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At least 19 recordsLinked to original sources
PubMed2004

Cholangiography can discriminate sclerosing cholangitis with autoimmune pancreatitis from primary sclerosing cholangitis.

BACKGROUND: Sclerosing cholangitis with autoimmune pancreatitis has a cholangiographic appearance that is similar to that of primary sclerosing cholangitis, but only the former responds well to corticosteroid therapy. It, therefore, is necessary to distinguish between these two diseases. Cholangiography is the reference standard for the diagnosis of primary sclerosing cholangitis. The present study compared the characteristic findings for these two types of sclerosing cholangitis. METHODS: Cholangiograms from patients with primary sclerosing cholangitis (n = 29) and sclerosing cholangitis with autoimmune pancreatitis (n = 26) were studied with regard to length and region of stricture formation, and other characteristic findings. RESULTS: Band-like stricture, beaded or pruned-tree appearance, and diverticulum-like formation were significantly more frequent in primary sclerosing cholangitis. In contrast, segmental stricture, long stricture with prestenotic dilatation and stricture of the distal common bile duct were significantly more common in sclerosing cholangitis with autoimmune pancreatitis. Discriminant analysis based on these findings correctly identified 27 of 28 patients with primary sclerosing cholangitis and 25 of 26 patients with sclerosing cholangitis with autoimmune pancreatitis. It also identified a patient with an incorrect diagnosis of primary sclerosing cholangitis who proved, on review of a surgical specimen, to have findings consistent with lymphoplasmacytic sclerosing cholangitis. CONCLUSIONS: Characteristic cholangiographic features allow discrimination of sclerosing cholangitis with autoimmune pancreatitis and lymphoplasmacytic sclerosing cholangitis without pancreatitis from primary sclerosing cholangitis.

Adult↗
PubMed1994

Fibrous and obliterative cholangitis in liver allografts: evidence of recurrent primary sclerosing cholangitis?

Fibroobliterative lesions and fibrous cholangitis are characteristic histological lesions of primary sclerosing cholangitis. To determine whether such lesions can be found in the liver allograft, and whether they represent recurrent disease, we reviewed all consecutive histological material taken at greater than 6 mo after transplantation in a 3-yr period from a series of 207 liver transplantations (22 with primary sclerosing cholangitis, 185 controls without primary sclerosing cholangitis). Because patients with primary sclerosing cholangitis have a biliary system reconstructed by means of a Roux loop, we compared the findings with those from a further control group of patients who had received a Roux loop for reasons other than primary sclerosing cholangitis. Of 22 patients receiving liver transplants for primary sclerosing cholangitis, 7 (32%) patients had biopsy specimens showing features of biliary obstruction, 6 (27%) showed fibrous cholangitis, and 3 (14%) showed classic fibroobliterative lesions. These findings compared with 3 (14%), 1 (5%) and 0 of 22 Roux controls, and 19 (10%), 4 (2%) and 0 of 185 controls without primary sclerosing cholangitis, respectively. The three patients with fibroobliterative lesions either had clinical episodes of cholangitis or had microorganisms in the large bile ducts. However, both biliary obstructive features and fibrous cholangitis were more common in primary sclerosing cholangitis, and fibroobliterative lesions were found only in patients who received transplants for primary sclerosing cholangitis, despite the presence of cholangitis and Roux loops in control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Cholangitis score: a scoring system to predict severe cholangitis in gallstone pancreatitis.

