Tag Archives: primary sclerosing cholangitis

Liver Disease Associated with Inflammatory Bowel Disease

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A useful review on the hepatobiliary manifestations of inflammatory bowel disease (IBD): Inflamm Bowel Dis 2014; 1655-67.

A few topics/comments from review:

Primary sclerosing cholangitis (PSC):

  • “among those with PSC, about 70% to 80% have UC and 15% to 20% have CD.  Those IBD patients with PSC are more likely to develop malignant complications and to require liver transplantation. Conversely, only about 0.4% to 7.5% of patients with IBD will develop PSC.”
  • “Currently, no medical treatment has been proven to decrease the progression of PSC.”
  • “At the time of diagnosis of PSC, IBD must be ruled out and a complete colonoscopy with multiple segmental biopsies of the mucosa needs to be performed.”  Among PSC-IBD patients, “annual surveillance colonoscopy is recommended.”
  • Further surveillance recommendations (eg. annual imaging/CA 19-9 annually) discussed in Table 2.

Cholelithiasis: Gallstones are reported in 13% to 24% of all patients with CD.  In UC, the risk of cholelithiasis “does not seem to be increased.”

Drug-induced liver disease: (see liver tox website)

  • Thiopurines
  • Methotrexate
  • Sulfasalazine/mesalamine
  • Biologic agents

Viral hepatitis in immunosuppressed IBD patients:

Hepatitis B reactivation -algorithm for screening/management of latent hepatitis B provided in Figure 3

Other liver problems seen in IBD patients:

  • Portal Vein Thrombosis
  • Nonalcoholic Fatty Liver Disease
  • Secondary amyloidosis
  • Hepatic abscess

Related blog posts:

Link to NASPGHAN Lectures and Postgraduate Course

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Later this week, our national pediatric GI meeting (North American Society for Pediatric Gastroenterology Hepatology and Nutrition) is starting in Atlanta.  Many in my group are involved and presenting.

The following link (with permission from NASPGHAN) is to the website with links to all of these lectures:

NASPGHAN 2014 Atlanta meeting

For those interested only in the Syllabus for the Postgraduate Course:  NASPGHAN 2014 Postgraduate Course.

Topics include in this 200 page (online) book: primary sclerosing cholangitis, jaundiced infant, acute liver failure, “dreaded” endoscopy wake up calls, endoscopy for biliary tract disease, extraesophageal manifestations of gastroesophageal reflux, constipation, eosinophilic esophagitis, motility disorders, FODMAPs diet, nutrition for neurologically impaired, early onset inflammatory bowel disease, “luminitis” due to non-IBD causes, new IBD treatments, and diet-microbiome.

Should be great!

Also, to plan your meeting -go to NASPGHAN home page and use mobile guidebook: NASPGHAN 2014 has gone mobile using Guidebook!

Understanding Cholestatic Pruritus

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A recent review (Hepatology 2014; 60: 399-407) sorts out “facts and fiction” with regard to pruritus in cholestasis.

The authors note that for more than 2000 years there has been a search for the potential pruritogen in cholestasis, “when Aretaeus the Cappadocian (2nd century B.C.) stated that ‘pruritus in jaundiced patients is caused by prickly bilious particles.'”

Key points of review:

Pruritus affects a large number of hepatobiliary diseases

  • Hepatocellular cholestasis: intrahepatic cholestasis of pregnancy (ICP), benign recurrent intrahepatic cholestasis (BRIC), progressive familial intrahepatic cholestasis (PFIC1, PFIC2), Hepatitis C
  • Biliary-liver diseases: primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), PFIC3, Alagille, Drug-induced diseases
  • Obstructive cholestasis: gallstones, IgG4-associated cholangitis, biliary atresia, and other causes

Most recently lysophosphatidic acid LPA) and autotaxin (ATX) have been shown to be important pruritogen candidates in cholestasis

  • “ATX is the main source of circulating LPA levels…In cholestasis, serum ATX activity, but not other putative markers of itch such as serum bile salt levels or serum μ-opiod activity, were correlated with itch intensity.”
  • “Rifampicin was found to reduce ATX expression at the transcriptional level.”  This may explain rifampicin’s efficacy for pruritus in cholestasis.
  • “When the enterohepatic circulation is interrupted by nasobiliary drainage, circulating levels of ATX rapidly dropped concomitant with relief of pruritus.”  So, while ATX is not secreted into bile, other substances in bile, like steroid hormones, like play a role in the induction of ATX.

