UNLABELLED: Nowadays endoscopic sphincterotomy (SE) is considered to be a "gold standard" in the treatment of residual choledocholithiasis and biliary pancreatitis. Nevertheless patients after invasive procedures concerning bile ducts with destruction of Oddi's sphincter often have increased succeptibility to chronic infections of bile ducts. AIM: Assessment of the influence of SE on bacterial colonization, development of main bile duct chronic inflammation and recurrent choledocholithiasis. MATERIAL AND METHODS: We included to the study 50 patients with main bile duct lithiasis, who underwent endoscopic cholangiopancreatography (ERCP). Among them there were 32 women in age from 45 to 87 (mean 69.7 +/- 12.3) and 18 men in age from 39 to 84 (mean 59.8 +/- 11.56). The studied group was divided into 3 subgroups: In I (control) group were included 10 patients diagnosed with ERCP techniques because of jaundice of unknown origin. Those patients did't have ERCP or operative revision of bile ducts before, but all of them underwent cholecystectomy in the past. Each II and III group consisted of 20 patients, who underwent SE before 12-24 and 25-36 months earlier respectively. Sterile uodenoscope was inserted to the region of major duodenal papilla, and then a sterile brush was used to collect material to cytological smear (brushing) from main bile duct. In all groups 2 ml of bile were taken by a catheter to a syringe. On the basis of radiograms from ERCP findings, the width of main bile duct was assessed. In all patients blood cell count, aspartate and alanine aminotransferases, gammaglutamyltranspeptidase, alkaline phosphatase, amylase, bilirubin, C-reactive protein and procalcitonine levels were measured. RESULTS: In our study all 40 patients with previously performed endoscopic sphincterotomy (SE) had bacterial colonization in bile ducts, mostly with Gramm negative pathogens. The most virulent pathogens vere cultured from bile duct swabs from patients after two or more revisions of common bile duct, and after a longer time from sphincterotomy. Those patients had multibacterial bile duct infections (Escherichia coli + Pseudomonas aeruginosa; P. aeruginosa + Enterococcus faecalis; E. faecalis + Enterobacter cloacae + Candida albicans; P. aeruginosa + E. cloacae). E. coil and E. faecalis were most frequently cultured (20 and 16 cases respectively). It was observed that with length of time from endoscopic sphincterotomy, the width of main bile duct and also amount of cultured pathogens and their virulency grow. Elevated transaminases activity and serum procalcitonine levels were observed in studied groups. 9 patients after previous sphincterotomy had recurrent lithiasis. CONCLUSIONS: Sphincterotomy contributes to colonization of main bile duct with pathogenic bacteria. With length of time from endoscopic sphincterotomy, and amount of performed endoscopic sphincterotomies the amount of cultured pathogens, their virulency and drug resistance grow. Chronic infection of bile ducts after endoscopic sphincterotomy causes higher risk of recurrent lithiasis.
UNLABELLED: Nowadays endoscopic sphincterotomy (SE) is considered to be a "gold standard" in the treatment of residual choledocholithiasis and biliary pancreatitis. Nevertheless patients after invasive procedures concerning bile ducts with destruction of Oddi's sphincter often have increased succeptibility to chronic infections of bile ducts. AIM: Assessment of the influence of SE on bacterial colonization, development of main bile duct chronic inflammation and recurrent choledocholithiasis. MATERIAL AND METHODS: We included to the study 50 patients with main bile duct lithiasis, who underwent endoscopic cholangiopancreatography (ERCP). Among them there were 32 women in age from 45 to 87 (mean 69.7 +/- 12.3) and 18 men in age from 39 to 84 (mean 59.8 +/- 11.56). The studied group was divided into 3 subgroups: In I (control) group were included 10 patients diagnosed with ERCP techniques because of jaundice of unknown origin. Those patients did't have ERCP or operative revision of bile ducts before, but all of them underwent cholecystectomy in the past. Each II and III group consisted of 20 patients, who underwent SE before 12-24 and 25-36 months earlier respectively. Sterile uodenoscope was inserted to the region of major duodenal papilla, and then a sterile brush was used to collect material to cytological smear (brushing) from main bile duct. In all groups 2 ml of bile were taken by a catheter to a syringe. On the basis of radiograms from ERCP findings, the width of main bile duct was assessed. In all patients blood cell count, aspartate and alanine aminotransferases, gammaglutamyltranspeptidase, alkaline phosphatase, amylase, bilirubin, C-reactive protein and procalcitonine levels were measured. RESULTS: In our study all 40 patients with previously performed endoscopic sphincterotomy (SE) had bacterial colonization in bile ducts, mostly with Gramm negative pathogens. The most virulent pathogens vere cultured from bile duct swabs from patients after two or more revisions of common bile duct, and after a longer time from sphincterotomy. Those patients had multibacterial bile duct infections (Escherichia coli + Pseudomonas aeruginosa; P. aeruginosa + Enterococcus faecalis; E. faecalis + Enterobacter cloacae + Candida albicans; P. aeruginosa + E. cloacae). E. coil and E. faecalis were most frequently cultured (20 and 16 cases respectively). It was observed that with length of time from endoscopic sphincterotomy, the width of main bile duct and also amount of cultured pathogens and their virulency grow. Elevated transaminases activity and serum procalcitonine levels were observed in studied groups. 9 patients after previous sphincterotomy had recurrent lithiasis. CONCLUSIONS: Sphincterotomy contributes to colonization of main bile duct with pathogenic bacteria. With length of time from endoscopic sphincterotomy, and amount of performed endoscopic sphincterotomies the amount of cultured pathogens, their virulency and drug resistance grow. Chronic infection of bile ducts after endoscopic sphincterotomy causes higher risk of recurrent lithiasis.