Urinary Trypsinogen-2 Research Articles

Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis: a prospective study

OBJECTIVE: The management of patients with acute pancreatitis is complicated by the inability to distinguish mild from severe disease during the early stages. It has been previously shown that urinary trypsinogen activation peptide (TAP) and hematocrit (Hct) may serve as early predictors of severity in patients with acute pancreatitis. To establish which marker is more accurate in the determination of severity in patients with acute pancreatitis, a prospective study was performed. METHODS: A consecutive series of patients admitted with pain consistent with acute pancreatitis and an amylase of three times the upper limit of normal were included. The admission and 24-h Hct was obtained. A urine sample was obtained within 12 h of admission. Urinary TAP was determined using a modified solid phase ELISA. Severity was defined by the Atlanta Symposium, as the presence of organ failure and/or pancreatic necrosis. RESULTS: Fifty-eight consecutive patients with acute pancreatitis participated. There were 33 men and 25 women with a mean age of 60 ± 19. Thirty-nine patients had mild disease; 19 had severe disease. Urinary TAP was elevated in 26 patients. All patients with severe pancreatitis were correctly identified as having severe disease by an elevated urinary TAP (sensitivity 100%, specificity 77%). The admission Hct was higher than 47 in only three patients, all with mild disease. Of the patients with a rise in Hct, eight had mild disease, and only one had severe disease. Using a Hct of 44 as a cutoff did not affect the accuracy. There was no association between a rise in Hct and failure of Hct to decrease in the determination of severity. CONCLUSIONS: In comparison to admission Hct, urinary TAP was more accurate in determining severity in patients with acute pancreatitis by Atlanta, APACHE II, and Ranson criteria. We conclude that urinary TAP is a more accurate predictor of severity in patients with acute pancreatitis compared with Hct. Urinary TAP should be used to determine severity in patients early in the course of acute pancreatitis.

Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis: a prospective study.

The management of patients with acute pancreatitis is complicated by the inability to distinguish mild from severe disease during the early stages. It has been previously shown that urinary trypsinogen activation peptide (TAP) and hematocrit (Hct) may serve as early predictors of severity in patients with acute pancreatitis. To establish which marker is more accurate in the determination of severity in patients with acute pancreatitis, a prospective study was performed. A consecutive series of patients admitted with pain consistent with acute pancreatitis and an amylase of three times the upper limit of normal were included. The admission and 24-h Hct was obtained. A urine sample was obtained within 12 h of admission. Urinary TAP was determined using a modified solid phase ELISA. Severity was defined by the Atlanta Symposium, as the presence of organ failure and/or pancreatic necrosis. Fifty-eight consecutive patients with acute pancreatitis participated. There were 33 men and 25 women with a mean age of 60 +/- 19. Thirty-nine patients had mild disease; 19 had severe disease. Urinary TAP was elevated in 26 patients. All patients with severe pancreatitis were correctly identified as having severe disease by an elevated urinary TAP (sensitivity 100%, specificity 77%). The admission Hct was higher than 47 in only three patients, all with mild disease. Of the patients with a rise in Hct, eight had mild disease, and only one had severe disease. Using a Hct of 44 as a cutoff did not affect the accuracy. There was no association between a rise in Hct and failure of Hct to decrease in the determination of severity. In comparison to admission Hct, urinary TAP was more accurate in determining severity in patients with acute pancreatitis by Atlanta, APACHE II, and Ranson criteria. We conclude that urinary TAP is a more accurate predictor of severity in patients with acute pancreatitis compared with Hct. Urinary TAP should be used to determine severity in patients early in the course of acute pancreatitis.

Predicting the Severity of Acute Pancreatitis by Rapid Measurement of Trypsinogen-2 in Urine

