Abstract:IBD presenting as AP was more frequent among the pediatric population with IBD in comparison to adults. It was more common in patients with colitis than in those with ileal disease, suggesting that patients with idiopathic AP should be observed carefully for a possible diagnosis of IBD.
“…The relationship between IBD and autoimmune pancreatitis (AIP) is mainly confined to UC[13,14]. Several studies have reported positive associations between risk for acute pancreatitis and IBD severity[15-17]. To our knowledge, however, no study has evaluated the clinical course of UC patients who develop pancreatitis according to its etiology.…”
AIMTo investigate the clinical course of ulcerative colitis (UC) patients who develop acute pancreatitis.METHODSWe analyzed 3307 UC patients from the inflammatory bowel disease registry at Asan Medical Center from June 1989 to May 2015. The clinical course of UC patients who developed acute pancreatitis was compared with that of non-pancreatitis UC patients.RESULTSAmong 51 patients who developed acute pancreatitis, 13 (0.40%) had autoimmune, 10 (0.30%) had aminosalicylate-induced, and 13 (1.73%) had thiopurine-induced pancreatitis. All 13 patients with autoimmune pancreatitis (AIP) had type 2 AIP. Two (15.4%) patients had pre-existing AIP, and three (23.1%) patients developed AIP and UC simultaneously. Compared to non-pancreatitis patients, AIP patients had UC diagnosed at a significantly younger age (median, 22.9 years vs 36.4 years; P = 0.001). AIP and aminosalicylate-induced pancreatitis patients had more extensive UC compared to non-pancreatitis patients. All patients with pancreatitis recovered uneventfully, and there were no recurrences. Biologics were used more frequently in aminosalicylate- and thiopurine-induced pancreatitis patients compared to non-pancreatitis patients [adjusted OR (95%CI), 5.16 (1.42-18.67) and 6.90 (1.83-25.98), respectively]. Biologic utilization rate was similar among AIP and non-pancreatitis patients [OR (95%CI), 0.84 (0.11-6.66)]. Colectomy rates for autoimmune, aminosalicylate-induced, and thiopurine-induced pancreatitis, and for non-pancreatitis patients were 15.4% (2/13), 20% (2/10), 15.4% (2/13), and 7.3% (239/3256), respectively; the rates were not significantly different after adjusting for baseline disease extent.CONCLUSIONPancreatitis patients show a non-significant increase in colectomy, after adjusting for baseline disease extent.
“…The relationship between IBD and autoimmune pancreatitis (AIP) is mainly confined to UC[13,14]. Several studies have reported positive associations between risk for acute pancreatitis and IBD severity[15-17]. To our knowledge, however, no study has evaluated the clinical course of UC patients who develop pancreatitis according to its etiology.…”
AIMTo investigate the clinical course of ulcerative colitis (UC) patients who develop acute pancreatitis.METHODSWe analyzed 3307 UC patients from the inflammatory bowel disease registry at Asan Medical Center from June 1989 to May 2015. The clinical course of UC patients who developed acute pancreatitis was compared with that of non-pancreatitis UC patients.RESULTSAmong 51 patients who developed acute pancreatitis, 13 (0.40%) had autoimmune, 10 (0.30%) had aminosalicylate-induced, and 13 (1.73%) had thiopurine-induced pancreatitis. All 13 patients with autoimmune pancreatitis (AIP) had type 2 AIP. Two (15.4%) patients had pre-existing AIP, and three (23.1%) patients developed AIP and UC simultaneously. Compared to non-pancreatitis patients, AIP patients had UC diagnosed at a significantly younger age (median, 22.9 years vs 36.4 years; P = 0.001). AIP and aminosalicylate-induced pancreatitis patients had more extensive UC compared to non-pancreatitis patients. All patients with pancreatitis recovered uneventfully, and there were no recurrences. Biologics were used more frequently in aminosalicylate- and thiopurine-induced pancreatitis patients compared to non-pancreatitis patients [adjusted OR (95%CI), 5.16 (1.42-18.67) and 6.90 (1.83-25.98), respectively]. Biologic utilization rate was similar among AIP and non-pancreatitis patients [OR (95%CI), 0.84 (0.11-6.66)]. Colectomy rates for autoimmune, aminosalicylate-induced, and thiopurine-induced pancreatitis, and for non-pancreatitis patients were 15.4% (2/13), 20% (2/10), 15.4% (2/13), and 7.3% (239/3256), respectively; the rates were not significantly different after adjusting for baseline disease extent.CONCLUSIONPancreatitis patients show a non-significant increase in colectomy, after adjusting for baseline disease extent.
“…11,12 Our patient's case is unique in that the diagnosis of Crohn's disease came after multiple bouts of pancreatitis, circumstances reported in only a few other cases. 8,9 To our knowledge, this is also the first reported case of pancreatic panniculitis coinciding with pancreatitis and Crohn's disease.…”
Section: Diagnosismentioning
confidence: 82%
“…Pancreatitis without an obvious cause has been diagnosed in patients with Crohn's disease, though an explanation for this relationship has yet to be identified. [4][5][6][7][8][9][10][11][12] The inflammatory process triggered in the walls of the proposed mechanism for this concurrence is that reflux of duodenal contents into the pancreatic duct activates zymogens. 7,10 Then again, as with our patient, pancreatitis also exists without duodenal involvement.…”
“…A multifactorial pathogenesis is recognized, but in some patients idiopathic forms may occur before the onset of IBD. [13] In children, idiopathic chronic pancreatitis occur ten months before the diagnosis of CD with a severe phenotype. [14] Clinical and biological surveys have shown that 20%-30% of patients with pancreatitis remain unknown or idiopathic (Table 1).…”
It is important to establish a correct diagnostic approach based on etiology and to assess the most appropriate therapeutic strategy, thus avoiding complications and improving the quality of life of children with IBD.
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