ABSTRACT
A new rapid immunoinhibition pancreatic amylase assay was compared to total amylase and lipase in an unbiased sample of 1005 emergency department patients with suspicion of pancreatitis, of which 55 had a final diagnosis of pancreatitis. Imprecision of the assays for both amylases (less than 2.5%) were better than for lipase (less than 6.1%). Correlation (R2) of pancreatic amylase with total amylase was 0.991 but only 0.789 with lipase. Using Receiver Operator Characteristics analysis, the best diagnostic cutoff point for all three enzymes was near the upper limit of the reference interval. With pancreatic amylase, sensitivity, specificity, and predictive values for positive and negative results are, respectively, 85.5, 92.5, 39.8, and 99.1%; we found similar values for lipase but poorer values (78.2, 92.0, 36.1, and 98.7%) for total amylase. Tests combination did not improve the diagnostic performance significantly. In the diagnosis of pancreatitis, pancreatic amylase (p = 0.037) and lipase (p = 0.049) had better diagnostic performance than total amylase. The correct diagnosis of pancreatitis could be achieved in 47 instead of 43 patients with either pancreatic amylase or lipase as opposed to total amylase among 1005 patients in this study. We conclude that pancreatic amylase and lipase are incrementally better diagnostic tools than total amylase for the diagnosis of pancreatitis.
Subject(s)
Amylases/blood , Clinical Enzyme Tests , Lipase/blood , Pancreas/enzymology , Pancreatitis/diagnosis , Acute Disease , Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Chronic Disease , Humans , Linear Models , Middle Aged , Predictive Value of Tests , Prospective Studies , Sensitivity and Specificity , Single-Blind Method , Time FactorsABSTRACT
Addition of arachidonic acid to suspensions of human blood leukocytes induces the synthesis of small amounts only of the C-5 lipoxygenase products as demonstrated by HPLC. However, the coincubation of blood platelets with the leukocytes always resulted in an activation of the C-5 lipoxygenase and formation of (5S)-5-hydroxy-6,8,11,14-icosatetraenoic acid, (5S,12S)-5,12-dihydroxy-6,8,10,14-icosatetraenoic acid, and leukotriene B4 from exogenous arachidonic acid. It was found that the activation of arachidonic acid metabolism in leukocytes was caused by a labile compound because the synthesis of the C-5 lipoxygenase products did not occur when platelets were preincubated for 1 min or more with the substrate prior to the addition of the leukocytes. The use of cyclooxygenase inhibitors did not suppress the activation of the leukocytes by the platelets. However, the addition of 5,8,11,14-icosatetraynoic acid, an inhibitor of cyclooxygenase and C-12 and C-15 lipoxygenases, completely suppressed the formation of leukotrienes, although this substance is not an inhibitor of the C-5 lipoxygenase in human leukocytes. This indicated that a product of the C-12 lipoxygenase was likely the mediator of the stimulatory effect of platelets on leukocyte arachidonic acid metabolism. The finding that the direct addition of (12S)-12-hydroperoxy-5,8,10,14-icosatetraenoic acid, but not of the corresponding hydroxy derivative, could activate the leukocyte's C-5 lipoxygenase confirmed this hypothesis. These data demonstrate that an interaction between C-12 and C-5 lipoxygenases can promote the formation of leukotrienes and support the possibility of a cooperation between platelets and leukocytes in inflammation and hypersensitivity reactions. Furthermore, the finding provides a new interest for the platelet C-12 lipoxygenase.