Current therapeutic recommendations (dosing recommendations provided by authors in Table 3)

  • 1st line: Cholestyramine (except in ICP in which ursodeoxycholic acid is considered 1st line)
  • 2nd line: Rifampicin
  • 3rd line: naltrexone
  • 4th line: sertraline
  • Experimental: ondansetron, phenobarbitol, propranolol, lidocaine, dronabinol, butorphanol, phototherapy, nasobiliary drainage, plasmapharesis (and similar treatments), biliary diversion
  • Liver transplantation

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Withdrawing Immunosuppression with Autoimmune Hepatitis

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A recent retrospective study indicates that withdrawal of immunosuppression in autoimmune hepatitis (AIH) can be successful in carefully selected children (J Pediatr 2014; 164: 714-19).

A cohort of 56 children with AIH were followed for a median of 5.6 years and with a median age of 11 years (62% female).  Demographics noted that cirrhosis was present in 14%, primary sclerosing cholangitis 21%, and AIH type II in 9%.

Key findings:

  • Biochemical remission with immunosuppression was achieved in 76% of all patients at a median of 1.2 years; 23% of these patients experienced a subsequent relapse.
  • Withdrawal of immunosuppression was successful in 14 of 16 of patients with type 1 AIH who had been treated for a median of 2.0 years after diagnosis.
  • When the authors excluded patients with inflammatory bowel disease, they noted that the probability of achieving a sustained immunosuppression-free remission was 42% at 5 years.  Sustained remission was defined as biochemical remission for >1 year, liver biopsy without inflammation, and no relapses.
  • Patients less likely to reach a biochemical remission with immunosuppression included patients with cirrhosis, elevated INR, positive ANCA titer, and patients with coexisting autoimmune disorder.

In their discussion, the authors note that treatment withdrawal is “generally considered more successful after at least 3 years of therapy,” though only 50% of their patients who had therapy withdrawn had been treated that long.  In addition, they state that while coexisting immune disorders often result in more frequent relapses, the one exception in the literature is celiac disease when patients adhere to a strict gluten-free diet.  They also urge all patients diagnosed with AIH to undergo testing for celiac disease and thyroid disease.

Limitations of the study include the following: small numbers of patients, single center (Utah), retrospective design, and cholangiography was not performed uniformly.

Take-home message: In patients doing well with AIH for 2-3 years & with normalized liver histology, it may be possible to withdraw immunosuppression.

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) and specific medical management interventions should be confirmed by prescribing physician.  Application of the information in a particular situation remains the professional responsibility of the practitioner.

 

Population-Based Outcomes for Primary Sclerosing Cholangitis

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A study from the Netherlands examined the outcomes for Primary Sclerosing Cholangitis (PSC) (Hepatology 2013; 2045-55). Using four independent hospital databases with 44 hospitals, allowed the investigators to identify 590 PSC patients from a population of almost 8 million. Median followup was 92 months. Mean age at diagnosis was 38.9 years.  A second comparison cohort of 450 patients was identified from three Dutch transplantation centers outside the study area.  134 (30%) of this cohort were present in the population-based cohort.  An IBD comparison group of 722 cases was identified as well from a population of 271,000 patients.

Results:

  • Prevalence: 6 per 100,000.  This is significantly lower than previous estimates.  The authors emphasize the problem with previous epidemiology studies and the need for population-based studies with rigorous case-finding.
  • Survival, estimated at 21.3 years for the entire cohort following diagnosis, was better than previous studies and this may indicate less selection bias than tertiary referral center studies.  It could also reflect diagnosis of milder cases with newer imaging techniques.
  • 402 (68%) of PSC patients were diagnosed with inflammatory bowel disease.
  • 23 (4%) had autoimmune hepatitis overlap.
  • Colorectal cancer was 10-fold increased compared to ulcerative colitis controls and developed at a younger age (39 years compared with 59 years).
  • Cholangiocarcinoma (CCA) was nearly 400-fold increased risk.  The cumulative risk of CCA was estimated at 20% after 30 years following PSC diagnosis.
  • During followup, there were 97 deaths; 73 (75%) were PSC-related.