BACKGROUND/PURPOSES: Emergency biliary decompression and stone extraction are mandatory for patients with gallstone pancreatitis who have ampullary stone impaction or persistent stones and pus in the bile duct (severe cholangitis). The aim of this study was to devise a simple scoring system for the prediction of complicating severe cholangitis in gallstone pancreatitis. METHODS: Clinical signs, laboratory data, and ultrasonography (US) findings at the time of admission, and the bile duct pathology at the time of bile duct exploration, were reviewed in 66 patients with gallstone pancreatitis. Variables which discriminated 26 patients with bile duct stones from 40 without were defined as predictive factors of bile duct stones. The receiver operating characteristic (ROC) curve was used to determine the optimal cutoff values of numerical variables. One point was allocated to each predictive factor, and the total score was defined as the cholangitis score (CS). Bile duct pathology identified at the time of bile duct exploration was graded into three categories: mild, moderate, and severe cholangitis. A threshold value of the CS, claimed to be predictive of severe cholangitis, was determined by using the ROC curve. RESULTS: The scoring system consisted of four predictive factors: (1) pyrexia (temperature > or =38 degrees C), (2) elevated serum bilirubin (> or =2.2 mg/dl), (3) dilated bile duct (> or =11 mm maximum diameter on US), and (4) bile duct stones detected on US. The scoring system predicted severe cholangitis with 92% sensitivity and 98% specificity in patients with scores of three or four points. CONCLUSIONS: Patients with gallstone pancreatitis who meet three or four of the above predictive factors at the time of admission are likely to have severe cholangitis, and should be rapidly treated by biliary decompression and stone extraction.

Acute Disease↗
PubMed2002

Bacterial cholangitis causing secondary sclerosing cholangitis: a case report.

BACKGROUND: Although bacterial cholangitis is frequently mentioned as a cause of secondary sclerosing cholangitis, it appears to be extremely rare, with only one documented case ever reported. CASE PRESENTATION: A 48-year-old woman presented with an episode of acute biliary pancreatitis that was complicated by pancreatic abcess formation. After 3 months she had an episode of severe pyogenic (E. Coli) cholangitis that recurred over the subsequent 7 months on a further two occasions. Initially, cholangiography suggested the presence of extra-biliary intrahepatic abcesses while repeated investigations demonstrated development of multiple segmental biliary duct strictures. After maintenance antibiotic treatment was started, no episodes of cholangitis occurred over a 14-month period. CONCLUSIONS: Sclerosing cholangitis can rapidly develop after an episode of bacterial cholangitis. Extra-biliary involvement of the hepatic parenchyma with abcess formation may be a risk factor for developing this rare but particularly severe complication.

Abdominal Abscess↗
PubMed1990

Trichosporon cholangitis associated with hyperbilirubinemia, and findings suggesting primary sclerosing cholangitis on endoscopic retrograde cholangiopancreatography.

Usually, ascending cholangitis is a bacterial process. However, in the debilitated or immunocompromised patient, mycotic cholangitis must be placed in the differential diagnosis. We report a patient with cryptogenic cirrhosis whose presenting problem in his terminal hospitalization was spontaneous bacterial peritonitis, for which he was treated with broad-spectrum antibiotics. Endoscopic retrograde cholangiopancreatogram was performed during the hospital course to explain his profound hyperbilirubinemia. The findings were grossly consistent with primary sclerosing cholangitis or cholangiocarcinoma. The patient subsequently continued to deteriorate, and died with hepatic and renal failure. At autopsy, he was found to have choledocholithiasis, marked biliary duct proliferation, and ascending cholangitis, with Trichosporon demonstrated histologically to be invading the bile ducts. To our knowledge, this is the first reported case of Trichosporon cholangitis.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1998

Recurrence of primary biliary cirrhosis, autoimmune cholangitis and primary sclerosing cholangitis after liver transplantation.

Given the usually prolonged natural history of primary biliary cirrhosis, autoimmune cholangitis, and primary sclerosing cholangitis, and the relatively recent introduction of orthotopic liver transplantation, our understanding of recurrence of these autoimmune diseases after orthotopic liver transplantation has been slow to evolve. Present data suggest that after orthotopic liver transplantation, patients with primary biliary cirrhosis will have persistence of serum antimitochondrial antibodies, develop histologic lesions suggestive of recurrent primary biliary cirrhosis with a frequency in the 8% to 16% range at 2 to 5 years after orthotopic liver transplantation, but will demonstrate little if any symptomatic disease as a consequence. Although data are extremely limited, autoimmune cholangitis patients will have a similar post-transplant course (without antimitochondrial antibodies). Recurrence of primary sclerosing cholangitis remains the most controversial, however, these patients probably develop nonanastomotic intrahepatic and extrahepatic strictures more frequently than patients without primary sclerosing cholangitis, with a frequency in the 20% to 25% range at 3 to 5 years. With longer patient follow-up and additional studies, it is hoped that our understanding of recurrent autoimmune biliary diseases will grow considerably in the future.

