Post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common serious adverse event, and the average incidence in a prospective series of patients has been reported to be 1.3–7.6%. The development of PEP depends on patient- and procedure-related factors, and even on the endoscopic techniques/maneuvers. In the previous meta-analyses, various factors including suspected sphincter of Oddi dysfunction, female sex, history of acute pancreatitis, precut sphincterotomy, and pancreatic injection were predicted to be the risk factors for PEP. It is essential to identify which variables definitely contribute to this adverse event, so that unnecessary diagnostic endoscopic retrograde cholangiopancreatography (ERCP) can be avoided or other endoscopic or pharmacological preventive measures can be considered.
Although the mechanisms are not clear, PEP is considered to occur due to an inflammatory cascade triggered by injury to the acinar cells, that leads to the systemic release of cytokines by various chemical, enzymatic, microbiologic, mechanical, hydrostatic, or thermal processes. Among these, pancreatic fat is gaining attention as the likely risk factor for acute pancreatitis. Recent studies reported that pancreatic fat adjacent to the acinar cells is associated with tissue damage in acute pancreatitis, by a direct toxic effect on the pancreatic parenchyma. Furthermore, hypertriglyceridemia-induced pancreatitis generally has poor clinical outcomes compared to that induced by other etiologies. These results suggest that the triglycerides are released from adipocytes, and the pancreatic triglyceride lipase as well as trypsin, apart from its traditional known role in acinar injury, could also play a role in adipocyte injury.
In the previous study on fatty pancreas, fatty pancreas tended to be associated with recurrent acute pancreatitis. Unfortunately, however, the study failed to demonstrate statistical significance, and visually measured pancreatic fat based on endoscopic ultrasonography (EUS) findings, which may have a concern about interobserver variations. Until now, there is still a lack of sufficient evidence between fatty pancreas and the development of PEP. In our study, therefore, we evaluated the presence of fatty pancreas using abdominal computed tomography (CT) scan, which can provide quantitative and reliable information. Thereafter, we identified the potential risk factors for the development of PEP, including fatty pancreas.

Cohort/Group Label

All patients who underwent computerized tomography (CT) for an accurate diagnosis of benign or malignant pancreatic biliary tract disease, followed by continuous endoscopic retrograde cholangiopancrea

Cohort/Group Description

Fatty change in the pancreas was prospectively evaluated from unenhanced image of the abdominal CT scan. Pancreatic attenuation was measured in three nontumorous pancreatic parenchyma (pancreatic head, body, and tail) and spleen, respectively, with areas of 1.0 cm2 in three different sections. The contrast-enhanced CT images were also reviewed simultaneously with the unenhanced images to identify the pathologic parenchymal lesion, pancreatic duct, and vascular structures. Consequently, pathologic parenchymal lesions such as tumors or vascular structures were excluded from the measurement. In addition, the investigator was careful not to include the peripheral margin of the pancreas to avoid the artifact of the partial volume effect. When the margins of the pancreas were not precisely delineated with adjacent peri-pancreatic fat, we measured pancreatic attenuation as close to the splenic vein as possible and containing as much of the pancreatic parenchyma as possible. We also measured splenic attenuation on unenhanced CT images by averaging the measurements in Housfield units (HU) from three 1.0 cm2 regions in different parts of the spleen for the reference. A threshold of <36 HU of average pancreatic attenuation was considered fatty pancreas. The investigator, who measured pancreatic attenuation, kept the blinding for clinical outcomes including the development of PEP.

Not collect nor Archive

All patients who underwent computerized tomography (CT) for an accurate diagnosis of benign or malignant pancreatic biliary tract disease, followed by continuous endoscopic retrograde cholangiopancreatography for therapeutic purposes

To calculate the sample size, we referred to our unpublished data (IRB no.2020-08-007) that calculated the proportion of fatty pancreas based on CT evaluation. In the study, the percentage (%) of fatty pancreas based on CT evaluation was 46.4% (215/463) while the percentage (%) of non-fatty pancreas was 54.6% (248/463). Furthermore, we reported that the percentage (%) of PEP in fatty pancreas group was 7.9% (17/215) while the percentage (%) of PEP in non-fatty pancreas group was 2.4% (6/248). Thus, to achieve a power of at least 0.80 and detect 5.5% of an absolute difference between the two groups with an alpha level of 0.05, the number of samples required for chi-square test was 500 patients as total cohort including 267 patients in fatty pancreas group and 233 patients in non-fatty pancreas group. Assuming a 5% dropout rate, the final sample size was set at 527 as total cohort including 282 patients in fatty pancreas group and 245 patients in non-fatty pancreas group.

Gender

Age

Description

1. All patients who underwent computerized tomography (CT) for an accurate diagnosis of benign or malignant pancreatic biliary tract disease, followed by continuous endoscopic retrograde cholangiopancreatography for therapeutic purposes
2. Age of 19 or more years old

1. Patients diagnosed with acute pancreatitis within 2 weeks before endoscopic retrograde cholangiopancreatography
2. Patients diagnosed with chronic pancreatitis
3. Patients with a very low probability of developing pancreatitis after endoscopic retrograde cholangiopancreatography because the papilla has already been opened after endoscopic retrograde cholangiopancreatography

Risk of intra-pancreatic localization of pancreatitis after endoscopic retrograde cholangiopancreatography

Until 24 hours after index intervention

Other risk factors affecting pancreatitis after endoscopic retrograde cholangiopancreatography

Until 5 weeks after index intervention

Other risk factors affecting pancreatitis after endoscopic retrograde cholangiopancreatography

Until 5 weeks after index intervention

Pancreatic average attenuation and the risk of pancreatitis and ROC analysis

Until 5 weeks after index intervention

All other adverse events

Until 7 days after index intervention