The article is devoted to the evaluation of methods for the prevention of post-manipulation pancreatitis based on the analysis of hyperamylasemia in patients with acute biliary pancreatitis, who underwent transpapillary interventions.Aim of the study. To assess the impact of a new method of preventing post-manipulation complications on the rate of regression of hyperamylasemia in acute biliary pancreatitis.Materials and methods. In 2015-2021, 70 patients with proven acute biliary pancreatitis who underwent transpapillary interventions were included. Men -16 (23%), women 54 (77%). In 56 patients (Group 1), complications were prevented after the intervention by submucosal infi ltration of a 0.5% lidocaine/novocaine solution, 10 ml. 14 patients (Group 2) used the new technique in the prevention of complications (priority certifi cate No. 2021137430 dated 12/16/2021). The level of amylasemia was monitored 6-8 hours after papillotomy, then daily until normalization. In 10 patients of the 2nd group, stenting with a plastic stent was also used.Results. The time for regression of hyperamylasemia to 100 units/l between groups 1 and 2 was 6.8±1.9 days versus 4.5±2.3 and diff ered signifi cantly. Without a stent, the level of amylasemia in the 2nd group returned to normal within 2 days, with the use of a stent -within 4 days, without statistical diff erences. Evaluation of the rate of regression of reactive hyperamylasemia in patients with normal amylase levels at the time of endoscopic intervention revealed a reduction in the duration of the period of hyperamylasemia when using double PBB. Comparison of the rate of regression of hyperamylasemia in acute biliary pancreatitis with conventional PBB with changes in reactive hyperamylasemia after EPT without PBB showed a similar picture.
Conclusions.1. A new technique for the prevention of post-manipulation complications is promising and requires additional evaluation. 2. PBB after the intervention does not signifi cantly aff ect the rate of regression of hyperamylasemia. 3. Stenting of the pancreatic duct in acute biliary pancreatitis tends to prolong the duration of hyperamylasemia.