Pancreatic involvement in Salmonella infection.

CONTEXT: Salmonella has been identified as a causative agent of acute pancreatitis. OBJECTIVE: We prospectively evaluated the frequency of acute pancreatitis, pancreatic enzyme elevation and morphological pancreatic abnormalities in patients with Salmonella infection. SUBJECTS: Thirty consecutive patients with salmonellosis (Salmonella enterica serovar Enteritidis: n=25; Salmonella enterica serovar Typhimurium: n=5) and 30 sex- and age-matched healthy subjects were studied. MAIN OUTCOME MEASURES: All subjects underwent serum amylase and lipase determination and ultrasonography. RESULTS: None of the subjects developed acute pancreatitis. Two patients (6.7%) and two controls showed serum amylase activity above the upper reference limit whereas, in five patients (16.7%) and one control subject (3.3%), the serum lipase activity appeared above the upper reference limit. Salmonella infection significantly increased serum activity of lipase (P<0.001) while it did not significantly affect serum amylase levels (P=0.204). Serum lipase activity was significantly higher in patients infected by Salmonella enterica serovar Typhimurium than in those infected by Salmonella enterica serovar Enteritidis (P=0.012). Ultrasonography did not show pancreatic abnormalities in any of the subjects. CONCLUSIONS: Our data demonstrated an elevation of serum lipase activity in gastroenteritis due to Salmonella infection, but this elevation does not seem to have clinical significance. The elevation of serum lipase seems to be particularly related to infection from Salmonella enterica serovar Typhimurium.

Mutations of the CFTR gene in pancreatic disease.

INTRODUCTION: An association has been found between CFTR gene mutations and chronic pancreatitis; however, there is a lack of information about the frequency of CFTR gene mutations in acute pancreatitis and in pancreatic cancer. AIM: To prospectively evaluate the prevalence of CFTR gene mutations in acute pancreatitis, chronic pancreatitis, and pancreatic cancer. METHODOLOGY: Ninety-eight consecutive patients were studied and divided into 3 groups: 34 patients with acute pancreatitis, 46 patients with chronic pancreatitis, and 18 patients with pancreatic cancer. The mutation analysis of the CFTR gene was carried out using diagnostic commercial kits for the simultaneous detection of 29 mutations and Tn polymorphism. RESULTS: Among the 98 patients studied, 12 (12.2%) had CFTR gene mutations: 2 of the 34 patients (5.9%) with acute pancreatitis, 9 of the 46 (19.6%) with chronic pancreatitis, and 1 of the 18 (5.6%) with pancreatic cancer. All the mutations were found in heterozygosis (2 DeltaF508, 1 W1282X, and 9 T5 allele). CONCLUSION: Our prospective study adds further information about the frequency of CFTR mutations in patients with a single episode of acute pancreatitis. Furthermore, our results suggest an association of CFTR gene mutations with chronic alcoholic pancreatitis and emphasize the need for a multicenter study, possibly multinational, to conclusively establish the role of CFTR mutations as a genetic susceptibility factor for this disease.

Early activation of peripheral lymphocytes in human acute pancreatitis.

BACKGROUND: The CD69 antigen is an indicator of early lymphocyte activation. GOALS: To evaluate the early activation of peripheral lymphocytes T, B, and NK in patients with acute pancreatitis in comparison with patients with acute abdomen of nonpancreatic origin. STUDY: Thirty patients with acute pancreatitis were studied; 20 of them had the mild form of the disease and 10 had the severe form. Thirty patients with nonpancreatic acute abdomen were used as controls. All patients were enrolled within 48 hours of the onset of pain. In all patients, leukocytes and total lymphocyte and lymphocyte subset counts (CD4+, CD8+, CD56+, CD19+, CD4+CD69+, CD8+CD69+, CD56+CD69+, CD19+CD69+) were determined upon hospital admission. RESULTS: The percentage of total lymphocytes was significantly lower in acute pancreatitis patients than in those with nonpancreatic acute abdomen (P = 0.014); patients with severe pancreatitis had a percentage of total lymphocytes significantly lower when compared with patients with mild pancreatitis (P < 0.001). The CD19+CD69+ count was significantly lower in patients with severe pancreatitis (24.6 +/- 14.6%) than in patients with mild pancreatitis (46.7 +/- 16.5%; = 0.006). The counts of the other lymphocyte subsets were not statistically different between patients with acute pancreatitis and those with nonpancreatic acute abdomen, as well as between patients with mild and severe acute pancreatitis. CONCLUSIONS: Patients with severe pancreatitis show impaired early activation of peripheral CD19+ cells.

Mechanisms involved in the onset of post-ERCP pancreatitis.

In various prospective studies, the frequency of post-ERCP pancreatitis ranges from 1 to 14%. After exposure to trigger events, injury to the gland occurs extremely rapidly. In experimental models of acute pancreatitis, it has been suggested that digestive enzyme activation might occur within acinar cells and it has been shown that in the early stages of acute pancreatitis induced by secretagogues or by diet, there is a co-localization of digestive enzymes and lysosomal hydrolases within large cytoplasm vacuoles; this co-localization mechanism might result in activation of the digestive enzyme. In this article, we will review the trigger events which may determine the final effect of acute pancreatitis during ERCP and endoscopic sphincterotomy: mechanical, chemical, enzymatic and microbiological. Nonetheless, factors related to the patient and the physician will be considered. Finally, the hypothesis of activation of chemokines by endoscopic maneuvers as a cause of acute pancreatitis will be described.

Pancreatic involvement during the early phase of shock.

BACKGROUND: There is a lack of data concerning pancreatic involvement during shock. AIM: To evaluate possible pancreatic alterations in the early phase of shock. SETTING: Twelve consecutive patients with shock were studied within 2 hours from the onset of illness. Seven patients died during the hospital stay: 3 within 4 hours from admission, 3 within 4-8 hours and 1 within 12 hours. MAIN OUTCOME MEASURES: Amylase, lipase, C-reactive protein, amyloid A, interleukin 6, procalcitonin and vascular cell adhesion molecule-1 serum concentrations were determined on admission and 4, 8, and 12 hours afterward. All patients underwent imaging studies of the pancreas. RESULTS: None of the patients developed clinical signs or morphological alterations compatible with acute pancreatitis. Serum amylase levels were above the upper reference limit in 7 patients (58.3%) and serum lipase levels in 2 patients (16.7%; P=0.062). There were no significant differences found between survivors and non-survivors in the serum concentrations of all the proteins studied. CONCLUSIONS: In patients with shock, amylase seems to be more frequently elevated than lipase. None of the patients showed pancreatic alterations at imaging techniques.