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Background: Increased serum antibodies against carbonic anhydrase II (CA-II Ab) or IgG4 levels have been reported in cases of autoimmune chronic pancreatitis (ACP)., Aim: To assess the relevance of serum CA-II Ab and IgG4 levels for the diagnosis of ACP in idiopathic CP (ICP) versus alcoholic CP and Sjogren's syndrome (SS)., Subjects: This was a multicentre study involving 227 subjects divided into four groups: ICP (n = 54), normal controls (n = 54, paired by age and sex with ICP patients), alcoholic CP (n = 86), and SS (n = 33)., Methods: CA-II Ab was measured by ELISA and confirmed by western blotting. A score of easy clinical use with major clinical, morphological, and biochemical parameters for the diagnosis of ACP was applied., Results: The percentage of patients with increased serum CA-II Ab was higher in the ICP group (28%) than in controls (1.9%) and in patients with alcoholic CP (10.5%), but lower than in patients with SS (64%). The proportion with elevated IgG4 levels was higher in the ICP group (15%) compared with controls (1.9%) and SS (0%) but not significantly different from alcoholic CP (8%). Most ICP patients (7/8) with high IgG4 levels exhibited increased CA-II Ab and a compatible ACP score. A definitive diagnosis of ACP by histological analysis was associated with other autoimmune disorders, an increase in both serum IgG4 and CA-II Ab levels, and IgG4 positive plasma cells., Conclusions: The increase in serum IgG4 levels was strongly associated with elevated CA-II Ab levels, manifestations compatible with ACP, and lymphoplasmacytic infiltration when surgical specimens were available.

Background: Bacterial translocation implies the transit of viable gastric microflora from the intestinal lumen through the intestinal wall to the mesenteric ganglia and seems to be the mechanism by which microflora reach necrotic tissue in acute pancreatitis (AP). This occurs in 40-70% of necrotizing hemorrhagic AP and plays a major role in up to 80% of deaths from this cause., Aims: To analyze the possible influence of bacterial decontamination in the gut on bacterial translocation in severe experimental AP., Methods: Severe AP was induced in 43 male Sprague-Dawley rats by administration of 0.2 ml of 2.5% taurodeoxycholate sodium in NaOH glycyl-glycine buffer after cannulizing the bilio-pancreatic duct through the duodenum and clamping the common bile duct in the hepatic junction. The rats were divided into two groups: a) control group: 24 rats in which only AP was induced; b) problem group: 19 rats that underwent bacterial decontamination through the administration of 4 mg/ml gentamicin, bacitracin and neomycin in the drinking water during the 5 days prior to AP induction. Twenty-four hours after AP induction, laparotomy was performed and a sample for the culture of mesenteric lymphatic ganglia, pancreas, liver, spleen, peritoneum and cecum was obtained., Results: Seven rats in the control group died. Of the 17 rats that survived 24 hours, positive cultures in the pancreas were obtained in nine. In the problem group, two rats died within 24 hours. Of the remaining 17 rats, positive pancreatic cultures were obtained in 2 while in 15 pancreatic cultures were negative. No microflora were cultured in the peritoneum. The microflora most frequently cultivated were Escherichia coli, enterococcus and proteus. No differences were found in the percentage of Gram-positive and Gram-negative bacteria between the two groups., Conclusions: a) The majority of the bacteria in AP tissue originate in the intestinal microflora, E. coli being the most prevalent. b) One of the main mechanisms in this process is bacterial translocation via the lymphatic pathway; transit directly through the transperitoneal pathway is not essential. c) Bacterial translocation already occurs in the earlier phases of AP. d) Bacterial decontamination prior to AP decreases the frequency of bacterial translocation and does not interfere in the Gram-positive/Gram negative balance, nor does it increase fungal infections.

To study the role that continuous drinking plays in the pain of chronic pancreatitis, we have examined 67 patients with alcoholic chronic pancreatitis with pain and 29 patients without pain, and we report on their alcoholic habits. Drinking habits played a part 92 (67.6%) of 136 times in patients with pain; in 185 without pain, 86 (46.5%) had continued their drinking habit (p < 0.001). Advanced pancreatic exocrine insufficiency was seen in 27 patients; 11 of them had pain during follow-up, whereas 16 did not. The nondrinker rate was similar in patients with and without pain, whereas among 69 patients with better pancreatic exocrine function, 56 had pain episodes and 13 did not. Alcoholic consumers were significantly more in number in the pain group: 70.4% versus 35% of the no pain group (p < 0.002). Our study shows that drinking alcohol in patients with chronic pancreatitis increased the frequency of painful episodes when there was relatively good pancreatic function, whereas in severe pancreatic insufficiency drinking had less influence on the development of pain.

