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In exocrine insufficiency, pancreatic enzyme supplementation can prevent malnutrition and steatorrhea-related symptoms. Although the optimal dose varies according to dietary fat content and individual patient characteristics, many patients are prescribed a fixed dose. We prospectively evaluated if patient-education on flexible dosing improves treatment efficacy in exocrine insufficiency due to chronic pancreatitis. Between August 2010 and October 2012, exocrine insufficient patients using a fixed enzyme dose of 1 to 6 capsules per day were included. In the first 4 weeks of the trial (phase I), patients continued this dose. In week 5, patients were educated in flexible dosing (depending on the fat intake and presence of steatorrhea, patients varied the amount of capsules up to a maximum of 16 per day), which was applied in the last 4 weeks of the trial (phase II). During the study, patients were treated with Panzytrat25000 containing 25,000 units of lipase. The faecal fat absorption (CFA) was measured at the end of phase I and II. The enzyme dose, steatorrhea-related symptoms, and BMI were assessed at the end of phases I and II, and after 3 and 6 months. Symptoms of steatorrhea were assessed with a scoring system, consisting of questions regarding stool frequency, consistency, stickiness, and abdominal cramps and/or flatulence. The scale ranged from 0-8, with higher scores indicating more severe symptoms. Ten patients were included (50%male; median age of 53).With flexible dosing, the median CFA improved from 87% to 90% (p value 0.23, Table 1). The mean enzyme dose increased from 3 to 10 capsules per day and steatorrhea-related symptoms improved. Both effects were significant and persistent in the longer term. BMI did not change during the first 9 weeks, but significantly improved thereafter. In exocrine insufficiency, patient-education on flexible dosing increased the daily enzyme dosage and improved treatment efficacy. Therefore, it should be routinely applied in enzyme supplementation therapy. Table 1. Treatment outcomes during the fixed and flexible treatment phases, and after 3 and 6 months follow-up

Introduction: Pancreatoduodenectomy (PD) has become a standard operation with low mortality in high-volume centers, however perioperative morbidity remains substantial, mainly due to postoperative pancreatic fistula (POPF). Development of preoperative protective measures is hampered by a lack of strictly preoperative risk stratification. Predictive power of single parameters can be enhanced by optimally weighed combination of risk factors in an artificial neuronal network (ANN). Methods: A panel of clinical and radiological parameters were assessed retrospectively from patients with pancreatoduodenectomy in our institution and risk factors analysis for the endpoint POPF (clinically relevant Grade B/C of ISGPS definition) were identified. Preoperatively available parameters were used for prediction of a high risk pancreas in an ANN. Internal validation of the thereby identified risk group was performed by testing for POPF and other relevant complications. Results A total of 471 patients with PD operated from 2001 to 2012 were included. Out of twelve clinical and radiological risk factors for POPF B/C, the most powerful was a soft pancreas. When an ANN was trained to predict a soft high-risk pancreas, correct prediction was achieved in 83% in the test group. Patients predicted to have a high-risk pancreas had a significantly higher rate of POPF and severe complications compared to the low-risk group (POPF B/C (38% vs 8%, p=0.000), intraabdominal abscess (23% vs 10%, p=0.000), severe complications (26% vs 13%, p=0.003), severe postpancreatectomy hemorrhage (18% vs 6%, p=0.012)), as well as a five-fold elevated mortality (5% vs 1%, p=0.034). Conclusion Clinical and radiological parameters combined in an ANNmodel can correctly predict a high-risk pancreas and severe complications already before the operation.

the increase was +36.8% (high dose) and +27.2% (low dose). Significant increases compared to baseline were observed in CNA (low: +5.3; high: +7.6; p

Introduction: In 1992, fibrosing colonopathy was noted in patients with cystic fibrosis (CF). High doses of pancreatic enzyme supplements were felt to be an etiologic factor. We developed an algorithm for decreasing pancreatic enzyme doses of patients who were receiving doses higher than those recommended by the CF foundation. Aims: To decrease pancreatic enzyme doses in patients with CF receiving high doses by 1) identifying the factors responsible for the presumed need for high doses, 2) identifying the successful interventions associated with the use of lower doses. Methods: We surveyed all patient charts at our CF center and determined their dose of pancreatic enzymes (lipase unitslkg/meal). All patients who were receiving more than 3000 lipase unitslkg/meal were included in the study. Charts were analyzed for reasons for excessive dosing, medications and factors responsible for decreasing enzyme dosing. A computerized program (SPSS 9.0) was used for statistical analysis. Results: Of the 176 patients followed at the CF center, 58 patients (33%) were on high doses of enzymes. Mean age at the time of intervention was 12.6 years z 4.6 SD. Prior to intervention, mean dose of enzyme supplementation was 6372 ::': 3143 SD lipase unitslkg/meal. Following intervention, the mean dose was 3414 ::': 1145 SD lipase unitslkg/meal (p less than 0.001). Dosage of enzyme was changed in 56 patients (97%). Preparation type was changed in 40 patients (69%). Interventions included change in timing of enzyme administration in 21 patients (44%), dietary changes after analysis of diet history in 30 patients (58%): addition of fiber in 6 patients (15.4%), removal of excess juice intake in 1 patient (2.1%). Dose of histamine receptor (H2) blockers were changed in 38 patients (66%); 16 were decreased, 22 increased. A stool softener was added in 17 patients (29%). Conclusions: The identification of the reason for high doses of pancreatic enzymes and the development of a systematic approach for all patients in a CF center allows for the successful intervention and the use of lower and more appropriate pancreatic enzyme replacement therapy.