Autoimmune Diseases↗
PubMed2003

Long-term evaluation of a rat model of chronic cholangitis resembling human primary sclerosing cholangitis.

Primary sclerosing cholangitis (PSC) is a chronic cholestatic disorder with a presumed autoimmune aetiopathogenesis. We have recently described a novel organ-specific rat model of fibrosing cholangitis induced by intrabiliary administration of the hapten-reagent 2,4,6-trinitrobenzenesulfonic acid (TNBS) with similarities to human PSC. In the present report, we have evaluated the long-term outcome of TNBS-induced cholangitis in this model. Mild stenosis of the common bile duct of female Lewis rats (n = 18) was achieved by subtotal ligation and cholangitis induced by TNBS injection (50 mg/kg) into the dilated bile duct after a second laparotomy. After 8 and 12 months, we found no evidence of cholangitis in serum chemistry or histology or retrograde cholangiography of TNBS-treated rats. Antineutrophil cytoplasmic antibodies were positive in 75% of animals but were not predictive of liver damage. Tumour necrosis factor-alpha levels were not elevated in serum or in mononuclear spleen cell supernatants. Our findings suggest that a single initial insult is not sufficient to trigger chronic progressive inflammation. Rather, perpetuation of inflammation probably requires additional stimuli.

Alanine Transaminase↗
PubMed1998

Sarcoidosis, sclerosing cholangitis, and chronic atrophic autoimmune gastritis: a case of infiltrative sclerosing cholangitis.

We report a patient in whom sarcoidosis coexisted with sclerosing cholangitis and chronic atrophic autoimmune gastritis. There are some autoimmune diseases associated with primary sclerosing cholangitis; the difference between sarcoidosis and all other autoimmune diseases associated with primary sclerosing cholangitis is the ability of the former to damage the biliary tree. Moreover, when sarcoidosis behaves like cholestasis it can damage the biliary tree, mimicking primary sclerosing cholangitis, with high immunoglobulin M but without inflammatory bowel disease and p-ANCAs negative. We believe that it should be regarded as a single disease "infiltrative sclerosing cholangitis" because this is not a primary disease and sarcoidosis would be responsible for a beaded biliary tree.

Adult↗
PubMed1992

HLA class II genes in primary sclerosing cholangitis and chronic inflammatory bowel disease: no HLA-DRw52a association in Swedish patients with sclerosing cholangitis.

The familial predisposition to chronic inflammatory bowel disease and the increased concordance rate in monozygotic twins with Crohn's disease, suggest that genetic factors influence disease susceptibility. A 100% association with the supertypic HLA class II specificity DRw52a was recently described in white North American patients with primary sclerosing cholangitis, with or without concurrent ulcerative colitis. HLA class II alleles of the DR, DQ, and DP subregions were determined by genomic typing techniques in a large group of Swedish patients with ulcerative colitis or Crohn's disease as well as in a series of patients with primary sclerosing cholangitis. No statistically significant HLA class II association was observed in any of the investigated diseases or when the patients were subgrouped according to disease site or occurrence of extraintestinal manifestations, except an insignificant increase of the DRw17, DQw2 haplotype in patients with primary sclerosing cholangitis. The failure to confirm the well established DRw17 association in Swedish patients with sclerosing cholangitis probably represents a statistical type II error. Furthermore, this study did not verify the recently described strong DRw52a association in sclerosing cholangitis--52% of the patients were DRw52a positive compared with 28% of the controls (p less than 0.05, pc NS). This discrepancy was probably caused by different typing techniques. The DRw52a specificity was determined directly by hybridising HLA-DRB3 genes, group specifically amplified by the polymerase chain reaction, with an allele specific oligonucleotide probe, whereas in the previously mentioned study DRw52a was assigned by indirect serological criteria, which overestimate the frequency of this allele.

