Trypsin secretion and turnover in patients with acute pancreatitis

Abstract

Studies in humans have shown that pancreatic enzyme secretion is reduced during acute pancreatitis. It is not known, however, whether the reduction is due to impaired synthesis or disruption of the secretory pathway. The rate of secretion and turnover of trypsin was measured in 12 patients with acute pancreatitis of variable etiology and severity (median Ranson's score 2.5, range 0-5, 4 with severe necrotizing disease) and eight healthy volunteers by 4-h primed/continuous intravenous infusions of 1-(13)C-labeled l-leucine, and collection of pancreatic secretions by duodenal perfusion and sampling. Trypsin secretion was reduced from 476 +/- 73 to 153 +/- 60 U/h (means +/- SE, P = 0.005) in acute pancreatitis, with the greatest reductions being observed in patients with necrotizing disease (32 +/- 7 U/h, P = 0.003). The time for newly labeled trypsin to first appear in digestive juice was not, however, delayed in pancreatitis patients (87.2 +/- 11.1 vs. 94.7 +/- 4.9 min); on the contrary, there was an early appearance of newly labeled trypsin at 30 min in patients with severe necrotizing pancreatitis (P < 0.05). Calculated zymogen pool turnover was unchanged, but pool size was decreased (P = 0.01). Despite low rates of luminal secretion, trypsin continues to be synthesized in patients with acute pancreatitis. Our findings could be explained by post-Golgi leakage of enzymes from acinar cells or by loss of synthetic function in some cells with preservation in others.

Immediate oral feeding in patients with mild acute pancreatitis is safe and may accelerate recovery—A randomized clinical study

“…2,3 It has been shown, both experimentally and in humans, that the secretion of pancreatic juice and trypsin is reduced during acute pancreatitis. 4,5 In mild acute pancreatitis, current practice has been initial fasting until abdominal pain has resolved and levels of pancreatic and inflammatory markers have decreased. Oral refeeding has been initiated with small amounts of a diet, rich in carbohydrates and proteins and low in fat, then gradually increasing the intake during 3-7 days in order to avoid pain and pancreatitis relapse.…”

Effects of Pantoprazole in experimental acute pancreatitis

“…Pancreatic juice protein profiling has been used mainly to determine malignancy in Intraductal Papillary Mucinous Neoplasias (IPMN) (Shirai et al 2007). However, changes in pancreatic juice protein content are not specific for any pre-malignant or malignant lesion, but also observed during AP (O'Keefe et al 2005) as a leakage of proteins into the pancreatic juice, which can be also regarded as an additional marker of pancreatic tissue damage in AP (Hartwig et al 1999). We observed this phenomenon of protein leakage with a change in the spectra in SAP which may be a consequence of disturbed cellular membrane integrity.…”

Oral refeeding in mild acute pancreatitis: An old challenge

“…So, we can speculate that the basal and stimulated pancreatic enzyme secretion, in particular pancreatic secretory response to CCK, may be woken markedly early, after the onset of AP, as have been shown in experimental studies [13,14] . Evidence allows us to conclude that in human pancreatitis the injured pancreas may be less responsive to stimulation by food than previously considered [15,16] .…”