Functional Recovery of the Exocrine Pancreas after Acute Pancreatitis

Abstract

A tubeless pancreatic function test (BTP test) using N-benzoyl-l-tyrosyl-p-aminobenzoic acid was used to assess exocrine function from urinary recovery of p-aminobenzoic acid produced by hydrolysis of the peptide by chymotrypsin. Patients with acute pancreatitis were studied at various time intervals after the acute attack and compared with controls with abdominal pain that was not pancreatic in origin. The initial BTP test carried out in the convalescent period was abnormal in all of 30 patients with acute pancreatitis but normal in 10 patients with non-pancreatic abdominal pain and also in 8 patients who had recovered from an attack of acute pancreatitis 2-6 years previously. Results were improved or normal in 12 of 15 patients re-tested 1 year after the attack of pancreatitis, but 4 out of 6 still had abnormal results 2-6 months after the attack. The data suggest that an attack of acute pancreatitis may impair exocrine pancreatic function for several months.

Exocrine pancreatic changes following acute attack of biliary pancreatitis

“…This is in agreement with results published by other authors [8,11,31], but our results differ from those reported by Bozkurt et al [15] who used Lundh's test a month after the acute episode, and included patients who had undergone a necrosectomy, without regard for etiology, and reported severe or moderate insufficiency in 26 and 74% of the patients, respectively. However, we must remember that particular criteria were used to determine severity, so that it is hard to make a comparison between these results and our own.…”

“…It is evident from a review of papers published that in some there is no assessment of severity [9], and in others radiological [31] and clinical [8,10,31] criteria or laparotomy findings [8,11,15] are used, and that it is uncommon to quantify the percentage of pancreatic necrosis [8,9,11,14,31]. It needs to be pointed out that the authors of some of the papers reviewed include cases where necrosectomy or even pancreatectomy has been performed, for example Büchler [13] and Angelini [14].…”

“…when a clinical and analytical return to normal occurs and oral feeding is resumed [6-13, 15, 27-29], but differing results are reported on recovery of the function after the acute episode. Some authors report progressive recovery of the function back to its normal level over a varying period of time [7][8][9][10][11][12]27], while others have found a persisting functional deficit [13,28,30].…”

Protective effect of a microtubule stabilizer taxol on caerulein-induced acute pancreatitis in rat.

“…This secretory blockade is seen in various experimental models of acute pancreatitis (33) and in most patients of clinical acute pancreatitis (34). For example, in a model of acute hemorrhagic pancreatitis induced by feeding young female mice a choline-deficient, ethionine-supplemented diet (35), pancreatic digestive enzyme secretion is blocked and colocalization of digestive enzyme zymogen with lysosomal hydrolases is observed as well as in caerulein-induced pancreatitis (36,37).…”

Membrane Proteome Analysis of Cerulein-Stimulated Pancreatic Acinar Cells: Implication for Early Event of Acute Pancreatitis

“…2 Pancreatic exocrine dysfunction after acute pancreatitis is observed not only in patients with gallstone pancreatitis but also in those with alcoholic and idiopathic pancreatitis. 3 These studies demonstrate that possible involvement of CCK, which affects exocrine function of pancreas, in the pathogenesis of acute pancreatitis. Pancreatitis induced by cerulein, a CCK analogue, is one of the widely used experimental models of acute pancreatitis that exhibits the biochemical, morphological, and pathophysiological similarities to various aspects of human pancreatitis.…”