Unlabelled: The purpose of this study was to assess the role of duodenal diverticula as an etiologic factor in acute pancreatitis., Methods and Patients: We have reviewed the records of patients with diverticulum of the second portion of the duodenum diagnosed by gastroduodenal radiology or endoscopy during the period 1991-1992 in our hospital. As a control group we studied patients without duodenal diverticulum. All subjects underwent biliary-pancreatic ultrasonography. Thirty-eight patients had a duodenal diverticulum and gallstones 36 had a duodenal diverticulum but no gallstones; 21 had gallstones alone; and, finally, 42 patients were free of duodenal diverticulum and gallstones., Results: Patients with duodenal diverticula had a greater prevalence of gallstones than those without (51.3% VS 33.3%, p < 0.005). Of the thirty-eight patients with duodenal diverticula and gallstones 23.7% had acute pancreatitis. None of the 21 patients without duodenal diverticulum and with gallstones had acute pancreatitis, p < 0.05. The median age of patients with duodenal diverticulum without gallstones was 64.25 years, range 34-85, and the age of those with duodenal diverticulum and gallstones was 70.4 years, range 37-87, p < 0.05., Conclusions: 1) Gallstones may cause acute pancreatitis in patients with D2 duodenal diverticula. 2) Patients with a D2 duodenal diverticulum frequently have gallstones. 3) The fact that the age of patients with duodenal diverticulum was lower than that of patients with both duodenal diverticulum and gallstones suggests that duodenal diverticula may play a role in the pathogenesis of gallstones.

Early recognition of severity of acute pancreatitis is very uncertain. For this reason it is necessary to have objective criteria to predict with accuracy the course of the disease. The aim of this study was to examine the value of the determination of the acute phase reactants: C reactive protein (CRP), alpha 1-antitrypsin (alpha-AT) and alpha 1-glycoprotein acid (alpha-GA) as prognostic indicators of acute pancreatitis on admission and on the third day. We have studied 40 patients with acute pancreatitis and serum concentrations of CRP, alpha-AT and alpha-GP were related to the Ranson Index. On admission the median levels of CRP: 74 mg/L, alpha-AT: 208 mg% and alpha-GA: 303 mg% were significantly higher (p less than 0.001) in patients with Ranson Index greater than or equal to 3 than in those with Ranson Index less than or equal to 2 (CRP: 166 mg/L, alpha-AT: 303 mg% and alpha-GA: 121 mg%). The values which differentiated patients with better and worse prognosis were: CRP 100 mg/L (sensitivity 100% and specificity 86%); alpha--AT 275 mg% (sensitivity 71% and specificity 85%); and alpha-GA 90 mg% (sensitivity 87.5% and specificity 57.9%). CRP, and to a lesser degree the alpha-AT and alpha-GA, were related to the duration of the ileus, and to the severe complications of the acute pancreatitis.

Background: Increased serum antibodies against carbonic anhydrase II (CA-II Ab) or IgG4 levels have been reported in cases of autoimmune chronic pancreatitis (ACP). Aim: To assess the relevance of serum CA-Il Ab and lgG4 levels for the diagnosis of ACP in idiopathic CP (ICP) versus alcoholic CP and Sjögren's syndrome (SS). Subjects: This was a multicentre study involving 227 subjects divided into four groups: ICP (n = 54), normal controls (n = 54, paired by age and sex with ICP patients), alcoholic CP (n = 86), and SS (n = 33). Methods: CA-II Ab was measured by ELISA and confirmed by western blotting. A score of easy clinical use with major clinical, morphological, and biochemical parameters for the diagnosis of ACP was applied. Results: The percentage of patients with increased serum CA-II Ab was higher in the ICP group (28%) than in controls (1.9%) and in patients with alcoholic CP (10.5%), but lower than in patients with SS (64%). The proportion with elevated IgG4 levels was higher in the ICP group (15%) compared with controls (1.9%) and SS (0%) but not significantly different from alcoholic CP (8%). Most ICP patients (7/8) with high lgG4 levels exhibited increased CA-II Ab and a compatible ACP score. A definitive diagnosis of ACP by histological analysis was associated with other autoimmune disorders, an increase in both serum lgG4 and CA-II Ab levels, and IgG4 positive plasma cells. Conclusions: The increase in serum 1gG4 levels was strongly associated with elevated CA-II Ab levels, manifestations compatible with ACP, and lymphoplasmacytic infiltration when surgical specimens were available. [ABSTRACT FROM AUTHOR]

A case study is presented concerning two patients with rheumatic diseases, a 61-year-old female with acute pancreatitis caused by cholelithiasis and a 51-year-old female patient diagnosed with scleroderma. It states the first patients was diagnosed with systematic lupus erythematosus (SLE) and Sjogren's syndrome and talks about chronic calcifying of the pancreas in both patients. It comments on the potential for calcification in chronic pancreatitis.