Blotting, Southern↗
PubMed2001

Rapid progress of acute suppurative cholangitis to secondary sclerosing cholangitis sequentially followed-up by endoscopic retrograde cholangiography.

A 66-year-old man was admitted to our hospital because of right hypochondralgia and fever after colonic polypectomy. Endoscopic examination revealed purulent bile excretion from the duodenal papilla orifice; based on this finding, acute suppurative cholangitis was diagnosed. An endoscopic retrograde cholangiography revealed no abnormality in the biliary tree. However, chronic cholestasis persisted, and endoscopic cholangiography performed 4 months later disclosed a beaded appearance of the intrahepatic bile ducts; this sign is a characteristic finding of sclerosing cholangitis. This is the first report of rapid progression of acute suppurative cholangitis to secondary sclerosing cholangitis sequentially followed-up by endoscopic retrograde cholangiography.

Acute Disease↗
PubMed2002

Regulation of organic anion transporters in a new rat model of acute and chronic cholangitis resembling human primary sclerosing cholangitis.

BACKGROUND/AIMS: Primary sclerosing cholangitis (PSC) is a cholestatic liver disease of unknown etiology. Although the primary defect affects cholangiocytes, cholestatic injury of hepatocytes may promote further liver damage. Since down-regulation of hepatocellular organic anion transporters is implicated in the molecular pathogenesis of cholestasis, expression of these transporters was determined in a novel rat model, which closely resembles human PSC. METHODS: Hepatic protein and mRNA expression of basolateral (Ntcp, Oatp1, 2 and 4) and canalicular (Mrp2, Bsep) organic anion transporters were analyzed 1, 4 and 12 weeks after induction of experimental PSC by 2,4,6-trinitrobenzenesulfonic acid (TNBS). RESULTS: Specific down-regulation of basolateral and canalicular transport systems except Oatp4 and Bsep proteins occurred during the acute phase of inflammation. In chronic cholangitis 12 weeks after TNBS Mrp2 protein and mRNA remained down-regulated by 40-50% of controls (P<0.05). In addition Oatp1 protein was also reduced by 40+/-13% (P<0.05), whereas all other transporters returned to control values. CONCLUSIONS: In chronic cholangitis only canalicular Mrp2 expression remained down-regulated. This might represent the first injury to hepatocytes in chronic cholangitis as an extension of liver injury from the level of cholangiocytes to hepatocytes in PSC.

ATP-Binding Cassette Transporters↗
PubMed2004

IgG4-related sclerosing cholangitis with and without hepatic inflammatory pseudotumor, and sclerosing pancreatitis-associated sclerosing cholangitis: do they belong to a spectrum of sclerosing pancreatitis?

Sclerosing cholangitis (SC) is a heterogeneous disease entity. Different etiologies such as choledocholithiasis, biliary tumor, or pericholangitis can manifest as SC. Hepatic inflammatory pseudotumor (IP) is rarely associated with SC (sclerosing cholangitis associated with hepatic inflammatory pseudotumor; SC-hepatic IP), but sclerosing pancreatitis (SP) is not infrequently associated with bile duct lesions (sclerosing pancreatitis-associated sclerosing cholangitis; SP-SC). In this study, we compared the histologic changes of hepatic hilar and extrahepatic bile duct lesions of SC (7 cases), SC-hepatic IP (5 cases), SP-SC (5 cases), and typical primary sclerosing cholangitis (PSC) (5 cases). Histologically, all SP-SC cases showed extensive and dense fibrosis with marked lymphoplasmacytic infiltration, many eosinophils, and obliterative phlebitis. Four cases of SC showed bile duct lesions similar to those of SP-SC, whereas other three cases of SC showed milder lymphoplasmacytic infiltration, scant eosinophilic cell infiltration, and no obliterative phlebitis. All SC-hepatic IP cases showed bile duct lesions identical to those of SP-SC. Immunohistochemically, many IgG4-positive plasma cells were found in the bile duct lesions of all SP-SC cases, 4 SC cases with marked lymphoplasmacytic infiltration, and all SC-hepatic IP cases. By contrast, IgG4-positive plasma cells were scarce or hardly found in the remaining 3 SC cases and all PSC cases. In conclusion, 4 SC cases and all SC-hepatic IP cases showed bile duct lesions identical to those of SP-SC, suggesting that these three conditions may be a single disease entity. Their pathogenesis may be similar or closely related to that of SP, and in that respect they may represent an IgG4-related biliary disease. They may respond to steroid therapy as SP does.

