Abstract
Introduction: After self-expanding metal stents (SEMS) insertion for malignant biliary obstruction, occlusion cholangitis by tumor ingrowth or overgrowth is one of major problems, which leads to the delay of chemotherapy or SEMS dysfunction. However, acute cholangitis without stent occlusion also develops clinically. Pathophysiology and prognosis in patients with non-occlusion cholangitis remains unclear. The aim of this study is to evaluate the risk factors for non-occlusion cholangitis and its impact on prognosis. Methods: From April 2011 to April 2016, SEMS were inserted for the first time in 74 patients with malignant distal biliary obstruction at Kitano Hospital. Non-occlusion cholangitis was diagnosed when CT and/or endoscopic retrograde cholangiopancreatography revealed no stent occlusion in patients with fever and abnormal liver function tests. Incidence rate of non-occlusion cholangitis after SEMS insertion was evaluated based on Kaplan-Meier method, the prognoses in incidence and non-incidence groups were compared, and the different characteristics of patients between both groups were analyzed using cox regression analysis. Results: Among 74 patients who received SEMS insertion, non-occlusion cholangitis was observed in 31 patients (41.9%). The median duration between SEMS insertion and the onset of non-occlusion cholangitis was 141 days. Cumulative incidence rate at 100 and 365 days after SEMS insertion were 30.0% and 66.3%, respectively. With the passage of time after SEMS insertion, cumulative survival rate of incidence group was lower than non-incidence group, although there was no significant difference (P= 0.63) (Figure 1). In the multivariate analysis, significant risk factors for non-occlusion cholangitis were pancreatic cancer (hazard ratio [HR] 4.83, P= 0.007) and duodenal invasion (hazard ratio [HR] 2.45, P= 0.04).Figure 1Conclusion: Our data suggests that non-occlusion cholangitis occurs frequently and can impact on longterm prognosis of cancer patients. When pancreatic cancer invades duodenum, duodenal hypoperistalsis easily induces duodenobiliary reflux through SEMS. Therefore, biliary drainage preserving Oddi sphincter function, such as percutaneous and endoscopic ultrasound-guided approaches, might be better to improve long-term prognosis in patients with pancreatic cancer accompanied with duodenal invasion. In conclusion, duodenobiliary reflux by duodenoal invasion of pancreastic cancer would be major cause of non-occlusion cholangitis.
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