrowhead). (b) Coronal fluorine 18 (18F) fluorodeoxyglucose positron emission tomographic (PET) scan shows an area of increased activity (arrow), which corresponds to the tumor extension in a.

 

Figure 18B
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  		Figure 18b.  Intrabiliary metastases from colonic adenocarcinoma. (a) Coronal delayed gadolinium-enhanced T1-weighted MR image (minimum intensity projection) shows longitudinal tumor growth within the bile ducts (arrows) and biliary dilatation (arrowhead). (b) Coronal fluorine 18 (18F) fluorodeoxyglucose positron emission tomographic (PET) scan shows an area of increased activity (arrow), which corresponds to the tumor extension in a.

 

Imaging findings of metastases that show intrabiliary growth may mimic all three morphologic forms of CCA (53,54). There are no imaging features that allow reliable distinction of biliary metastases from CCA; therefore, diagnosis is based solely on history and histologic findings (52). Immunochemistry can solve the problem in difficult cases; metastatic colon carcinoma shows cytokeratin 20 (CK20) positivity and cytokeratin 7 (CK7) negativity in contradistinction to the adjacent bile duct epithelium, which is CK7 positive and CK20 negative (55).

Biliary Tract Melanoma
Bile duct melanoma may arise primarily from the biliary epithelium or can result from metastases from a primary location elsewhere. Malignant melanoma exhibits a remarkable ability to metastasize to diverse locations in the body. At histologic analysis, melanoma demonstrates melanin cells that show positive immunoreactivity to HMB-45, melan-A, and S100 markers (56) (Fig 19a).


Figure 19A
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  		Figure 19a.  Primary malignant melanoma of the hepatic duct. (a) Photomicrograph (original magnification, 400;x H-E stain) shows nests of tumor cells with large nuclei, prominent nucleoli, and abundant eosinophilic cytoplasm. Melanin pigment is evident (arrowheads). The tumor arose within a large hepatic duct near the hilum. (b) Transverse gray-scale sonogram shows an expansile soft-tissue mass of variable echogenicity (arrows) in the common hepatic duct.

 

Figure 19B
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  		Figure 19b.  Primary malignant melanoma of the hepatic duct. (a) Photomicrograph (original magnification, 400;x H-E stain) shows nests of tumor cells with large nuclei, prominent nucleoli, and abundant eosinophilic cytoplasm. Melanin pigment is evident (arrowheads). The tumor arose within a large hepatic duct near the hilum. (b) Transverse gray-scale sonogram shows an expansile soft-tissue mass of variable echogenicity (arrows) in the common hepatic duct.

 

Biliary melanoma manifests as an intraluminal polypoid soft-tissue mass with associated biliary dilatation, thus simulating the CCA type with intraluminal growth (Fig 19b). Imaging features at CT and US are nonspecific. However, the polypoid mass may demonstrate high signal intensity on T1-weighted images and low signal intensity on T2-weighted images owing to its melanin content (57).

Lymphoma of the Bile Ducts
Lymphomatous involvement of the biliary system is rare and is usually a secondary manifestation of systemic disease (58). Most biliary lymphomas are of the non-Hodgkin type. Lymphomas demonstrate variegated histomorphologic and immunocytochemical features (Fig 20a). Primary malignant lymphoma arising from the biliary ducts is extremely rare and was described by Nguyen in 1982 (59). In general, patients present with systemic symptoms and abdominal pain; however, a small percentage of patients present solely with symptoms of obstructive jaundice (58).


Figure 20A
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  		Figure 20a.  Non-Hodgkin lymphoma. (a) Photomicrograph (original magnification, x400; H-E stain) of a tumor shows infiltrating lymphoid cells. (b) Oblique sagittal gray-scale sonogram shows a soft-tissue mass with a longitudinal growth pattern (arrow) in a bile duct. (c) Coronal 18F-fluorodeoxyglucose PET scan shows an area of increased activity (arrow), which corresponds to the tumor extension in b.