Adult↗
PubMed2000

Primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune cholangitis.

Primary biliary cirrhosis (PBC), and autoimmune cholangitis are presumed to be autoimmune cholestatic diseases, but the relevant antigens are unknown. Primary biliary cirrhosis is diagnosed by a positive serum mitochondrial antibody test. It usually affects women and has a very long course, culminating in liver transplantation or death. Ursodeoxycholic acid is probably the appropriate treatment. Primary sclerosing cholangitis (PSC) is marked by progressive destruction of extrahepatic and intrahepatic bile ducts. There is no specific diagnostic test or treatment. Cholangiocarcinoma is the dreaded complication and precludes liver transplantation, the only chance of a cure. Autoimmune cholangitis overlaps PBC and autoimmune chronic hepatitis. It is a rare condition, resembling PBC but with a negative serum mitochondrial antibody test; however, serum antinuclear antibodies and smooth muscle antibodies are present in high titers.

Autoimmune Diseases↗
PubMed1997

Ursodiol for primary sclerosing cholangitis. Mayo Primary Sclerosing Cholangitis-Ursodeoxycholic Acid Study Group.

BACKGROUND: There is no satisfactory medical therapy for patients with primary sclerosing cholangitis. Ursodiol (ursodeoxycholic acid) benefits patients with primary biliary cirrhosis, another cholestatic liver disease. METHODS: From May 1989 to July 1995, we enrolled 105 patients with well-documented primary sclerosing cholangitis in a randomized, double-blind study comparing ursodiol (13 to 15 mg per kilogram of body weight per day in divided doses) with placebo. The primary outcome was the time to treatment failure, defined as death; liver transplantation; histologic progression by two stages (of four) or progression to cirrhosis; the development of varices, ascites, or encephalopathy; sustained quadrupling of the serum bilirubin concentration; marked worsening of fatigue or pruritus; inability to tolerate the drug; or voluntary withdrawal from the study. RESULTS: We analyzed data on the 51 patients in each group with at least 3 months of follow-up; the median follow-up was 2.2 years. There was no significant difference between the groups in time to treatment failure (relative risk of treatment failure in the ursodiol group, 1.01; 95 percent confidence interval, 0.6 to 1.7). During the first two years of follow-up, treatment was unsuccessful in 17 of 32 patients (53 percent) in the placebo group and 16 of 31 (52 percent) in the ursodiol group. There were also no differences in time to treatment failure for patients with early-stage disease or in time to liver transplantation. Ursodiol, but not placebo, was associated with improvement in serum alkaline phosphatase, aspartate aminotransferase, bilirubin, and albumin levels at one and two years. CONCLUSIONS: In a group of patients with well-defined primary sclerosing cholangitis, ursodiol provided no clinical benefit.

Adult↗
PubMed1988

Cholangitis glandularis proliferans. A histologic variant of primary sclerosing cholangitis with distinctive clinical and pathological features.

This is the first report in the American literature of a recently described histologic variant of primary sclerosing cholangitis (PSC). Only six examples of this unique entity, called cholangitis glandularis proliferans (CGP), or proliferative cholangitis, have previously been reported. This disorder typically presents as painless jaundice but differs clinically from PSC by occurring predominantly in females and lacking an association with inflammatory bowel disease. The unique histological features are characterized by florid intramural proliferation of glandular elements in addition to an intense inflammatory component. Anatomically, the lesion is confined to the extrahepatic biliary tree, which enables its successful surgical extirpation since it does not appear to be progressive.

Adult↗
PubMed1997

Hepatic hilar inflammatory pseudotumor mimicking cholangiocarcinoma with cholangitis and phlebitis--a variant of primary sclerosing cholangitis?

