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Raffaele Pezzilli

Publications and source records attributed to Raffaele Pezzilli.

At least 55 records · Page 3Linked to original sources

Immune-manipulation of the inflammatory response in acute pancreatitis. What can be expected?

Severe acute pancreatitis still has a high mortality rate and multiple organ failure is considered to be a severe complication of the disease. Activated polymorphonuclear leukocytes have an important role in the development of multiple organ failure which may result from acute pancreatitis and they are an important pathogenetic factor in the severity of this disease. Therefore, a logical therapeutic approach is to limit the organ damage by selective suppression of inflammatory mediators involved in the systemic inflammatory response syndrome and protect against systemic complication. In this paper, we review the recent literature data on the possible manipulation of the immune response in acute pancreatitis.

Acute 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.

Abdomen, Acute↗

Anesthesiological risk and endoscopic sphincterotomy in acute biliary pancreatitis.

INTRODUCTION: The rate of complications after endoscopic sphincterotomy (ES) is about 10%, and early complications have been reported in 20% of patients considered unfit for surgery. AIM: To evaluate the early and long-term results of endoscopic intervention in relation to the anesthesiological risk for 87 patients with acute biliary pancreatitis. METHODOLOGY: All patients underwent endoscopic retrograde cholangiopancreatography (ERCP) and were evaluated according to the American Society of Anesthesiology (ASA) criteria immediately before the operative procedure. Patients' ASA scores were as follows: 49.4%, ASA 2; 29.9%, ASA 3; and 20.7%, ASA 4. RESULTS: The severity of acute pancreatitis was positively related to the anesthesiological grade (p = 0.014). Six patients (6.9%) had complications related to the endoscopic procedure. There was no significant relationship between the frequency of biliopancreatic complications during the follow-up (23/84, 27.4%) and the ASA grade. The frequency of cholecystectomy was inversely related to the ASA grade (p = 0.003). Seven patients (8.3%) died during the follow-up period: multivariate analysis showed that the ASA grade (odds ratio [OR], 10.9; 95% confidence interval [CI], 1.2-96.6; p = 0.001) and age (OR, 1.1; 95% CI, 1.0-1.3; p = 0.037) were significantly related to survival. CONCLUSIONS: Endoscopic treatment is safe and effective in patients at high anesthesiological risk with acute pancreatitis, and survival is significantly related to the ASA grade.

Acute Disease↗

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.

Acute Disease↗

Effect of secretin on serum pancreatic enzymes and on the Wirsung duct in chronic nonpathological pancreatic hyperenzymemia.

AIM: Chronic nonpathological pancreatic hyperenzymemia (CNPH) is a new syndrome characterized by an increase in serum pancreatic enzymes in the absence of pancreatic disease. The aim of this study was to increase our understanding of this condition by determining the serum pancreatic enzyme response as well as changes in the caliber of the Wirsung duct after secretin stimulation. METHODS: Twenty subjects with CNPH and 9 healthy subjects without CNPH were studied. Blood samples were drawn 5 and 0 min before and 5, 10, 15, 30, 45, and 60 min after intravenous injection of secretin (1 U/kg). Amylase, pancreatic isoamylase, and lipase concentrations were determined. The caliber of the Wirsung duct was measured by ultrasonography. RESULTS: The injection of secretin caused a marked and statistically significant (p < 0.05) increase in serum pancreatic enzymes in the subjects with CNPH that persisted for the duration of the study. The increase over the basal value was in the range of 1.2- to 1.6-fold for amylase, 1.4- to 2.1-fold for pancreatic isoamylase, and 2.6- to 4.2-fold for lipase. In the control subjects the increase was mild, but statistically significant (p < 0.05), ranging from 1.1- to 1.2-fold for amylase, 1.2- to 1.4-fold for pancreatic isoamylase, and 1.5- to 2.2-fold for lipase. The injection of secretin caused a slight increase in the diameter of the Wirsung duct in both groups of subjects, but this was statistically significant only during the first 30 min of the study. CONCLUSIONS: The serum pancreatic enzyme response to secretin was more marked in CNPH than in controls. The Wirsung duct showed no alterations after secretin injection that would help to explain the hyperenzymemia.

Adult↗

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.

Acute Disease↗

An update on recurrent acute pancreatitis: data from five European countries.

OBJECTIVE: A great number of studies have been published on acute pancreatitis, but few have focused on the recurrent form. In this study, we have sought to determine the relative frequency and mortality of recurrent acute pancreatitis, and also to update our knowledge of its etiological factors. METHODS: Patients were selected from a total of 1068 persons included in a previous European study of acute pancreatitis. All were admitted to a hospital with an attack of acute pancreatitis between January, 1990 and December, 1994. Data for each patient was recorded on a standardized form. RESULTS: Of the 1068 with acute pancreatitis, 288 (27%) had recurrent pancreatitis; the majority (78.8%) were men, with a mean age of 43 yr (range 16-95 yr). Regarding etiology, alcohol was the most frequent factor (57%), followed by gallstones (25%), other factors (7.6%), and no identified factor (10.4%). Of the 288 patients, 17 (5.9%) died, all of whom had necrotizing pancreatitis; among all of the patients with necrotizing pancreatitis (141 of 288), the mortality was 12.1%. These percentages are lower than those for patients who had a single attack (8.5% and 18.6%, respectively), but not to a statistically significant degree. Mortality was significantly lower among patients with alcoholic pancreatitis (6.9%) than among those with biliary (30%) (p < 0.002) or idiopathic pancreatitis (25%) (p < 0.04). Most of the deaths (82.4%) occurred at the second attack of pancreatitis. CONCLUSION: Acute recurrent pancreatitis remains a frequent disease, with alcohol being the most frequent etiological factor. Mortality is similar to that of a single episode of acute pancreatitis, and it is significantly lower among patients with alcohol as the etiology.

