title: The lethal toxicity of pancreatic ascites fluid in severe acute necrotizing pancreatitis.
abstract: OBJECTIVE
  The pathogenesis and the molecular mechanisms of the development and progression of the acute pancreatitis (AP) are not clearly understood. Ascites fluid is known to be important in the clinical progression of AP. We present the lethal toxicity of human pancreatic ascites fluid for experimental pancreatitis, with the therapeutic course of severe necrotizing AP.
  
  
  METHODS
  The material was in a 33-year-old male admitted with epigastric pain. An abdominal CT revealed that his pancreas was swollen and contained pancreatic fluid collection extending to the pelvic cavity. He had complicated acute renal failure, sepsis, and DIC, and received hemodialysis, and continuous arterial infusion therapy (CAI). The peripancreatic infection was acquired, and percutaneous interventional radiology (IVR) was performed for the abscess drainage. The drained liquid around the pancreas contained high molecular cytokines, protease, and bacterial contamination. To evaluate the toxicity of the ascites fluid, we gave it intraperitoneally to rats in which pancreatitis had been induced and rats that had undergone a sham operation; these rats died immediately. The consistent irrigation and drainage of the abscess was administered and the patient's general condition improved. At this time, we gave the drained material intraperitoneally to other rats with induced pancreatitis and sham operation, but all these rats survived.
  
  
  RESULTS
  These experimental results suggested that pancreatitis-associated ascites fluid contained a lethal toxicity. For curing this disease, elimination of these potential toxic mediators was essential. Our intensive IVR-based therapy improved the patient's prognosis.
  
  
  CONCLUSIONS
  Downregulating this inflammatory process leads to a decrease in the mortality of severe acute pancreatitis.
authors.affiliation: Department of Surgery, Teikyo University School of Medicine, Ichihara Hospital, 3426-3 Anesaki Ichihara, 299-0111 Chiba, Japan. sugimoto@med.teikyo-u.ac.jp
authors.forename: Maki
authors.initials: M
authors.lastname: Sugimoto
authors.forename: Tadahiro
authors.initials: T
authors.lastname: Takada
authors.forename: Hideki
authors.initials: H
authors.lastname: Yasuda
authors.forename: Ikuo
authors.initials: I
authors.lastname: Nagashima
authors.forename: Hodaka
authors.initials: H
authors.lastname: Amano
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yoshida
authors.forename: Fumihiko
authors.initials: F
authors.lastname: Miura
authors.forename: Toyohiko
authors.initials: T
authors.lastname: Uchida
authors.forename: Takahiro
authors.initials: T
authors.lastname: Isaka
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Toyota
authors.forename: Keita
authors.initials: K
authors.lastname: Wada
authors.forename: Kenji
authors.initials: K
authors.lastname: Takagi
authors.forename: Kenichiro
authors.initials: K
authors.lastname: Kato
mesh_terms: D000328:Adult; D000818:Animals; D001202:Ascitic Fluid / Q000737:chemistry / Q000378:metabolism* / Q000382:microbiology; D006801:Humans; D007274:Injections, Intraperitoneal; D008297:Male; D023421:Models, Animal; D010179:Pancreas / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D014057:Tomography, X-Ray Computed