Background. Trypsinogen activation peptide (TAP) reflects the amount of activation trypsinogen, not taking into account how much trypsin is active or linked to specific inhibitors. TAP is released into the peritoneal cavity and circulates after which the peptide, thanks to its small size, is rapidly metabolized in the kidney and excreted in the urine. It seems logical that the greater the quantity of trypsinogen activated, the more the pancreas is damaged. The aim of the study was to evaluate the serum TAP concentration elevation after ERCP and to establish its role in the early diagnosis of post-procedural acute pancreatitis. The second aim was to explore whether the administration of gabexate mesylate could prevent the activation of tripsinogen by blocking trypsin activation. Methods. Sixty-five patients were enrolled in the study. Patients who were under 18 years of age, patients with a recent onset of acute pancreatitis, those who were pregnant, and patients with a known allergy to gabexate mesylate were excluded. In all patients, a 5 mL blood sample was taken immediately before the endoscopic examination and 1, 2, 3, 4 and 6 hours post-ERCP. A two mL sample of urine was also collected before ERCP and 2, 4 and 6 hours after the completion of the ERCP. Serum and urine TAPs were assayed using a technique previously described [Pancreas 2004;29:298-305]. The detection limit was 1.0 ng/mL and healthy subjects had no detectable values of TAP in serum and in urine. Serum trypsinogen concentrations were determined using commercially available RIA-kits (Sorin Biomedica). The detection limit was 2.5 ng/mL and the reference values of our laboratory were 10-57 ng/mL. The use of gabexate mesylate was decided by the endoscopist. Post-ERCP acute pancreatitis was defined as the appearance of typical abdominal pain associated with an increase in serum amylase activity greater than 3 times the upper reference limit. The severity of the pancreatitis was assessed by clinically-based Atlanta criteria. Results. In the 65 patients who completed the study, 2-hour post-ERCP serum TAP concentrations were elevated (P=0.034 vs. pre-ERCP) whereas these concentrations significantly declined at 4 hours (P=0.006). Urine TAP showed a similar behavior. Mean serum trypsinogen concentrations were slightly below the upper reference limit before ERCP and then significantly increased thereafter. Serum and urine TAP levels, as well as serum trypsinogen concentration, showed no significant differences between patients who developed acute pancreatitis and those who did not. Within the group of the patients who received gabexate mesylate, serum TAP concentrations were significantly lower at 1 and 2 hours after ERCP in the patients who developed acute pancreatitis (P=0.033 and P=0.041, respectively). Conclusions. Serum and urine concentrations of TAP are detectable very early in patients who undergo ERCP, i.e. within the first 6 hours. As for the other pancreatic enzymes, serum and urine TAP determination is of limited value in diagnosing post-ERCP acute pancreatic damage if used alone. Finally, more studies are necessary to precisely establish the role of TAP determination in patients treated prophylactically with drugs capable of blocking the activation of trypsin.

Serum and Urine Trypsinogen Activation Peptide in Assessing Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis / A. Barassi, R. Pezzilli, R. Capra, A. Mariani, A. Gabrielli, A.M. Morselli Labate, R. Pacciolla, G. MELZI D'ERIL. - In: CLINICAL CHEMISTRY. - ISSN 0009-9147. - 56:Suppl. 6(2010), pp. A105-A105. ((Intervento presentato al 62. convegno Annual Meeting of Clinical Chemistry tenutosi a Anaheim nel 2010.

Serum and Urine Trypsinogen Activation Peptide in Assessing Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis

A. Barassi
Primo
;
R. Pacciolla
Penultimo
;
G. MELZI D'ERIL
Ultimo
2010

Abstract

Background. Trypsinogen activation peptide (TAP) reflects the amount of activation trypsinogen, not taking into account how much trypsin is active or linked to specific inhibitors. TAP is released into the peritoneal cavity and circulates after which the peptide, thanks to its small size, is rapidly metabolized in the kidney and excreted in the urine. It seems logical that the greater the quantity of trypsinogen activated, the more the pancreas is damaged. The aim of the study was to evaluate the serum TAP concentration elevation after ERCP and to establish its role in the early diagnosis of post-procedural acute pancreatitis. The second aim was to explore whether the administration of gabexate mesylate could prevent the activation of tripsinogen by blocking trypsin activation. Methods. Sixty-five patients were enrolled in the study. Patients who were under 18 years of age, patients with a recent onset of acute pancreatitis, those who were pregnant, and patients with a known allergy to gabexate mesylate were excluded. In all patients, a 5 mL blood sample was taken immediately before the endoscopic examination and 1, 2, 3, 4 and 6 hours post-ERCP. A two mL sample of urine was also collected before ERCP and 2, 4 and 6 hours after the completion of the ERCP. Serum and urine TAPs were assayed using a technique previously described [Pancreas 2004;29:298-305]. The detection limit was 1.0 ng/mL and healthy subjects had no detectable values of TAP in serum and in urine. Serum trypsinogen concentrations were determined using commercially available RIA-kits (Sorin Biomedica). The detection limit was 2.5 ng/mL and the reference values of our laboratory were 10-57 ng/mL. The use of gabexate mesylate was decided by the endoscopist. Post-ERCP acute pancreatitis was defined as the appearance of typical abdominal pain associated with an increase in serum amylase activity greater than 3 times the upper reference limit. The severity of the pancreatitis was assessed by clinically-based Atlanta criteria. Results. In the 65 patients who completed the study, 2-hour post-ERCP serum TAP concentrations were elevated (P=0.034 vs. pre-ERCP) whereas these concentrations significantly declined at 4 hours (P=0.006). Urine TAP showed a similar behavior. Mean serum trypsinogen concentrations were slightly below the upper reference limit before ERCP and then significantly increased thereafter. Serum and urine TAP levels, as well as serum trypsinogen concentration, showed no significant differences between patients who developed acute pancreatitis and those who did not. Within the group of the patients who received gabexate mesylate, serum TAP concentrations were significantly lower at 1 and 2 hours after ERCP in the patients who developed acute pancreatitis (P=0.033 and P=0.041, respectively). Conclusions. Serum and urine concentrations of TAP are detectable very early in patients who undergo ERCP, i.e. within the first 6 hours. As for the other pancreatic enzymes, serum and urine TAP determination is of limited value in diagnosing post-ERCP acute pancreatic damage if used alone. Finally, more studies are necessary to precisely establish the role of TAP determination in patients treated prophylactically with drugs capable of blocking the activation of trypsin.
Settore BIO/12 - Biochimica Clinica e Biologia Molecolare Clinica
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/194427
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