title: [Stimulation of immunoglobulin E formation in chronic pancreatitis by alcohol drinking and exocrine pancreatic insufficiency].
abstract: Many patients with chronic pancreatitis (CP) complain of several types of food intolerance despite elimination of fat and alcohol. Since there are no data on serum immunoglobulin E (IgE) concentrations in CP, IgE concentrations in serum were detected in 97 persons with CP and 50 controls. IgE was analyzed by the use of a highly sensitive fluoro-enzyme-immunoassay. In CP, a significantly raised IgE level (mean +/- SEM; 286.1 +/- 49 KU/L; p < 0.0001) was detected compared with controls (65.2 +/- 13 KU/L). CP-patients without alcohol consumption and normal exocrine pancreatic function were found to have only slightly elevated serum IgE values (120.2 +/- 54 KU/L), whereas patients with exocrine insufficiency treated with enzyme supplementation showed an IgE level of 153.7 +/- 51 and exocrine insufficient patients without treatment of 261.0 +/- 173 KU/L (p = 0.01). IgE levels were far more elevated in the corresponding groups with continued alcohol consumption (> 25 g/day). Alcohol consuming patients with CP and normal pancreatic function had a mean serum IgE of 295.0 +/- 114 KU/L, while patients with alcohol consumption and sufficiently treated exocrine pancreatic insufficiency showed a serum IgE of 393.7 +/- 147 KU/L (p = 0.03). Non-enzyme supplemented patients with CP and exocrine pancreatic insufficiency were characterized by approximately 10-fold increased serum IgE (1080.0 +/- 313 KU/L; p = 0.001). Non-allergic, alcohol consuming patients with CP have significantly increased serum IgE values. Since patients without alcohol consumption and normal pancreatic function or sufficiently treated exocrine insufficiency showed clearly lower IgE values than non-compliant patients with manifest exocrine pancreatic insufficiency, these results are compatible with the assumption that a reduced rate of antigen digestion in exocrine pancreatic insufficiency may lead to an increased intestinal antigen load, stimulating an abnormal humoral immune response with IgE production. Alcohol may further contribute to this by damaging the mucosal barrier.
authors.affiliation: Funktionelle Gewebediagnostik Med. Klinik I, Universität Erlangen-Nürnberg. Martin.Raithel@med1.imed.uni-erlangen.de
authors.forename: M
authors.initials: M
authors.lastname: Raithel
authors.forename: H
authors.initials: H
authors.lastname: Dormann
authors.forename: M
authors.initials: M
authors.lastname: Farnbacher
authors.forename: M
authors.initials: M
authors.lastname: Weidenhiller
authors.forename: E G
authors.initials: EG
authors.lastname: Hahn
authors.forename: H T
authors.initials: HT
authors.lastname: Schneider
mesh_terms: D000328:Adult; D000368:Aged; D000428:Alcohol Drinking / Q000009:adverse effects* / Q000276:immunology; D002908:Chronic Disease; D010188:Exocrine Pancreatic Insufficiency / Q000276:immunology*; D005260:Female; D005512:Food Hypersensitivity / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000276:immunology*; D012307:Risk Factors; D016312:Treatment Refusal
chemical_list: D007073:Immunoglobulin E