Inflammatory pseudotumor (IPT) of the liver is rare. We present a case of hepatic IPT mimicking cholangiocarcinoma in which the tumor was located at the left porta hepatis. The patient was a 64-year-old man in whom abnormal liver function test results had been noted incidentally during an annual health checkup in 1993: the patient declined to go to the hospital for further examination. At the annual health checkup the following year, abnormal liver function test results were noticed again, and this time he did go to a hospital, where a hepatic mass was found. Laboratory test results were unremarkable. Based on the location of the lesion and the findings of a variety of imaging modalities, such as ultrasound and computed tomography examination, the lesion was preoperatively diagnosed as hilar cholangiocarcinoma and was surgically resected. Pathologic examination of the resected lesion, however, revealed that it was not a true tumor but an inflammatory pseudotumor with marked destructive and sclerosing cholangitis mimicking primary sclerosing cholangitis (PSC) and obliterative phlebitis. Since the location and features of the tumor in the present case are very pertinent to the relationship between IPT and PSC, we describe its clinical and histologic features and discuss the findings in relation to PSC in the context of our literature review.

Bile Duct Neoplasms↗
PubMed1991

Lymphoplasmacytic sclerosing pancreatitis with cholangitis: a variant of primary sclerosing cholangitis extensively involving pancreas.

Pancreatic involvement in primary sclerosing cholangitis (PSC) is an extremely rare condition, and its pathologic features are poorly documented. We report two cases of an unusual lymphoplasmacytic sclerosing inflammatory disease involving the total pancreas, common bile duct, gallbladder, and, in one patient, the lip. Two elderly men presented with waxing and waning obstructive jaundice, and exhibited radiologic and ultrasonographic findings highly suggestive of pancreatic carcinoma. Gross appearance of the pancreas showed firm and mass-like enlargement with regional lymph node swelling. Histologic findings were characterized by diffuse lymphoplasmacytic infiltration with marked interstitial fibrosis and acinar atrophy, obliterated phlebitis of the pancreatic veins, and involvement of the portal vein. Similar inflammatory processes involved the bile duct and the gallbladder. Lymphoplasmacytic sclerosing pancreatitis with cholangitis is thought to be a more appropriate term for this condition, of which a similar lesion has been previously noted in a single case of "PSC involving pancreas". Differences in age, radiologic appearance, and the negative history of ulcerative colitis exist, but the two cases in this study could be considered as a variant of PSC extensively involving pancreas, which can readily be mistaken for pancreatic carcinoma.

Aged↗
PubMed1996

Antimitochondrial antibody-negative chronic nonsuppurative destructive cholangitis. Atypical primary biliary cirrhosis or autoimmune cholangitis?

We investigated whether autoimmune cholangitis (AC) has specific features that constitute an entity other than primary biliary cirrhosis (PBC). We compared clinical, laboratory, and liver biopsy features; response to treatment; and the follow-up of two groups of patients. The first group comprised seven patients with AC criteria-PBC with negative antimitochondrial antibodies (AMAs) and positive antinuclear antibodies (ANAs)-termed the PBC AMA-negative group; the second was made up of another seven PBC patients with positive AMA, labeled the PBC AMA-positive group. We found that the PBC AMA-negative group had, besides negative AMAs and positive ANAs, a significantly higher incidence of asthenia, a higher and earlier incidence of liver failure, and higher ANA titers and serum immunoglobulin G levels than the PBC AMA-positive group. There were no significant differences in the other laboratory tests, although the PBC AMA-negative group showed higher serum bilirubin and aminotransferase and lower serum alkaline phosphatase and immunoglobulin M levels. Liver histological data were similar in both groups. Patients in the PBC AMA-negative group, with more markedly abnormal liver tests, responded to immunosuppressive therapy. We concluded that patients with criteria for PBC but with negative AMAs and positive ANAs have a few specific features that fall between PBC and autoimmune chronic hepatitis. This finding suggests that these patients have a different disease, for which autoimmune cholangitis seems to be an appropriate name.

Adult↗