Cholangiocarcinoma and pancreatic cancer are the most common causes of malignant biliary obstruction. The majority of patients are diagnosed at a late stage when surgical resection is rarely possible. In these cases, palliative chemotherapy and radiotherapy provide only limited benefit and are associated with poor survival. Radiofrequency ablation (RFA) is a procedure for locoregional control of tumours, whereby a high-frequency alternating current turned into thermal energy causes coagulative necrosis of the tissue surrounding the catheter. The subsequent release of debris and tumour antigens by necrotic cells can stimulate local and systemic immunity. The development of endoluminal RFA catheters has led to the emergence of endoscopically delivered RFA, a treatment mainly used for malignant biliary strictures to prolong survival and/or stent patency. Other indications include recanalisation of occluded biliary stents and treatment of intraductal ampullary adenoma or benign biliary strictures. This article presents a comprehensive review of endobiliary RFA, mainly focusing on its use in patients with malignant biliary obstruction. The available data suggest that biliary RFA may be a promising modality, having positive impacts on survival and stent patency and boasting a reasonable safety profile. However, further studies with better characterised and stratified patient populations are needed before the method becomes accepted within routine clinical practice.

Radiofrequency ablation (RFA) is a mini-invasive loco-regional ablation technique that is increasingly being used as a palliative treatment for pancreatic cancer and cholangiocarcinoma. Ablation-triggered immune system stimulation has been proposed as a mechanism behind the systemic effects of RFA. The aim of our study was to investigate the immune response to endoluminal biliary RFA. Peripheral blood samples were collected from patients with pancreatic cancer and cholangiocarcinoma randomised to receive endoluminal biliary radiofrequency ablation + stent (19 patients) or stent only (21 patients). We observed an early increase in IL-6 levels and a delayed increase in CXCL1, CXCL5, and CXCL11 levels as well as an increase in CD8+ and NK cells. However, these changes were not specific to RFA treatment. Explicitly in response to RFA, we observed a delayed increase in serum CXCL1 levels and an early decrease in the number of anti-inflammatory CD206+ blood monocytes. Our study provides the first evidence of endoluminal biliary RFA-based regulation of the systemic immune response in patients with pancreatic cancer and cholangiocarcinoma. These changes were characterised by a general inflammatory response. RFA-specific activation of the adaptive immune system was not confirmed.

Background Acute pancreatitis (AP) is a relatively rare but serious complication that can occur after organ transplantation. Material/Methods The aim of this study was to evaluate the incidence, potential risk factors, and course of AP in patients following liver transplantation at a single large-volume transplant center. Results Out of a total of 1850 transplanted patients, 49 (2.8%) were diagnosed with AP. Of this group, 37 (75.5%) had a mild form of AP and 12 (24.5%) had a severe form of AP. The mortality rate was 10% overall and 42% in the group of patients with severe AP. An early form of AP (<30 days from transplantation) occurred in 13 patients (26.5%), most of whom presented with severe AP (10 patients, 76.9%); 4 patients died (40%). A late form of AP was diagnosed in 36 patients (73.5%), most of whom had mild AP (34 patients, 94.4%); 1 of 2 patients with severe AP died. The most common AP etiologies were post-ERCP (38.8%), idiopathic (34.7%), and postoperative (18.4%). Chronic HBV infection was a risk factor for development of AP ( P =0.01). Conclusions AP in liver transplant recipients was more frequent and more severe than in the general population. This unfavorable course was associated with the occurrence of AP in the early post-transplant period. Liver transplantation due to complications of HBV infection was a risk factor for the development of AP.

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