Related blog posts:

PSC 2013 Review

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A recent review of PSC was published (Gastroenterology 2013; 145: 521-36).  This review is a little more detailed than a previous review noted in this blog less than 6 months ago (Staying current with PSC | gutsandgrowth).

A couple of useful comments from the review:

  • “An increased serum level of alkaline phosphatase is the most common biochemical abnormality detected in patients with PSC.  In some cases, it is the only biochemical alteration observed, such as in patients with intrahepatic involvement.”
  • “Typically, a liver biopsy is not required to diagnose PSC unless small duct PSC is suspected or if there are concerns that a patient also has AIH.”  Cholangiography is the best way to identify PSC.
  • “Patients diagnosed with PSC should undergo colonoscopy… to determine if they have IBD, even when there are no symptoms.”
  • Autoimmune hepatitis-PSC overlap is thought to occur in ≤6% of cases.  AIH-PSC should be suspected if there are biochemical features of AIH (positive serology, increased transaminases), histology suggestive of AIH, or in AIH patients that become refractory to treatment.
  • No controlled trials have identified effective medical treatments.  Studied medications have included corticosteroids, etanercept, tacrolimus, cyclosporine, azathioprine, methotrexate, infliximab, and ursodeoxycholic acid.  The latter may increase disease progression, particularly at higher doses.

Also noted:

Hepatology 2013; 58: 1392-1400. “Primary Sclerosing Cholangitis, Autoimmune Hepatitis, and Overlap in Utah Children: Epidemiology and Natural History”

In this study the authors identified 607 cases of IBD, 29 cases of PSC, 12 cases of ASC (overlap), and 44 cases of AIH.  “Cholangiocarcinoma developed in 2 of the 29 PSC patients (6.9%).  PSC occurred in 9.9% of patients with ulcerative colitis (UC) and 0.6% of patients with Crohn’s disease.”

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Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) and specific medical management interventions should be confirmed by prescribing physician.  Application of the information in a particular situation remains the professional responsibility of the practitioner.

Staying current with PSC

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A recent article provides a useful review for primary sclerosing cholangitis (PSC) (Clin Gastroenterol Hepatol 2013; 11: 898-907).

This blog has previously discussed PSC (links below); however, the above reference is succinct and covers the key issues.  A couple of points that I found particularly helpful:

Cancer surveillance:

  • Cholangiocarcinoma (CCA): recommends “consider annual imaging (MRCP or Ultrasound) along with serum CA19-9 levels” to monitor for cholangiocarcinoma.  If there is a dominant stricture, proceed with ERCP with brushings. In pediatrics, the age to start screening is less clear, usually not presenting until beyond the late teen years, though CCA has been diagnosed in one case report at 14 years of age (NEJM 2003; 348: 1464).
  • Gallbladder cancer (30-40-fold higher risk than general population): If gallbladder polyp identified that is ≥0.8 cm, recommends cholecystectomy.  If smaller, may also want to remove if normal synthetic function; otherwise repeat imaging in 3-6 months.
  • Colon cancer: colonoscopy every 1-2 years in those with coexistent IBD (70% of patients with PSC have IBD).

Diagnosis: 44-56% of patients are asymptomatic at time of diagnosis, picked up due to abnormal serum liver tests or on cross-sectional imaging.

Small-duct PSC: occurs in the setting of features of PSC (histology, biochemistry) without abnormal cholangiogram.  This represents 11-17% of PSC patients and is difficult to identify in patients without IBD. Over time, 25% will develop large-duct PSC. Small-duct PSC does not appear to result in increased risk of CCA.

Overlap syndrome with autoimmune hepatitis: patients with typical PSC but with 5- to 10-fold aminotransferase elevations should be suspected of having an overlap syndrome and may benefit from treatments directed at autoimmune hepatitis.  Other features often include histology with an interface hepatitis and the presence of auto-antibodies. This situation is more common in children and young adults.