 

Figure 20B
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  		Figure 20b.  Non-Hodgkin lymphoma. (a) Photomicrograph (original magnification, x400; H-E stain) of a tumor shows infiltrating lymphoid cells. (b) Oblique sagittal gray-scale sonogram shows a soft-tissue mass with a longitudinal growth pattern (arrow) in a bile duct. (c) Coronal 18F-fluorodeoxyglucose PET scan shows an area of increased activity (arrow), which corresponds to the tumor extension in b.

 

Figure 20C
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  		Figure 20c.  Non-Hodgkin lymphoma. (a) Photomicrograph (original magnification, x400; H-E stain) of a tumor shows infiltrating lymphoid cells. (b) Oblique sagittal gray-scale sonogram shows a soft-tissue mass with a longitudinal growth pattern (arrow) in a bile duct. (c) Coronal 18F-fluorodeoxyglucose PET scan shows an area of increased activity (arrow), which corresponds to the tumor extension in b.

 

Imaging findings of bile duct lymphomas include biliary strictures and a soft-tissue mass causing biliary obstruction and are similar to those of CCA (58,60) (Fig 20b, 20c).

Leukemic Involvement of the Bile Ducts
Leukemic involvement of the biliary ducts is rare. Acute myelogenous leukemia may manifest as biliary stricture formation and may mimic the periductal-infiltrating type of CCA (61,62) (Fig 21). Granulocytic sarcoma (chloroma) can involve the extrahepatic biliary ducts either de novo or concurrently with acute or chronic myeloproliferative disorders. Chloroma appears as a soft-tissue mass in the bile ducts and is radiologically indistinguishable from CCA (63–65).


Figure 21
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  		Figure 21.  Acute myeloid leukemia with an intrabiliary growth pattern. Oblique coronal gray-scale sonogram shows a soft-tissue mass with longitudinal intrabiliary growth (arrow) and upstream ductal dilatation (arrowhead).

 

Carcinoid Tumors of the Bile Ducts
Carcinoid tumors of the biliary tract are rare and account for 0.2%–2% of all gastrointestinal carcinoid tumors (66). Carcinoid tumor of the extrahepatic bile duct is extremely rare, with fewer than 34 cases reported in the English-language literature. The most common anatomic sites were the common bile duct (58%), perihilar region (28%), cystic duct (11%), and common hepatic duct (3%) (67). Carcinoid tumors are usually slow-growing neoplasms with low malignant potential and hence are amenable to aggressive surgical management (68). Preoperative diagnosis is difficult because they mimic the signs and symptoms of CCA. Unlike CCA, biliary carcinoid tumors occur more commonly in younger patients and in women. Aggressive local invasion by the primary tumor is rare, and metastases occur in less than one-third of patients. The final diagnosis is usually confirmed with immunohistochemical studies (69).

Imaging findings of carcinoid tumors of the biliary tract are diverse and nonspecific. They may appear as a long-segment biliary stricture with associated wall thickening (Fig 22) or as a large exophytic mass, thus mimicking the periductal-infiltrating or mass-forming types of CCA.


Figure 22
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  		Figure 22.  Biliary carcinoid tumor. Axial arterial phase gadolinium-enhanced fat-saturated 3D gradient-echo T1-weighted MR image shows focal enhancement of the wall of the common bile duct (arrow). At histopathologic analysis, this finding was proved to represent a carcinoid tumor.

 


   Conclusions
Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Inflammatory or Infectious...
 Hepatobiliary Tumors That Mimic...
 Conclusions
References
 
There is a broad spectrum of inflammatory and neoplastic disorders of the intrahepatic and extrahepatic biliary system that resemble CCA in terms of clinical, pathologic, and imaging findings. Some entities may show characteristic imaging findings that permit accurate diagnosis. However, biopsy may be required to achieve definitive histopathologic characterization in most cases. Precise distinction of various biliary disorders from the more ominous CCA allows optimal patient treatment.


