The pancreas as a site of granulomatous inflammation in Crohn's disease

Gschwantler, Michael; Kogelbauer, Gabriele; Klose, Wolfgang; Bibus, B; Tscholakoff, D; Weiß, W.

doi:10.1016/0016-5085(95)90226-0

Cited by 81 publications

(41 citation statements)

References 10 publications

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“…[124][125][126][127][128] It can also occur in patients with PSC, as the bile and pancreatic ducts can be affected by the same autoimmune process resulting in ''sclerosing pancreatitis'' in association with PSC. 129 The ''idiopathic acute pancreatitis'' group may not fit into the drug-induced category or any of the above-mentioned causes.…”

Section: Acute Pancreatitismentioning

confidence: 99%

Hepatopancreatobiliary manifestations and complications associated with inflammatory bowel disease

Navaneethan¹,

Shen²

2010

Inflammatory Bowel Diseases

183

127

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Diseases involving the hepatopancreatobiliary (HPB) system are frequently encountered in patients with inflammatory bowel disease (IBD). Hepatobiliary manifestations constitute some of the most common extraintestinal manifestations of IBD. They appear to occur with similar frequency in patients with Crohn's disease or ulcerative colitis. HPB manifestations may occur in following settings: 1) disease possibly associated with a shared pathogenetic mechanism with IBD including primary sclerosing cholangitis (PSC), small-duct PSC/pericholangitis and PSC/autoimmune hepatitis overlap, acute and chronic pancreatitis related to IBD; 2) diseases which parallel structural and physiological changes seen with IBD, including cholelithiasis, portal vein thrombosis, and hepatic abscess; and 3) diseases related to adverse effects associated with treatment of IBD, including drug-induced hepatitis, pancreatitis (purine-based agents), or liver cirrhosis (methotrexate), and reactivation of hepatitis B, and biologic agent-associated hepatosplenic lymphoma. Less common HPB manifestations that have been described in association with IBD include autoimmune pancreatitis (AIP), IgG4-associated cholangitis (IAC), primary biliary cirrhosis (PBC), fatty liver, granulomatous hepatitis, and amyloidosis. PSC is the most significant hepatobiliary manifestation associated with IBD and poses substantial challenges in management requiring a multidisciplinary approach. The natural disease course of PSC may progress to cirrhosis and ultimately require liver transplantation in spite of total proctocolectomy with ileal-pouch anal anastomosis. The association between AIP, IAC, and elevated serum IgG4 in patients with PSC is intriguing. The recently reported association between IAC and IBD may open the door to investigate these complex disorders. Further studies are warranted to help understand the pathogenesis of HPB manifestations associated with IBD, which would help clinicians better manage these patients. An interdisciplinary approach, involving gastroenterologists, hepatologists, and, in advanced cases, general, colorectal, and transplant surgeons is advocated.

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Section: Acute Pancreatitismentioning

confidence: 99%

Hepatopancreatobiliary manifestations and complications associated with inflammatory bowel disease

Navaneethan¹,

Shen²

2010

Inflammatory Bowel Diseases

183

127

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“…16 In rare cases the pancreas may be affected by Crohn's disease, presenting as a mass lesion in the head of the organ. 17 In immunocompromised patients, tuberculous infection can (1) have granulomas without caseous necrosis, (2) have caseous necrosis with granulomas, (3) have only caseous necrosis without granulomas, and (4) be suppurative, with AFB positivity. 18 The cases described above belonged to group 3, with numerous AFB in the smears.…”

Section: Discussionmentioning

confidence: 99%

Cytologic Diagnosis of Pancreatic Tuberculosis in Immunocompetent and Immunocompromised Patients

et al. 2005

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“…In such cases, including other pancreatitis associated autoimmune disease, etc. [14][15][16][17][18], clinicians should be careful for the following systemic symptoms, and check several autoantibodies, LE cell test, total hemolytic complement (CH50), rheumatoid factor, Á-globulin, and/or examine biopsy [19] at an early stage in order to give appropriate treatment.…”

Section: Discussionmentioning

confidence: 99%