title: Altered gut flora and environment in patients with severe SIRS.
abstract: BACKGROUND
  The gut is considered an important target organ of injury after severe insult such as sepsis, trauma, and shock. The impact of bacterial translocation or mesenteric lymph on systemic inflammatory response and multiple organ damage has been investigated in animals, but dynamic changes in the gut flora and environment have not been fully clarified in critically ill patients. In the present study, we quantitatively evaluated changes in the gut microflora and environment in patients with severe systemic inflammatory response syndrome (SIRS).
  
  
  METHODS
  Twenty-five patients with severe SIRS, who fulfilled the criteria for SIRS, had a serum CRP level >10 mg/dL, and were treated in the intensive care unit for more than 2 days, were included in our study. SIRS was a result of sepsis in 18 patients, trauma in 6, and burn in 1. A fecal sample was used for quantitative evaluation of microflora (bacterial counts of 10 key groups including Bifidobacterium and Lactobacillus) by plate or tube technique and of the gut environment (pH and 9 organic acids by high speed liquid chromatography). Data obtained from patients were compared with corresponding data from healthy volunteers.
  
  
  RESULTS
  Analysis of fecal flora confirmed that patients with severe SIRS had significantly lower total anaerobic bacterial counts (especially 2-4 log fewer "beneficial" Bifidobacterium and Lactobacillus) and 2 log higher "pathogenic" Staphylococcus and Pseudomonas group counts than those of healthy volunteers. Concentrations of total organic acids (especially "beneficial" short-chain fatty acids such as acetic acid, propionic acid, and butyric acid) in the feces were significantly decreased in the patients, whereas pH was markedly increased.
  
  
  CONCLUSIONS
  The gut flora and environment are significantly altered in patients with severe SIRS. Abnormal gut flora and environment may affect systemic inflammatory response after severe insult.
authors.affiliation: Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, 2-15 Yamadaoka, Suita-shi, Osaka 565-0871, Japan. shimiken@hp-emerg.med.osaka-u.ac.jp
authors.forename: Kentaro
authors.initials: K
authors.lastname: Shimizu
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogura
authors.forename: Miki
authors.initials: M
authors.lastname: Goto
authors.forename: Takashi
authors.initials: T
authors.lastname: Asahara
authors.forename: Koji
authors.initials: K
authors.lastname: Nomoto
authors.forename: Masami
authors.initials: M
authors.lastname: Morotomi
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Yoshiya
authors.forename: Asako
authors.initials: A
authors.lastname: Matsushima
authors.forename: Yuka
authors.initials: Y
authors.lastname: Sumi
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Kuwagata
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tanaka
authors.forename: Takeshi
authors.initials: T
authors.lastname: Shimazu
authors.forename: Hisashi
authors.initials: H
authors.lastname: Sugimoto
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001421:Bacteria, Anaerobic / Q000302:isolation & purification*; D002264:Carboxylic Acids / Q000032:analysis*; D016022:Case-Control Studies; D015169:Colony Count, Microbial; D005243:Feces / Q000737:chemistry / Q000382:microbiology; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007378:Interleukins / Q000097:blood; D007422:Intestines / Q000737:chemistry* / Q000382:microbiology*; D008297:Male; D008875:Middle Aged; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000382:microbiology*; D018180:Thrombomodulin / Q000097:blood
chemical_list: D002264:Carboxylic Acids; D007378:Interleukins; D018180:Thrombomodulin