title: The clinical significance of hyperamylasemia in organophosphate poisoning.
abstract: OBJECTIVE
  Hyperamylasemia with a presumptive diagnosis of acute pancreatitis has been reported following organophosphate poisoning but there are no large-scale studies incorporating more specific diagnostic criteria.
  
  
  METHODS
  Retrospective review of the medical records of 159 patients with a diagnosis of organophosphate poisoning over 3 years. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels, and the clinical manifestations were analyzed.
  
  
  RESULTS
  Serum amylase data was available for 121 of the 159 study patients. Hyperamylasemia (amylase > or = 360 U/L) was found in 44 patients (36%). Lipase was measured in 28 patients with hyperamylasemia; 9 of 28 had hyperlipasemia (lipase > or = 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. A presumptive diagnosis of painless acute pancreatitis was diagnosed by hyperlipasemia associated with hyperamylasemia, clinical severity, serum LDH, and leukocyte counts. Two patients with presumptive pancreatitis died. Shock, coma, and hypoalbuminemia were the factors predicting fatality.
  
  
  CONCLUSIONS
  Hyperamylasemia is frequent in severe organophosphate poisoning. However, hyperamylasemia is not synonymous with acute pancreatitis and pancreatic amylase is not a reliable parameter in the diagnosis of organophosphate-induced pancreatitis due to its low sensitivity and specificity. Lipase assay is indicated in patients with hyperamylasemia for early diagnosis of pancreatitis. Proper image studies and even pathological examination are also needed to confirm the extent of pancreatic injury. With prompt diagnosis and appropriate treatment, a complete recovery can be anticipated unless the patient has otherwise unrelated complications.
authors.affiliation: Veterans General Hospital-Taipei and School of Medicine, National Yang-Ming University, Taiwan. wclee@mail.vghtpe.gov.tw
authors.forename: W C
authors.initials: WC
authors.lastname: Lee
authors.forename: C C
authors.initials: CC
authors.lastname: Yang
authors.forename: J F
authors.initials: JF
authors.lastname: Deng
authors.forename: M L
authors.initials: ML
authors.lastname: Wu
authors.forename: J
authors.initials: J
authors.lastname: Ger
authors.forename: H C
authors.initials: HC
authors.lastname: Lin
authors.forename: F Y
authors.initials: FY
authors.lastname: Chang
authors.forename: S D
authors.initials: SD
authors.lastname: Lee
mesh_terms: D000208:Acute Disease; D000328:Adult; D000681:Amylases / Q000097:blood* / Q000378:metabolism; D002802:Cholinesterases / Q000097:blood / Q000378:metabolism; D005260:Female; D006801:Humans; D008049:Lipase / Q000097:blood / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D062025:Organophosphate Poisoning; D010179:Pancreas / Q000201:enzymology; D010195:Pancreatitis / Q000097:blood / Q000139:chemically induced / Q000175:diagnosis / Q000378:metabolism; D012189:Retrospective Studies; D012463:Saliva / Q000201:enzymology
chemical_list: D008049:Lipase; D002802:Cholinesterases; D000681:Amylases