Acute Disease↗

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.

Aged↗

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.

Acute Disease↗

A search for acute necrotic pancreatitis in early stages of alcoholic chronic pancreatitis.

OBJECTIVES: Various investigators believe that alcoholic chronic pancreatitis is the result of recurrent episodes of acute necrotic pancreatitis. The aim of this work is to study pancreatic histology in early stages of the disease to search for evidence of these acute episodes. STUDY: Of about 650 patients with alcoholic pancreatitis seen during the 30-year period from 1972 to 2002, 45 underwent surgery for this disease, all within 2 years of clinical onset. Of these 45, tissue samples adequate for study were obtained from 42, and this was the study material. Tissue samples were prepared for histologic examination by standard procedures. RESULTS: Areas of pancreatic necrosis were seen in tissue samples of only three (7%) of the 42 patients, and in all three cases chronic lesions were also present. No evidence of localized scarring that could be attributed to prior episodes of focal necrotic pancreatitis was found. A typical feature was the patchy distribution of the lesions in largely normal pancreatic tissue. The main lesions observed were perilobular and intralobular fibrosis, dilation of acini and ducts, and protein plugs in dilated ducts surrounded by periductal fibrosis. CONCLUSIONS: This study shows that, in the early stages of alcoholic chronic pancreatitis, signs of acute necrotic pancreatitis are very infrequent and, when present, they are associated with chronic lesions. These findings suggest that alcoholic pancreatitis begins as a chronic disease.

Adult↗

Effect of intravenous infusion of amino acids on pancreatic secretion.

BACKGROUND/AIMS: The effect of intravenous administration of amino acids on exocrine pancreatic secretion is controversial. Since amino acids are used in parenteral nutrition of patients with acute pancreatitis or other pancreatic diseases, it seemed useful to establish whether or not they affect pancreatic secretion. METHODOLOGY: Four patients having an external transduodenal drainage of the main pancreatic duct performed after sphincteroplasty for common bile duct stones were studied. Two of them had undergone a Billroth II gastrectomy in the past. Pancreatic secretion was stimulated with low doses of secretin (0.1 CU/kg/h) and cerulein (10 ng/kg/h); after 75 min of stimulation, when pancreatic secretion was stable, a solution of L-amino acids (Freamine III 8.5%) was infused intravenously at a rate of 150 mL/h, for two hours. The volume of pancreatic secretion, bicarbonate and total protein was measured. RESULTS: The infusion of amino acids did not cause significant changes in pancreatic secretion. However, considering the results individually, they caused a clear increase of pancreatic secretion, mainly of bicarbonates (mean increase of 36%) in the two subjects who had not undergone previous surgical procedures and no increase in the two who had had a Billroth II gastrectomy. CONCLUSIONS: The results suggest that intravenous administration of amino acids stimulates exocrine pancreatic secretion in normal subjects but not in those who underwent previous gastrectomy. This stimulatory effect could be mediated by stimulation of gastric acid. This effect should be taken into consideration when amino acids are used in patients with acute pancreatitis or other pancreatic disorders.

Aged↗

Does gabexate mesilate affect serum concentrations of acute phase proteins after endoscopic retrograde cholangiopancreatography examination?

BACKGROUND/AIMS: To explore the possibility that the preventive effect of gabexate mesilate on endoscopic retrograde cholangiopancreatography-related acute pancreatitis may be mediated by its modulation of acute phase proteins. METHODOLOGY: Thirty consecutive patients who underwent endoscopic retrograde cholangiopancreatography were randomly assigned to receive 1g of gabexate mesilate (13 patients) or a placebo (17 patients) by continuous i.v. infusion starting 30 minutes before the endoscopy session and continuing for 12 hours afterward. In all patients, C-reactive protein, serum amyloid A and interleukin 6 serum concentrations were determined before endoscopy and 4, 8, 12 and 24 hours afterward. RESULTS: Interleukin 6 basal serum concentrations were not statistically different between patients who had been treated with gabexate mesilate and those who had received the placebo (P = 0.279), whereas C-reactive protein (P = 0.033) and serum amyloid A (P = 0.022) basal values were significantly lower in the gabexate mesilate group than in the placebo group. Compared to basal values, serum interleukin 6 concentrations significantly increased at 4 (P = 0.048) and at 8 (P = 0.025) hours; the increase of serum interleukin 6 concentrations was not significant at 12 (P = 0.092), but became significant at 24 (P = 0.025) hours. C-reactive protein and serum amyloid A serum concentrations increased significantly only at 12 (P = 0.001, P = 0.012, respectively) and 24 (P < 0.001, P = 0.013, respectively) hours. The modifications of serum concentrations of interleukin 6, C-reactive protein and serum amyloid A were not significantly different between the gabexate mesilate and the placebo groups. CONCLUSIONS: Gabexate mesilate does not affect serum concentrations of acute phase proteins after endoscopic retrograde cholangiopancreatography examination and it is able to prevent acute pancreatitis related to endoscopic retrograde cholangiopancreatography via a different mechanism than that explored in this study.

Acute Disease↗