Tu1150 Laboratory Predictors of Hyperamylasemia and Hyperlipasemia After Double Balloon Enteroscopy

Abstract

Objective The causal mechanism of acute pancreatitis after oral double balloon enteroscopy (DBE) is still uncertain. The most probable cause seems to be a mechanical straining of the endoscope with an over-tube on the pancreas. Hyperamylasemia and hyperlipasemia after DBE are frequent and usually asymptomatic. They do not represent the immediate risk factor of acute pancreatitis. The aim of this prospective study was to investigate several laboratory markers to predict patients in a higher risk of hyperamylasemia and hyperlipasemia and/or possible DBE-associated acute pancreatitis. Methods A total 38 patients (18 men and 20 women, mean age 51 years) with 44 DBEs and 30 matched healthy controls with no endoscopy entered the study. Following laboratory markers were investigated before, 4 hours and 24 hours after DBE and once in controls: serum hs-CRP, prokalcitonin, total S100 protein, cathepsin B, SPINK1, lactoferrin, E-selectin, alfa-1-antitrypsin, malondialdehyde, amylase and lipase. The mean time of DBE was 80 min. (range 20 210 min.), the mean number of push-and-pull cycles was 14 (range 1 41). We have not recorded any DBEassociated acute pancreatitis in this series. Results Serum amylase and lipase rose significantly with the maximum 4 hours after DBE, with increased abnormal values in 31/44 (70%) of serum amylase and 29/44 (66%) of serum lipase (p < 0.001 and p < 0.001). Serum cathepsin and procalcitonin decreased significantly 4 hours after DBE compared to healthy controls and patients' values before DBE (p = 0.018 and p = 0.031). There was a statistically significant, but clinically irrelevant, difference in malondialdehyde between males and females 4 hours after DBE (0.33±0.20 vs. 0.20±0.13 μmol/L; p = 0.012). No other gender-associated difference was recorded. There was a trend for an association between number of push-and-pull cycles in DBE and procalcitonin (r = -0.384; p = 0.011) and urine amylase (r = 0.313; p = 0.043) 4 hours after DBE; between procalcitonin and alfa-1-antitrypsin (r = 0.358; p = 0.021), cathepsin (r = 0.362; p = 0.020) and hs-CRP (r = 0.358; p = 0.021); and between E-selectin and malondialdehyde (r = 0.364; p = 0.019) 4 hours after DBE. Either serum amylase or lipase 4 hours after DBE did not correlate with any markers before DBE. Conclusions Our current results support our previous hypothesis that endoscope-induced mechanical straining during DBE is the most important factor responsible for the increase of amylase and lipase or even for progression to acute pancreatitis. We found no laboratory predictive markers that would identify in advance those patients in a higher risk. This study was supported by the research grant MH CZ NT11524-5/2010 and by the programme PRVOUK 37-08.