title: Cytokine genotypes in acute pancreatitis: association with etiology, severity, and cytokine levels in blood.
abstract: The circumstances that determine how acute pancreatitis (AP) becomes severe are unknown. Differences in cytokine genetic encoding may determine the severity or influence the etiology of AP. This article investigates the relationship between different polymorphisms of tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1), IL-1 receptor antagonist, IL-6, and IL-10 with the severity and etiology of AP and the serum levels of the cytokine encoded.
  
  
  METHODS
  Patients with AP were included prospectively. Severity of the disease was determined according to Atlanta classification. Serum levels of these cytokines were determined within the first 72 hours after the onset of symptoms. The following polymorphisms were determined by polymerase chain reaction: IL-1a -889, IL-1b +3954, IL-1b -511, variable number tandem repeats, IL-6 -174, IL-6 -597, IL-10 -592, TNF-alpha 308, TNF-alpha 238, and TNF-B250.
  
  
  RESULTS
  Eighty-four patients were included. The GA genotype of the TNF-alpha 238 polymorphism was associated with more frequent respiratory failure and shock than the GG genotype. Gallstone pancreatitis was associated with the CC genotype of the IL-6 -174 CC polymorphism.
  
  
  CONCLUSIONS
  AG genotype of the TNF-alpha 238 polymorphism is associated with organic failure in patients with AP. The CC genotype of the IL-6 174 polymorphism is associated with biliary etiology of acute pancreatitis.
authors.affiliation: Departments of Gastroenterology, Hospital General Universitario de Alicante, Alicante, Spain.
authors.forename: Enrique
authors.initials: E
authors.lastname: de-Madaria
authors.forename: Juan
authors.initials: J
authors.lastname: Martínez
authors.forename: Laura
authors.initials: L
authors.lastname: Sempere
authors.forename: Beatriz
authors.initials: B
authors.lastname: Lozano
authors.forename: José
authors.initials: J
authors.lastname: Sánchez-Payá
authors.forename: Francisco
authors.initials: F
authors.lastname: Uceda
authors.forename: Miguel
authors.initials: M
authors.lastname: Pérez-Mateo
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016207:Cytokines / Q000097:blood / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood / Q000235:genetics; D007375:Interleukin-1 / Q000097:blood / Q000235:genetics; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D012720:Severity of Illness Index; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
chemical_list: D016207:Cytokines; C508609:IL10 protein, human; C507763:IL1RN protein, human; C508600:IL6 protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10