ObjectiveTo investigate the etiology of pediatric pancreatitis and the effect of endoscopic retrograde cholangiopancreatography (ERCP) in it. MethodsPatients hospitalized for pancreatitis in West China Hospital of Sichuan University from Jan. 2008 to Jun. 2023 were included according to the inclusion and exclusion criteria. Totally, 241 cases (207 cases with acute pancreatitis and 34 with chronic pancreatitis) were included. Patients were divided into primary group (n=168) and recurrent group (n=73) according to their previous medical history. ResultsThe duration of hospitalization in the primary group was longer than that in the recurrent group [10.0 (7.0, 16.0) d vs. 7.5 (6.0, 11.8) d, P=0.012]. The proportion of acute pancreatitis in primary group (163/168, 97.0%) was higher than that in the recurrent group (44/73, 60.3%), P<0.001. There was no significant difference in the etiological component ratio between the primary and recurrent groups (χ2=7.504, P=0.347). However, in the primary group, the first etiology was biliary factors (38/163, 23.3%), and the second was biliary pancreatic anatomic abnormality (22/163, 13.5%). In the recurrence group, biliary pancreatic anatomic abnormality (13/44, 29.5%) was the first cause, and biliary factor (7/44, 15.9%) was the second cause. Among 207 cases with acute pancreatitis, there were 114 cases (55.1%) with clear etiology, including 45 cases (21.7%) of biliary factors, 35 cases (16.9%) of abnormal biliary pancreatic structure, 12 cases (5.8%) of traumatic factors, and 10 cases (4.8%) of drug-induced factors. In this study, 66 cases were treated with ERCP for pancreatitis, and a total of 103 ERCP operations were performed with cannulation success rate of 100%. Twenty-three cases (23/37, 62.2%) of acute pancreatitis resulted from biliary and biliary pancreatic structure abnormalities received ERCP. In biliary acute pancreatitis, the removal rate of choledocholithiasis in single ERCP operation was 80.0% (8/10). The clinical symptoms (abdominal pain, jaundice, and fever) of all cases were significantly improved after surgery, and no complications such as cholangitis, bleeding and perforation occurred. ConclusionsBiliary, congenital pancreatic anatomical abnormalities, drugs and trauma are the common causes of acute pancreatitis in children. ERCP is a safe and effective treatment for children with biliary pancreatitis, pancreatic anatomical abnormalities, and chronic pancreatitis.
ObjectiveTo investigate the effects of generic interleukin (IL)-17A gene knockout (IL-17AKO) on pancreatic and intestinal barrier on acute pancreatitis (AP) in mice. MethodsIL-17AKO mice and their wild type (WT) littermates were employed to induce AP using cerulein (CER) and sodium taurocholate (NaTC). In the CER-AP experiment, mice were randomly divided into three groups: WT control group, WT model group, and IL-17AKO model group (n=5). Mice in the model group were intraperitoneally injected with CER [50 μg/(kg·h), 7 injections], and control group received intraperitoneal injection the same amount of 0.9% NaCl. The mice were sacrificed at 12 hours after the first injection of CER. The levels of serum amylase, lipase and IL-6 were detected, and the pancreas was stained with hematoxylin-eosin (HE). In the NaTC-AP experiment, WT mice were randomly divided into sham group (n=3) and operation model group (n=6). Similarly, IL-17AKO mice were also randomly allocated to sham group (n=3) and operation model group (n=6). The mice in the sham group underwent a surgical procedure on the abdomen only, whereas in the model group, 50 μL 3.5% NaTC dissolved in saline solution was pumped into the pancreatobiliary duct. Serum amylase, lipase, and IL-6 levels were detected. Pancreas was stained with HE, and intestine was stained with Alcian blue-periodic acid-Schiff, Dolichos Biflorus Agglutinin and bacteria fluorescence in situ hybridization. ResultsIn the CER-AP experiment, there were no significant differences in serum amylase, lipase, IL-6, and pathological changes including edema, inflammation, necrosis, and total pathological score of the pancreas between IL-17AKO and WT mice (P>0.05). In the NaTC-AP experiment, compared to the WT model group, IL-17AKO did not significantly impact serum amylase, lipase, and pancreatic pathological changes (P>0.05). However, it did lead to an increased level of IL-6 (P<0.05), and showed no significant protective effect on intestinal injury in NaTC-AP. Compared to WT mice of sham group, IL-17AKO mice of sham group exhibited decreased expressions of glycosylated mucin in ileum and colon, disordered mucus layer structure, and increased bacterial invasion. ConclusionsIL-17AKO has no significant protective effect on pancreatic and intestinal barrier damage in AP mice. Furthermore, it was discovered that prior to modeling, IL-17AKO mice exhibited higher bacterial invasion, intestinal barrier disruption, and a systemic inflammatory response. These findings imply that IL-17A plays a crucial role in immune responses and the maintenance of physiological intestinal barrier function in mice.