title: [Cellular and humoral functions in acute pancreatitis].
abstract: Infectious complications are the leading cause of death in acute pancreatitis. Individual factors of immune defence could be of significance, whether or not a patient develops a severe course with infectious complications. In a prospective 5-year trial including 72 patients, we investigated 29 cellular and humoral markers of the body's defence system for their potential to indicate the severity and course of acute pancreatitis. Complement factors C3 and C4 as well as immunoglobulins IgG, IgM and IgA were normal, in general. Measurable levels of IL-1 alpha, IL-1 beta, IL-2 and sIL-2R could be detected only occasionally. Values of alpha 1-AT, TNF-alpha, TNF alpha-Rp75, neopterin, sICAM-1, IL-8, IL-1RA and sIL-6R did not correlate with a severe course. Due to the high magnitude of increase, CRP, IL-6 and granulocyte elastase were the best indicators of the inflammatory process. Delayed-type hypersensitivity response was the only early predictor of a severe course. It was superior over other cellular markers such as monocyte count or CD4+/CD8+ ratio. In vitro function of polymorphonuclear granulocytes (PMN) was not adequate to the severity of the disease already during the first week of illness. During further course, PMN motility and capacities to produce reactive oxygen species even worsened. The compromized PMN function could explain the frequent development of infectious complications in patients suffering from severe pancreatitis. These results should encourage new concepts of infection prophylaxis using stimulants of cellular defence.
authors.affiliation: Klinik für Chirurgie, Otto von Guericke-Universität Magdeburg, Deutschland.
authors.forename: H U
authors.initials: HU
authors.lastname: Schulz
authors.forename: D
authors.initials: D
authors.lastname: Schmidt
authors.forename: D
authors.initials: D
authors.lastname: Kunz
authors.forename: M
authors.initials: M
authors.lastname: Pross
authors.forename: A
authors.initials: A
authors.lastname: Gerber
authors.forename: G
authors.initials: G
authors.lastname: Weiss
authors.forename: A
authors.initials: A
authors.lastname: Sokolowski
authors.forename: H
authors.initials: H
authors.lastname: Struy
authors.forename: H
authors.initials: H
authors.lastname: Lippert
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000917:Antibody Formation / Q000276:immunology*; D016516:CD4-CD8 Ratio; D003167:Complement Activation / Q000276:immunology*; D005260:Female; D005609:Free Radicals; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007108:Immune Tolerance / Q000276:immunology; D007111:Immunity, Cellular / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000276:immunology*; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D005609:Free Radicals; D017382:Reactive Oxygen Species