Immunoglobulin G4-Related sclerosing cholangitis: this occurs most commonly in conjunction with autoimmune pancreatitis.  Since steroids can be effective, IgG4 levels should “be tested in all patients with suspected PSC, and, if elevated to consider an evaluation for IgG4-related disease.”

Medical management: “to date, there are no medical therapies that have been proven to alter the natural course of PSC.”  The discussion notes that standard doses of ursodeoxycholic acid (UDCA) may have protective effects against colorectal cancer in patients with coexisting IBD.  Higher doses of UDCA have been associated with a 2-fold risk of increased disease progression. Specific treatments for dominant strictures, pruritus, metabolic bone disease, and malabsorption are discussed.  In patients with cholestasis, monitoring fat-soluble vitamins is important.

Related blog posts:

What is the risk of colon cancer in IBD?

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Some recent studies have shown that colorectal cancer complicating IBD may not be as common as previously thought or may be decreasing in incidence (Gastroenterology 2012; 143: 375-81 & Gastroenterology 2012; 143: 382-89 ).

The first study used a nationwide cohort of 47,374 Danish patients with IBD over a 30-year period.  During a 178 million person-years of follow-up evaluation, 268 patients with ulcerative colitis (UC) and 70 patients with Crohn’s disease (CD) developed colorectal cancer (CRC).  The risk was comparable to the general population (RR 1.07)!  Furthermore, the relative risk for CRC decreased over sequential time periods: 1.34  (1979-88) to 0.57 (1999-2008).

Increased risk:

  • UC diagnosed in childhood or adolescence
  • longer disease duration
  • patients with primary sclerosing cholangitis

Their conclusion, ‘the overall risk of CRC in patients with UC has decreased markedly over time and no longer exceeds that of the general population, at least in the first decade after diagnosis.”  And, based on their data, patients with Crohn’s disease are not at increased risk for CRC.

The second study from California used a large Kaiser Permanente database from 1998-June 2010.  29 cancers were identified in CD (n=5603) and 53 in UC (n=10,895) patients.  The incidence per 100,000 for CRC was 75 for CD, 76 for UC, and 47 for general population.

These authors conclude that there is an increased risk of CRC in a community-based IBD population between 1998-2010 despite advances in medical treatment.

To understand the discrepancy of these reports, the same issue provides an editorial (page 288).  My take is that the current incidence of CRC is lower than in previous reports but that the risk factors identified in the Danish cohort (see above) likely remain important.

Additional references:

  • -Gastroenterol 2009; 136: 718. 22% of cancers occurred before recommended surveillance in adults (only 9% if exclusion of patients who had IBD and cancers diagnosed at same time).
  • Colon Cancer Survival Calculator http://www.mayoclinic.com/calcs-Gastro 2010; 138: 207-2177 (entire issue)
  • -JAMA 2009; 302: 649. Aspirin use likely increases survival after dx of colon cancer. Commentary-Gastro 2010;138: 2012.
  • -NEJM 2009; 361: 2449. molecular basis of colorectal cancer
  • -Gut 2008; 57: 1246. IBD and colon cancer
  • -IBD 2007; 4: 367. 5ASA Rx did not reduce rate of cancer in large study of UC/CD -review of 18,000 colorectal cancer cases. IBD increased risk of CRC 6-7-fold..
  • -Clin Gastro & Hep 2006; 4: 1346. aminosalicylates reduce CRC.
  • -Gastroenterol 2006; 130: 1030, 1039, 1350. 600 patients followed for 35 yrs: CRC by colitis duration: 2.5% @ 20yrs, 7.6% @ 30yrs, 10.8% @ 40yrs. 5 year survival was 73% among those with cancer. 2nd study showed main CRC risk in UC pts is among those with extensive colitis.
  • -Clin Gastro & Hepatol 2004; 2: 1088. Lower cancer risk in this cohort, n=1460. CRC 0.4 @10yrs, 1.1% @ 20yrs, 2.1% @ 30yrs. Lower CRC may be due to more surgery in Rx failures & use of 5-ASA.
  • -Clinical perspectives in Gastro 1999; 2: 9 & 25. (review) surveillance/ overview take 4 bx q10cm. start p 8yrs in pancolitis & 15yrs for left-sided dz. Cancer risk: ~5% at 20yrs + 1%/yr p 20yrs in pancolitis.
  • -Gastroenterol 2003; 125: 1311. Advancement of dysplasia to cancer in UC.