   Footnotes
 

Abbreviations: AIDS = acquired immunodeficiency syndrome, AIP = autoimmune pancreatitis, CCA = cholangiocarcinoma, ERCP = endoscopic retrograde cholangiopancreatography, H-E = hematoxylin-eosin, IPT = inflammatory pseudotumor, PSC = primary sclerosing cholangitis, RPC = recurrent pyogenic cholangitis, 3D = three-dimensional, XGC = xanthogranulomatous cholecystitis

2 Current address: Department of Diagnostic and Interventional Imaging, University of Texas Health Science Center, Houston, Tex. Back


   References
Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Inflammatory or Infectious...
 Hepatobiliary Tumors That Mimic...
 Conclusions
 References
 

  1. Hamilton SR, Aaltonen LA, eds. WHO classification of tumours: pathology and genetics of tumours of the digestive system. Lyon, France: IARC Press, 2000.
  2. Patel T. Cholangiocarcinoma. Nat Clin Pract Gastroenterol Hepatol 2006;3:33–42.[CrossRef][Medline]
  3. Terada T, Makimoto K, Terayama N, Suzuki Y, Nakanuma Y. Alpha-smooth muscle actin-positive stromal cells in cholangiocarcinomas, hepatocellular carcinomas and metastatic liver carcinomas. J Hepatol 1996;24:706–712.[CrossRef][Medline]
  4. Yamasaki S. Intrahepatic cholangiocarcinoma: macroscopic type and stage classification. J Hepatobiliary Pancreat Surg 2003;10:288–291.[CrossRef][Medline]
  5. Lacomis JM, Baron RL, Oliver JH 3rd, Nalesnik MA, Federle MP. Cholangiocarcinoma: delayed CT contrast enhancement patterns. Radiology 1997;203:98–104.[Abstract/Free Full Text]
  6. Lee WJ, Lim HK, Jang KM, et al. Radiologic spectrum of cholangiocarcinoma: emphasis on unusual manifestations and differential diagnoses. RadioGraphics 2001;21(spec issue):S97–S116.[Abstract/Free Full Text]
  7. Han JK, Choi BI, Kim AY, et al. Cholangiocarcinoma: pictorial essay of CT and cholangiographic findings. RadioGraphics 2002;22:173–187.[Abstract/Free Full Text]
  8. Clayton RA, Clarke DL, Currie EJ, Madhavan KK, Parks RW, Garden OJ. Incidence of benign pathology in patients undergoing hepatic resection for suspected malignancy. Surgeon 2003;1:32–38.[Medline]
  9. LaRusso NF, Shneider BL, Black D, et al. Primary sclerosing cholangitis: summary of a workshop. Hepatology 2006;44:746–764.[CrossRef][Medline]
  10. Burak K, Angulo P, Pasha TM, Egan K, Petz J, Lindor KD. Incidence and risk factors for cholangiocarcinoma in primary sclerosing cholangitis. Am J Gastroenterol 2004;99:523–526.[CrossRef][Medline]
  11. Vitellas KM, Keogan MT, Freed KS, et al. Radiologic manifestations of sclerosing cholangitis with emphasis on MR cholangiopancreatography. RadioGraphics 2000;20:959–975.[Abstract/Free Full Text]
  12. Elsayes KM, Oliveira EP, Narra VR, et al. MR and MRCP in the evaluation of primary sclerosing cholangitis: current applications and imaging findings. J Comput Assist Tomogr 2006;30:398–404.[CrossRef][Medline]
  13. Tsunoda T, Eto T, Yamada M, et al. Segmental primary sclerosing cholangitis mimicking bile duct cancer: report of a case and review of the Japanese literature. Jpn J Surg 1991;21:329–334.[CrossRef][Medline]
  14. Campbell WL, Ferris JV, Holbert BL, Thaete FL, Baron RL. Biliary tract carcinoma complicating primary sclerosing cholangitis: evaluation with CT, cholangiography, US, and MR imaging. Radiology 1998;207:41–50.[Abstract/Free Full Text]
