Stimulation of immunoglobulin E production in chronic pancreatitis by alcohol consumption and exocrine pancreatic insufficiency

Many patients with chronic pancreatitis (CP) complain of several types of f ood intolerance despite elimination of fat and alcohol. Since there are no data on serum immunoglobulin E (IgE) concentrations in CP, IgE concentratio ns in serum were detected in 97 persons with CP and 50 controls. IgE was an alyzed 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 func tion 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 insufficie nt 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 c onsumption (> 25 g/day). Alcohol consuming patients with CP and normal panc reatic function had a mean serum IgE of 295.0 +/- 114 KU/L, while patients with alcohol consumption and sufficiently treated exocrine pancreatic insuf ficiency showed a serum IgE of 393.7 +/- 147 KU/L (p = 0.03). Non-enzyme su pplemented patients with CP and exocrine pancreatic insufficiency were char acterized by approximately 10-fold increased serum IgE (1080.0 +/- 313 KU/L ; p = 0.001). Non-allergic, alcohol consuming patients with CP have significantly increas ed serum IgE values. Since patients without alcohol consumption and normal pancreatic function or sufficiently treated exocrine insufficiency showed c learly 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 insufficien cy may lead to an increased intestinal antigen load, stimulating an abnorma l humoral immune response with IgE production. Alcohol may further contribu te to this by damaging the mucosal barrier.