title: Immunosuppression in patients with severe acute pancreatitis.
abstract: BACKGROUND
  In severe acute pancreatitis (SAP), immunologic impairment in the early phase may be linked to subsequent infectious complications. In this study, immunologic alterations in patients with SAP were analyzed, and immunologic parameters related to infectious complications were clarified.
  
  
  METHODS
  A total of 101 patients with SAP were analyzed retrospectively. Various immunologic parameters on admission were analyzed and compared between the infection group and noninfection group during SAP. Furthermore, chronologic change in the lymphocyte count was investigated, and its utility for predicting infection was compared with conventional scoring systems.
  
  
  RESULTS
  Serum immunoglobulin G (IgG), serum IgM, lymphokine-activated killer cell activity, and natural killer cell activity were low, and the incidence of abnormally low values was 50.0%, 65.0%, 45.5%, and 42.4%, respectively. Serum complement factor 3 was significantly negatively correlated with the APACHE II score. The lymphocyte count was decreased below the normal range, and was significantly negatively correlated with the APACHE II score. CD4-, CD8-, and CD20-positive lymphocyte counts were below the normal range, and CD4- and CD8-positive lymphocyte counts were significantly lower in the infection group. The lymphocyte count on day 14 after admission was significantly lower in the infection group and was more useful for predicting infection than conventional scoring systems.
  
  
  CONCLUSIONS
  Immunosuppression occurs from the early phase in SAP, and quantitative impairment of lymphocytes, mainly T lymphocytes, may be closely related to infectious complications during SAP. CD4- and CD8-positive lymphocyte counts on admission and the lymphocyte count on day 14 after admission may be useful for predicting infection.
authors.affiliation: Department of Gastroenterological Surgery, Kobe University Graduate School of Medical Sciences, Chuo-ku, Kobe 650-0017, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Ueda
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Takeyama
authors.forename: Takeo
authors.initials: T
authors.lastname: Yasuda
authors.forename: Makoto
authors.initials: M
authors.lastname: Shinzeki
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Sawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Nakajima
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Ajiki
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Fujino
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Kuroda
mesh_terms: D018806:APACHE; D000208:Acute Disease; D003176:Complement C3; D003181:Complement C4; D005260:Female; D006801:Humans; D016867:Immunocompromised Host; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007239:Infections / Q000150:complications / Q000453:epidemiology; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000097:blood; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000150:complications / Q000276:immunology*; D012189:Retrospective Studies; D013601:T-Lymphocytes
chemical_list: C038245:C3 protein, human; D003176:Complement C3; D003181:Complement C4; D007074:Immunoglobulin G; D007075:Immunoglobulin M