title: [Changes in pro-inflammatory cytokines and media and peptide hormones during multiple organ dysfunction syndrome following acute abdominal diseases].
abstract: OBJECTIVE
  To inquire into effects of cytokines and other inflammatory media, and peptide hormones during multiple organ dysfunction syndrome (MODS) subsequent to acute abdominal diseases.
  
  
  METHODS
  In 19 patients with MODS due to acute abdominal diseases, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), thromboxane B(2) (TXB(2)), 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha)), endotoxin, gene-related peptide(CGRP), endothelin-1 (ET-1) and substance P (SP) in plasma, and lipid peroxide (LPO) and nitric oxide (NO) in serum were determined dynamically.
  
  
  RESULTS
  Both TNF-alpha and IL-6 at increased significantly in MODS patients; IL-6 on day 0 in patients without treatment of endoscopic retrograde bile duct drainage (ERBD) were higher than that in patients with correspondent treatment, IL-6 in severe acute cholangitis patients was higher than that in patients with acute necrotic pancreatitis, it approached 24,000 ng/L during toxic shock. TNF-alpha and IL-6 during early stage of MODS were higher than that during systemic inflammatory response syndrome (SIRS) respectively. Endotoxin and LPO levels in MODS patients increased significantly. The levels of NO in emergency patients with MODS was elevated, but lowered in patients with acute necrotic pancreatitis, hepatocarcinoma, advanced age's patients with long time fever due to hepatic abscess. TXB(2) and 6-keto-PGF(1alpha) during early stage rose significantly, both decreased after treatment. ET-1 and CGRP during early stage increased significantly, SP peaked on day 0.
  
  
  CONCLUSIONS
  The level of IL-6 persistently higher than 300 ng/L suggests the diagnosis of MODS. The levels of IL-6 and TNF-alpha could be taken as an indication of the degree of SIRS. NO maybe either increased or decreased, ET-1, CGRP, TXB(2), 6-keto-PGF(1alpha), endotoxin, and LPO are found to be increased MODS.
authors.affiliation: Department of Pharmacology, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Bu-wu
authors.initials: BW
authors.lastname: Fang
authors.forename: Qi
authors.initials: Q
authors.lastname: Qiu
authors.forename: Xian-zhong
authors.initials: XZ
authors.lastname: Wu
authors.forename: Li
authors.initials: L
authors.lastname: Kong
authors.forename: Ming-fang
authors.initials: MF
authors.lastname: Qin
authors.forename: Zhen-li
authors.initials: ZL
authors.lastname: Zhou
authors.forename: Nai-qiang
authors.initials: NQ
authors.lastname: Cui
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016207:Cytokines / Q000097:blood*; D004066:Digestive System Diseases / Q000150:complications / Q000378:metabolism*; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000209:etiology / Q000378:metabolism*; D036361:Peptide Hormones / Q000097:blood*; D018746:Systemic Inflammatory Response Syndrome / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D016207:Cytokines; D019332:Endothelin-1; D015850:Interleukin-6; D036361:Peptide Hormones; D014409:Tumor Necrosis Factor-alpha