  15. Campbell WL, Peterson MS, Federle MP, et al. Using CT and cholangiography to diagnose biliary tract carcinoma complicating primary sclerosing cholangitis. AJR Am J Roentgenol 2001;177: 1095–1100.[Abstract/Free Full Text]
  16. Abdalian R, Heathcote EJ. Sclerosing cholangitis: a focus on secondary causes. Hepatology 2006;44: 1063–1074.[CrossRef][Medline]
  17. Lim JH. Oriental cholangiohepatitis: pathologic, clinical, and radiologic features. AJR Am J Roentgenol 1991;157:1–8.[Abstract/Free Full Text]
  18. Park MS, Yu JS, Kim KW, et al. Recurrent pyogenic cholangitis: comparison between MR cholangiography and direct cholangiography. Radiology 2001;220:677–682.[Abstract/Free Full Text]
  19. Kruskal JB, Kane RA. Intraoperative sonography of the biliary system. AJR Am J Roentgenol 2001;177: 395–403.[Free Full Text]
  20. Kim MJ, Cha SW, Mitchell DG, Chung JJ, Park S, Chung JB. MR imaging findings in recurrent pyogenic cholangitis. AJR Am J Roentgenol 1999;173: 1545–1549.[Medline]
  21. vanSonnenberg E, Casola G, Cubberley DA, et al. Oriental cholangiohepatitis: diagnostic imaging and interventional management. AJR Am J Roentgenol 1986;146:327–331.[Abstract/Free Full Text]
  22. Keaveny AP, Karasik MS. Hepatobiliary and pancreatic infections in AIDS: Part II. AIDS Patient Care STDS 1998;12:451–456.[Medline]
  23. Dolmatch BL, Laing FC, Ferderle MP, Jeffrey RB, Cello J. AIDS-related cholangitis: radiographic findings in nine patients. Radiology 1987;163: 313–316.[Abstract/Free Full Text]
  24. Cello JP, Chan MF. Long-term follow-up of endoscopic retrograde cholangiopancreatography sphincterotomy for patients with acquired immune deficiency syndrome papillary stenosis. Am J Med 1995;99:600–603.[CrossRef][Medline]
  25. Finkelberg DL, Sahani D, Deshpande V, Brugge WR. Autoimmune pancreatitis. N Engl J Med 2006;355:2670–2676.[Free Full Text]
  26. Krasinskas AM, Raina A, Khalid A, Tublin M, Yadav D. Autoimmune pancreatitis. Gastroenterol Clin North Am 2007;36:239–257.[CrossRef][Medline]
  27. Patankar T, Prasad S, Shenoy A, Rathod K. Pulmonary inflammatory pseudotumour in children. Australas Radiol 2000;44:318–320.[CrossRef][Medline]
  28. Coffin CM, Humphrey PA, Dehner LP. Extrapulmonary inflammatory myofibroblastic tumor: a clinical and pathological survey. Semin Diagn Pathol 1998;15:85–101.[Medline]
  29. Dehner LP. Inflammatory myofibroblastic tumor: the continued definition of one type of so-called inflammatory pseudotumor. Am J Surg Pathol 2004; 28:1652–1654.[CrossRef][Medline]
  30. Arber DA, Weiss LM, Chang KL. Detection of Epstein-Barr virus in inflammatory pseudotumor. Semin Diagn Pathol 1998;15:155–160.[Medline]
  31. Pack GT, Baker HW. Total right hepatic lobectomy: report of a case. Ann Surg 1953;138:253–258.[Medline]
  32. Yan FH, Zhou KR, Jiang YP, Shi WB. Inflammatory pseudotumor of the liver: 13 cases of MRI findings. World J Gastroenterol 2001;7:422–424.[Medline]
  33. Tublin ME, Moser AJ, Marsh JW, Gamblin TC. Biliary inflammatory pseudotumor: imaging features in seven patients. AJR Am J Roentgenol 2007; 188:W44–W48.[Abstract/Free Full Text]