Colonic disease and PSC

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While primary sclerosing cholangitis (PSC) has been associated with inflammatory bowel disease, and ulcerative colitis (UC) in particular, the pathogenesis of this relationship has not been established.  A fascinating observation on this relationship is that an inflamed colon is important in PSC development (Clin Gastroenterol Hepatol 2012; 10: 439-41).

In this study which reviewed 2754 Irish patients with IBD, 59 (2.2%) had PSC.  PSC incidence correlated with increasing colonic involvement.  Among the 13 patients with Crohn’s disease, none had isolated small bowel disease.  The second part of the study involved a review of 82 separate PSC patients attending the Irish National liver transplant unit.  The majority of ulcerative colitis patients had a pancolitis; all 10 PSC patients with Crohn’s disease had colonic involvement.

Since PSC occurs without IBD, colonic inflammation is not necessary for PSC development.  However, in patients with IBD, colonic inflammation is very important.  In fact, in a previous study of 53 PSC-IBD patients, no UC patient status post a colectomy had recurrent liver disease following liver transplantation whereas seven patients with intact colons had recurrent disease following liver transplantation.

The authors speculate that bacterial translocation along with subsequent portal bacteremia may be an important step in pathogenesis among these patients.

Additional references/previous posts:

Challenges with primary sclerosing cholangitis

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Although primary sclerosing cholangitis (PSC) is an infrequent liver problem in pediatrics, it remains important.  PSC accounts for 2-3% of pediatric liver transplant cases.  A recent report updates some of the challenges for pediatric hepatologists (Shneider BL. Liver Transplantation 2012: 18: 277-81).

First the article examines some of the salient differences between children and adults.  The approach in adults may not apply well to children.  Some inherited diseases and immunologic defects may produce a similar clinical picture.   Specific differences include the following:

  • Defects in the adenosine triphosphate-binding cassette B4 (ABCB4 gene) (multidrug resistance protein 3) may cause a number of small-duct PSC in children
  • Cystic fibrosis can have a similar appearance
  • Overlap syndrome with autoimmune hepatitis is more common in children
  • Children with PSC often have higher alanine aminotransferase enzyme values than adults
  • Cholangiocarcinoma is rare in childhood, with 17 being the youngest reported case

Diagnosis usually requires, in addition to blood tests, cholangiography (eg MRCP), liver biopsy or both.  ERCP may not be needed depending on MRCP results.

Management: Pruritus may be managed with ursodeoxycholic acid (UDCA), bile acid binding resins, and rifampin.  Bone disease needs to be monitored along with fat soluble vitamin status.

  • While pruritus may improve with UDCA, high-dose UDCA (28-30mg/kg/day) has been associated with increased likelihood of negative endpoints.  It is not clear whether there may be detrimental effects at lower doses.
  • What about immunosuppression?  This (corticosteroids/thiopurines) is accepted in cases with AIH overlap.  Of course, what constitutes overlap is not certain.  So, in many cases, a trial of corticosteroids is considered.
  • Antibiotics?  Oral vancomycin has been tried in a small number with preliminary success.

As noted above, liver transplantation is a needed treatment in some cases. One concern with this approach has been recurrent PSC in about 10% at an average of 18 months after liver transplantation.

Additional references:

  • -Am J Gastro 2011; 106: 1638.  Use of high dose Urso increases risk of colonic neoplasia. n=150.
  • -Hepatology 2011; 54: 1842.  Guidelines on surveillance for PSC.  IF IBD yearly scope.  **Yearly U/S + CA 19-9 or yearly MRI.
  • -Liver Transplantation 201; 17: 925-933.  n=79 pediatric pts.  49% w IBD prior to OLT (46% w UC, 3%) & 9.8% developed IBD p OLT.  1 & 5yr survival for OLT 99% & 87%.  Recurrence in 9.8%.
  • -Clin Gastro & Hepatology 2011; 9: 434.  37% of PSC pts with CA 19-9 >129U/mL do NOT have cholangiocarcinoma.  n=7.
  • -Hepatology 2010; 51: 660-678.  update on dx/mgt.
  • -Gastroenterology 2010; 138: 1102.  genome associations with PSC.
  • -Hepatology 2009; 50: 808, 671 (ed).  Use of urso ~30/kg associated w WORSE outcome @5yrs. n=76 (& 74 controls)
  • -Clin Gastro & Hep 2009; 7:239. n=47 children w PSC.  59% w IBD, 25% w overlap syndrome
  • -JPGN 2008; 47: 61.  Use of oral vancomycin, 50mg/kg/day in patients with PSC/IBD was effective. n=14.
  • -Liver Tx 2008; 14: 735.  Review.  5 yr OLT survival 85%  ReTx rate higher (9.6% vs 4.9%).
  • -Hepatology 2008; 47: 9494-57.  Asymptomatic PSC common in AIH –might be higher than 10%.
  • -Gastroenterology 2008; 134: 975.  Natural hx/o small duct PSC in 83 pts (compared to controls).  Not likely increase in cholangiocarcinoma unless also large duct involvement.
  • -Gastroenterology 2008; 134: 706.  IAC is similar; IAC=IGG4 Associated Cholangitis
  • -Hepatology 2008; 47: 949.  8/79 w AIH also had PSC.
  • -J Pediatr 2007; 151: 255, 230.  association of CFTR mutations in PSC (26%); also present in disease control group with IBD (43%).
  • -Clin Gastro & Hep 2007; 5: 32.  Review vis-a-vis possible cholangiocarcinoma.
  • -Hepatology 2006; 44: 1063.  Review along w secondary causes.
  • -Liver Transplantation 2006; 12: 1813.  Recurrence post Tx 22% AIH, 18% PBC, 11% PSC.  (Review of 43 studies).
  • -Gastroenterology 2005; 129:1464.  High-dose actigall ineffective in 5 yr randomized controlled study.
  • -Gastroenterology 2003; 125: 1364.  Incidence of PSC.
  • -JPGN 2003; 37: 345 (57A). Use of vanco 50/kg/day x 4-6weeks in PSC, n=10, (56A) some pts c normal cholangiograms.
  • -Gastroenterology 2003; 124: 889. Urso prevents colon ca.
  • -Am J Gastro 2001; 96: 1558-62.  High dose UDCA, 25-30/kg/day may help long-term outlook
  • -JPGN 2001; 33:296. PSC-IBD.
  • -NEJM 2002; 346: 271-277.  case c Crohn’s.  PSC assoc c UC, celiac dz, pancreatic insufficiency.
  • -Ann Intern Med 2001; 134: 89-95.  Urso decreases colonic neoplasia in pts c UC & PSC.
    -NEJM 1997; 336: 691. Ursodeoxycolic acid & PSC.
  • -Gregorio et al. Autoimmune hepatitis/sclerosing cholangitis overlap syndrome in childhood: a 16-year prospective study. Hepatology 2001;33:544-553

NASPGHAN 2010 Pointers:
I. -“STOPSC criteria”: 2 of 3 diagnostic criteria needed:
1) elev GGT or alk phos
2) intra and/or extrahepatic bile duct irregularities on cholangiography (i.e. PTC, MRCP, ERCP) c/w PSC
3) liver biopsy abnormalities c/w chronic biliary injury

AND no evidence of a secondary cause of sclerosing cholangitis

 

II. SUMMARY OF KEY CLINICAL FEATURES:

 

  • -Sclerosing cholangitis  is associated with IBD, autoimmune and connective tissue disorders, abnormalities of immune function (i.e. immunodeficiencies, GvHD), infiltrative disorders (i.e. Langerhans cell histiocytosis, lymphoma).
  • -PSC may sometimes affect only small intrahepatic bile duct (“small duct PSC”), which may have a better outcome based on adult studies
  • -PSC may have overlapping features of AIH  (“autoimmune sclerosing cholangitis”)
  • -IgG4 –associated cholangitis: patients appear to have PSC with elev IgG4.  They seem to respond very well to steroid therapy in adult studies
  • -No therapy of proven benefit for PSC (ursodiol, antibiotics), some case series have suggested antibiotics may help PSC
  • -5 times higher rate of Colorectal Ca when UC pt has PSC.  Consider yearly endoscopy