Association between Inflammatory Bowel Disease and Pancreatitis: A PRISMA-Compliant Systematic Review

Background/Objectives. This systematic review was conducted to investigate the association between pancreatitis and IBD. Methods. MEDLINE, Embase, and CENTRAL were systematically searched for correlative studies till 2 November 2019. RevMan5.3 was used to estimate relevance. Results. Three studies with 166008 participants were included. The risk of pancreatitis significantly increased in the patients with CD (OR, 3.40; 95% CI, 2.70-4.28; P<0.00001) and UC (OR, 2.49; 95% CI, 1.91-3.26; P<0.00001). Increased risks of CD (OR, 12.90; 95% CI, 5.15-32.50; P<0.00001) and UC (OR, 2.80; 95% CI, 1.00-7.86; P=0.05) were found in patients with chronic pancreatitis. As for patients with acute pancreatitis, there were significant association of CD (OR, 3.70; 95% CI, 1.90-7.60; P=0.0002), but were not UC. Conclusions. The evidence confirmed an association between pancreatitis and IBD. When pancreatitis patients have chronic diarrhea and mucus blood stool or IBD patients have repeated abdominal pain and weight loss, they should consult pancreatic and gastrointestinal specialists

Kui Jie Tong Ameliorates Ulcerative Colitis by Regulating Gut Microbiota and NLRP3/Caspase-1 Classical Pyroptosis Signaling Pathway

Ulcerative colitis (UC) is one of the most refractory digestive diseases in the world. Kui jie tong (KJT) is an effective traditional Chinese medicine used clinically to treat UC. This study observed the regulatory effects of KJT on NIMA-related kinase 7- (NEK7-) activated nod-like receptor protein-3 (NLRP3)/caspase-1 classical pyroptosis pathway and intestinal flora in UC model rats. KJT components were analyzed using an ultraperformance liquid chromatography-tandem mass spectrometer (UPLC-MS/MS). A UC Sprague Dawley (SD) rat model was established using sodium dextran sulfate (DSS). Rats were randomly divided into four groups: control group (CG), UC model group (UG), KJT group (KG), and sulfasalazine (SASP) group (SG). After seven days of intervention, each group’s body weight, disease activity index (DAI) scores, and colon length were recorded. Intestinal mucosal injury to each group was observed using hematoxylin-eosin staining. Additionally, we investigated the expression levels of NEK7, NLRP3, ASC, caspase-1, and GSDMD in intestinal mucosa, as well as serum interleukin- (IL-) 1β, IL-18, and IL-33 proinflammatory factors. Intestinal microflora was analyzed using 16s rRNA sequencing. KJT controlled weight loss; decreased DAI scores; restored colon length; improved pathological injury in the colon; inhibited NEK7, NLRP3, ASC, caspase-1, cleaved-caspase-1, GSDMD, and GSDMD-N expression; and decreased IL-1β, IL-18, and IL-33 contents in UG rats’ serum and colon tissue (P <0.001 or P <0.05). KJT also increased Ruminococcaceae, unclassified_f_Ruminococcaceae, and unclassified_g_Ruminococcus_1 levels and decreased Erysipelotrichia, Erysipelotrichales, Erysipelotrichaceae, Turicibacter, and uncultured_bacterium_g_Turicibacter levels. KJT alleviated UC immune-inflammatory responses to NLRP3/caspase-1 by inhibiting the NEK-7-activated classic pyroptosis pathway and improving intestinal microflora