  34. Inaba K, Suzuki S, Yokoi Y, et al. Hepatic inflammatory pseudotumor mimicking intrahepatic cholangiocarcinoma: report of a case. Surg Today 2003;33:714–717.[CrossRef][Medline]
  35. Nonomura A, Minato H, Shimizu K, Kadoya M, Matsui O. Hepatic hilar inflammatory pseudotumor mimicking cholangiocarcinoma with cholangitis and phlebitis: a variant of primary sclerosing cholangitis? Pathol Res Pract 1997;193:519–525; discussion 526.[Medline]
  36. Lai EC, Lau WY. Mirizzi syndrome: history, present and future development. ANZ J Surg 2006;76: 251–257.[CrossRef][Medline]
  37. Pedrosa CS, Casanova R, de la Torre S, Villacorta J. CT findings in Mirizzi syndrome. J Comput Assist Tomogr 1983;7:419–425.[Medline]
  38. Strunk H, Teifke A, Menke H. Typical radiologic findings in Mirizzi syndrome [in German]. Rontgenblatter 1988;41:345–347.[Medline]
  39. Choi BW, Kim MJ, Chung JJ, Chung JB, Yoo HS, Lee JT. Radiologic findings of Mirizzi syndrome with emphasis on MRI. Yonsei Med J 2000;41: 144–146.[Medline]
  40. Becker CD, Hassler H, Terrier F. Preoperative diagnosis of the Mirizzi syndrome: limitations of sonography and computed tomography. AJR Am J Roentgenol 1984;143:591–596.[Abstract/Free Full Text]
  41. Kwon AH, Matsui Y, Uemura Y. Surgical procedures and histopathologic findings for patients with xanthogranulomatous cholecystitis. J Am Coll Surg 2004;199:204–210.[CrossRef][Medline]
  42. Goodman ZD, Ishak KG. Xanthogranulomatous cholecystitis. Am J Surg Pathol 1981;5:653–659.[Medline]
  43. Shuto R, Kiyosue H, Komatsu E, et al. CT and MR imaging findings of xanthogranulomatous cholecystitis: correlation with pathologic findings. Eur Radiol 2004;14:440–446.[CrossRef][Medline]
  44. Kawate S, Ohwada S, Ikota H, Hamada K, Kashiwabara K, Morishita Y. Xanthogranulomatous cholangitis causing obstructive jaundice: a case report. World J Gastroenterol 2006;12:4428–4430.[Medline]
  45. Cox CE, Davis-Allen A, Judson MA. Sarcoidosis. Med Clin North Am 2005;89:817–828.[CrossRef][Medline]
  46. Judson MA. Extrapulmonary sarcoidosis. Semin Respir Crit Care Med 2007;28:83–101.[CrossRef][Medline]
  47. Pungpapong S, Steers JL, Wallace MB, Krishna M, Keaveny AP. Hepatobiliary sarcoidosis mimicking Klatskin’s cholangiocarcinoma. Gastrointest Endosc 2006;64:124–125.[CrossRef][Medline]
  48. Alam I, Levenson SD, Ferrell LD, Bass NM. Diffuse intrahepatic biliary strictures in sarcoidosis resembling sclerosing cholangitis: case report and review of the literature. Dig Dis Sci 1997;42: 1295–1301.[CrossRef][Medline]
  49. Alazmi WM, McHenry L, Watkins JL, et al. Chemotherapy-induced sclerosing cholangitis: long-term response to endoscopic therapy. J Clin Gastroenterol 2006;40:353–357.[CrossRef][Medline]
  50. Leong JW, Ho JM, Ng HS, Raj JP. Early hepatocellular carcinoma presenting with biliary ductal invasion: a case report. Ann Acad Med Singapore 2000;29:101–104.[Medline]
  51. Qin LX, Tang ZY. Hepatocellular carcinoma with obstructive jaundice: diagnosis, treatment and prognosis. World J Gastroenterol 2003;9:385–391.[Medline]
  52. Riopel MA, Klimstra DS, Godellas CV, Blumgart LH, Westra WH. Intrabiliary growth of metastatic colonic adenocarcinoma: a pattern of intrahepatic spread easily confused with primary neoplasia of the biliary tract. Am J Surg Pathol 1997;21: 1030–1036.[CrossRef][Medline]
