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Pancreatic reaction after endoscopic papillosphincterotomy (EPT) is a common event occurring in about 70% of cases. Acute pancreatitis may also develop in 1%-6% of cases. Previous attempts to prevent this reaction with an inhibitor of exocrine pancreatic secretion such as somatostatin provided conflicting results. The somatostatin long-acting analogue octreotide has recently proposed for the prevention of ERCP/EPT-induced pancreatic reaction. Therefore we tested the prophylactic effect of a subcutaneous administration of octreotide in two different dosages in 60 consecutive patients undergoing EPT for common bile duct stones and benign papillary stenosis. They were given either octreotide 0.2 mg (20 cases), or octreotide 0.1 mg (20 cases), or placebo (20 cases) before the procedure. Serum amylase levels were determined at baseline and 2, 4, 8 and 24 hours thereafter. The differences were statistically significant at 2 hours between subjects pretreated with octreotide 0.2 mg and control subjects (p = 0.01); at 4 and 8 hours after the procedure between both octreotide-treated groups and control subjects (octreotide 0.1 mg: p0.05, at 4 and 8 hrs; octreotide 0.2 mg: p = 0.01, at 4 hrs, and p0.01, at 8 hrs). In patients with previous episodes of relapsing pancreatitis, the increase in serum amylase was significantly reduced in the octreotide 0.2 mg group vs control group, at 4 hrs (p0.05) and 8 hrs (p0.05). Our data suggest that octreotide 0.2 mg has a greater prophylactic efficacy than 0.1 mg in reducing pancreatic reaction after EPT.

Endoscopic papillosphincterotomy (EPT) has become a well-established therapeutic procedure in the management of common bile duct stones; however, in difficult cases with large stones or anatomic conditions limiting the amplitude of the sphincteric section, the procedure may fail. In these cases, the association with extracorporeal shock-wave lithotripsy (ESWL) has proved to be helpful. Twenty out of 21 patients in whom the endoscopic approach failed because of the presence of large stones in the biliary tree (15 cases) or anatomic conditions (5 cases) underwent ESWL treatment. Stone fragmentation was achieved in 18 of the 20 treated patients (90%), with spontaneous clearing of the fragments in 10 patients after ESWL sessions and in another 2 patients within three months. In 6 cases the residual fragments were extracted by means of endoscopy. The combined procedures were therefore successful in all the 18 cases in which stone fragmentation was obtained. Complications occurred in two cases after ESWL treatment (asymptomatic pancreatic reaction and severe bleeding from the papillary area). Clinical, ultrasound and biochemical evaluations at 6 and 12 months documented a normal condition in all but two treated subjects.

The interdigestive antro-duodenal motor activity was studied in 12 dyspeptic patients without gastritis (group A), 12 dyspeptic patients with chronic superficial antral gastritis (group B) and 8 healthy controls (group C) by manometric recording of phases of the interdigestive motility cycle (IDMC) prolonged over 240 minutes. A significantly lower incidence of migrating motor complexes (MMCs) starting from the antrum was observed in dyspeptic patients with gastritis vs dyspeptic patients without gastritis (p = 0.02) and in these latter vs controls (p0.01). Likewise, the overall number of MMCs was smaller in patients with gastritis vs controls (p = 0.02). Symptomatic evaluation was performed in the two groups of dyspeptic patients, without detecting any differences in frequency and severity of individual and overall complaints. Our results confirm the role of interdigestive antral motor abnormalities in the genesis of dyspeptic syndrome and suggest that the presence of associated chronic superficial gastritis may correlate with a further motor impairment.

Kallikrein is a protease involved in the inflammatory process causing acute pancreatitis. Attempts to prevent this process with antiprotease agents have been successful in experimental animal models but disappointing in humans. We studied 40 consecutive patients undergoing endoscopic papillosphincterotomy. This procedure can induce a transient, moderate pancreatic inflammatory reaction, characterized by hyperamylasemia, which in 1-6% of the patients may evolve to acute pancreatitis. To assess the capacity of C1 inhibitor, the main physiological inhibitor of kallikrein, to prevent such complications, we pretreated 20 patients with 3000 U of C1 inhibitor plasma concentrate i.v.; 20 patients served as controls. Serum levels of amylase and functional C1 inhibitor were determined before the procedure and after 2, 4, 8 and 24 hours. Serum levels of amylase in the control group (146 +/- 21 IU) and in the group treated with C1 inhibitor (158 +/- 25 IU) were similar before treatment. Four and 8 hours after the end of the procedure, amylase levels were significantly lower (p0.001) in the treated group (231 +/- 46 and 355 +/- 104 IU) than in the control subjects (969 +/- 229 and 923 +/- 207 IU). After 24 hours both groups had normal amylase levels. In treated patients, functional levels of C1 inhibitor increased from 104 +/- 30 to 175 +/- 30% and remained elevated throughout the observation period. These data indicate that C1 inhibitor plasma concentrate can prevent hyperamylasemia following pancreas injury, probably, by inhibiting the kallikrein-mediated inflammatory process. C1 inhibitor might benefit patients at high risk of pancreatitis who undergo endoscopic papillosphincterotomy.