In 5 human subjects, 95% pure cholecystokinin (CCK) given as a background infusion in doses of 42, 84, or 168 pmol kg-1 h-1 did not significantly alter acid secretion in response to graded doses (11-300 pmol kg-1 h-1) of synthetic human gastrin-17-I. The 168 pmol kg-1 h-1 dose of CCK produced maximal pancreatic amylase output. In 3 subjects, 337 pmol kg-1 h-1 of CCK slightly stimulated acid secretion when given alone and tended to reduce acid secretion in response to gastrin, but each of the subjects experienced cramping abdominal pain. The increment in acid secretion produced by CCK alone was similar to that produced by maximally effective doses of carboxyl-terminal octapeptide of CCK. In dogs with gastric and pancreatic fistulas, 168 pmol kg-1 h-1 of CCK produced maximal pancreatic protein output and slightly stimulated gastric acid secretion. In dogs with gastric fistulas and Heidenhain pouches, the lowest dose of CCK that inhibited gastrin-stimulated acid secretion was 674 pmol kg-1 h-1. We conclude that in man and dog 95% pure CCK weakly stimulates gastric acid secretion and inhibits gastrin-stimulated acid secretion but these actions occur only with doses of CCK that are maximal or supramaximal for pancreatic enzyme secretion. Because of the high dose requirement, these effects are unlikely to be physiologically significant.

We report a 13-mo-old patient with isolated congenital enterokinase deficiency and review the clinical features, diagnostic approach, and management of all 8 reported patients. Our patient presented with failure to thrive, diarrhea, and hypoproteinemia since birth. A normal sweat chloride with small intestinal histology, and nondetectable trypsin activity in the duodenal fluid should alert the physician to the possibility of isolated enterokinase deficiency. All reported patients, including our own, responded favorably to pancreatic enzyme replacement. In vitro studies of the small intestinal mucosal biopsy specimen suggest that enterokinase deficiency at least in part is due to altered enzymes with low enterokinase activity.

Summary Acute pancreatitis was induced by intraductal injection of bile or of trypsin into the pancreases of dogs. The histologic pattern resulting from the 2 different agents was dissimilar. In bile-induced pancreatitis the first change was a coagulation necrosis of the cells of a part of the lobule. In trypsin-induced pancreatitis, the earliest response was a marked hyperemia with vasodilation of the capillaries. Only later on did liquefaction necrosis of the cells occur. In both types, with the passage of time, secondary inflammatory changes with fatty necrosis were superimposed. Biochemically, these 2 types of pancreatitis were also different. In bile-induced pancreatitis proteolytic enzyme activity could not be recovered from the pancreatic tissue up to 1 hour after injection. In the pancreatic tissue of dogs in which pancreatitis was induced by trypsin, free proteolytic enzyme acttvity was present in the early stages of the disease. The data suggest different mechanisms for bile and for trypsin in the production of acute pancreatitis.

Summary Factors influencing mortality in experimental hemorrhagic pancreatitis were investigated. A control series showed that hemorrhagic pancreatitis produced by the bile injection technique gave 100 per cent mortality. Antibiotic therapy prevented mortality in such animals. Reduction of pancreatic enzymes by pretreatment of the animals with ethionine did not significantly reduce mortality, but did alter the course of the disease. The pancreas, removed imediately after bile injection and injected intraperitoneally, did not contain materials toxic to a normal animal. An experiment in which a section of the pancreas was placed extraperitoneally and then challenged by the bile injection technique demonstrated the importance of hypovolemic shock in the disease.

This study was designed to assess the effect of unsulfated synthetic human little gastrin (HG-17-I) on pancreatic secretion and gallbladder emptying in man. During continuous gastric and duodenal aspiration, 6 male subjects were given, on different days, either HG-17-I (7, 20, 60, 180 and 540 pmol kg-1 hr-1, cholecystokinin (0.1, 0.3, and 0.9 U kg-1 hr-1) or 238 pmol kg-1 (500 ng kg-1) of HG-17-I as a rapid intravenous injection. Trypsin output and bilirubin output increased significantly (P