  53. Okano K, Yamamoto J, Okabayashi T, et al. CT imaging of intrabiliary growth of colorectal liver metastases: a comparison of pathological findings of resected specimens. Br J Radiol 2002;75:497–501.[Abstract/Free Full Text]
  54. Wenzel DJ, Gaede JT, Wenzel LR. Case report: intrabiliary colonic metastasis mimicking primary biliary neoplasia. AJR Am J Roentgenol 2003;180: 1029–1032.[Free Full Text]
  55. Tokai H, Kawashita Y, Eguchi S, et al. A case of mucin producing liver metastases with intrabiliary extension. World J Gastroenterol 2006;12: 4918–4921.[Medline]
  56. Wagner MS, Shoup M, Pickleman J, Yong S. Primary malignant melanoma of the common bile duct: a case report and review of the literature. Arch Pathol Lab Med 2000;124:419–422.[Medline]
  57. Medina V, Darnell A, Bejarano N, Falco J, Musulen E, Martin J. Primary biliary tract malignant melanoma: US, CT, and MR findings. Abdom Imaging 2003;28:842–846.[Medline]
  58. Eliason SC, Grosso LE. Primary biliary malignant lymphoma clinically mimicking cholangiocarcinoma: a case report and review of the literature. Ann Diagn Pathol 2001;5:25–33.[CrossRef][Medline]
  59. Nguyen GK. Primary extranodal non-Hodgkin’s lymphoma of the extrahepatic bile ducts: report of a case. Cancer 1982;50:2218–2222.[Medline]
  60. Das K, Fisher A, Wilson DJ, dela Torre AN, Seguel J, Koneru B. Primary non-Hodgkin’s lymphoma of the bile ducts mimicking cholangiocarcinoma. Surgery 2003;134:496–500.[CrossRef][Medline]
  61. Rajesh G, Sadasivan S, Hiran KR, Nandakumar R, Balakrishnan V. Acute myeloid leukemia presenting as obstructive jaundice. Indian J Gastroenterol 2006;25:93–94.[Medline]
  62. Goor Y, Goor O, Michalewitcz R, Cabili S. Acute myeloid leukemia presenting as obstructive jaundice. J Clin Gastroenterol 2002;34:485–486.[CrossRef][Medline]
  63. Fleming DR, Slone SP. CML blast crisis resulting in biliary obstruction following BMT. Bone Marrow Transplant 1997;19:853–854.[CrossRef][Medline]
  64. Gonzalez-Vela MC, Val-Bernal JF, Mayorga M, Cagigal ML, Fernandez F, Mazorra F. Myeloid sarcoma of the extrahepatic bile ducts presenting as obstructive jaundice. APMIS 2006;114:666–668.[CrossRef][Medline]
  65. Kim HW, Choi SJ, Lee JH, et al. Nonleukemic granulocytic sarcoma in the bile duct: a case report. J Korean Med Sci 2006;21:745–748.[CrossRef][Medline]
  66. John BM, Song MH, Park YS, et al. A case of carcinoid tumor of the common bile duct [in Korean]. Korean J Gastroenterol 2006;47:320–323.[Medline]
  67. El Rassi ZS, Mohsine RM, Berger F, Thierry P, Partensky CC. Endocrine tumors of the extrahepatic bile ducts: pathological and clinical aspects, surgical management and outcome. Hepatogastro-enterology 2004;51:1295–1300.[Medline]
  68. Pawlik TM, Shah S, Eckhauser FE. Carcinoid tumor of the biliary tract: treating a rare cause of bile duct obstruction. Am Surg 2003;69:98–101.[Medline]
  69. Maitra A, Krueger JE, Tascilar M, et al. Carcinoid tumors of the extrahepatic bile ducts: a study of seven cases. Am J Surg Pathol 2000;24:1501–1510.[CrossRef][Medline]




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