Early identification of patients at risk of developing a severe attack of acute pancreatitis (AP) is of great importance because rapid therapeutic interventions improve outcome. At a cutoff of 50 microg/L, trypsinogen-2 measured by a rapid urinary dipstick is a sensitive and specific diagnostic test in AP. The trypsinogen-2 concentration correlates with the severity of the disease, and a test with a higher cutoff might therefore be useful for prediction of disease severity. We increased the detection limit of the urinary trypsinogen-2 test strip (Actim Pancreatitis) from 50 microg/L to 2000 microg/L and evaluated the prognostic value of this test. The results were compared with those obtained with serum C-reactive protein and the acute physiology and chronic health evaluation II (APACHE II) score. The study population consisted of 150 consecutive patients with AP (42 with severe disease). The sensitivity of the rapid urinary test strip (detection limit, 2000 microg/L) for prediction of severe AP, both on admission and at 24 h, was 62%; specificities were 87% and 85%, respectively, positive predictive values were 65% and 62%, and negative predictive values were 85% and 85%. C-Reactive protein had a sensitivity of only 38% on admission, but at 24 h, it was 83%; specificities were 90% and 70%, respectively, whereas positive predictive values were 59% and 52%, and NPVs were 79% and 91%, respectively. On admission the positive-likelihood ratio for the urinary trypsinogen-2 test strip was 4.8, and at 24 h it was 4.2; for C-reactive protein, the values were 3.7 and 2.7, respectively. The urinary trypsinogen-2 dipstick is a simple and rapid method for prediction of severe acute pancreatitis.

Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis. A prospective study

Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis. A prospective study

Évaluation clinique du trypsinogène-2 urinaire par le test rapide Actim pancreatitis™ au cours d'atteintes pancréatiques

Clinical evaluation of urinary trypsinogen-2 by rapid Actim pancreatitis™ test strip in pancreatic diseases. As a means of diagnosis of acute pancreatitis, Actim pancreatitis™ is a rapid test strip of detection of urinary trypsinogen-2 based on the immunochromatography sandwich principle. Serum and urinary amylase and serum lipase were measured in the same time as this urinary trypsinogen-2 test in 200 patients with abdominal pain from which 14 pancreatitis. Test performances were calculated and compared with the results of the enzyme measurements : sensitivity 79 %, specificity 96 %, positive predictive value of 58 % and negative predictive value of 98 %. Negative predictive value and sensitivity are equivalent whereas specificity and positive predictive value are better for the test. A positive result must, more than an elevation of the blood parameters, orientate the diagnosis towards a pancreatic disease. A negative result can pratically rule out this diagnosis. Without suppression of serum amylase and lipase measurements, Actim pancreatitis™ test is an additional element for the diagnosis of acute pancreatitis.

What’s new in the management of acute pancreatitis?

Acute severe pancreatitis remains a disease with multiple complications and high mortality rates. The body of knowledge about clinical pancreatitis is being subjected to rigorous evidence-based analysis, and relevant, practical guidelines have been issued. Great efforts are being made to identify and profile the mediators involved in the systemic hyperinflammatory response to acute pancreatic injury. Lexipafant, a platelet-activating factor antagonist that showed promising results in initial trials, failed to reduce the incidence of new organ failures or mortality in a large double-blind study. The search for an early and accurate prognostic marker for severity persists, with urinary trypsinogen activation peptide as a potentially suitable candidate. Patients with acute pancreatitis do not benefit from anti-secretory therapy with octreotide. Percutaneous, radiological, drainage techniques may eventually play an important role in the management of infected necrosis.

Time-course and clinical value of the urine trypsinogen-2 dipstick test in acute pancreatitis.

Urine trypsinogen-2 has been suggested as a marker of damage due to acute pancreatitis. Our aim was to assess the time-course and the clinical value of this test in acute pancreatitis. A urine trypsinogen-2 dipstick test was performed on 30 patients with acute pancreatitis upon admission to the emergency room, as well as on 30 patients with non-pancreatic acute abdominal pain, and in 30 healthy subjects. In 53.3% of the patients with acute pancreatitis the dipstick test showed abnormal urine trypsinogen-2 whereas this test gave negative results in all patients with non-pancreatic acute abdomen and in all healthy subjects. Patients with severe acute pancreatitis had a frequency of abnormal results of urine trypsinogen-2 (8/9, 88.9%; 95% CI, 51.8-99.7%) significantly higher (P = 0.031) than those with the mild disease (8/21, 38.1%; 95% CI, 18.1 -61.6%), while no significant differences were found in the urine trypsinogen-2 results between patients with biliary acute pancreatitis and those with non-biliary acute pancreatitis. Regarding the time-course of urine trypsinogen-2, there were no significant differences during the three days of the study. The specificity of urine trypsinogen-2 in the diagnosis of acute pancreatitis is good however its sensitivity is low.

Plasma and urinary trypsinogen activation peptide in healthy dogs, dogs with pancreatitis and dogs with other systemic diseases.

To determine the specificity and sensitivity of plasma and urinary trypsinogen activation peptide (TAP) concentrations in diagnosing pancreatitis in dogs. Retrospective analysis of clinical cases. Dogs were classified into three groups: healthy animals, dogs with confirmed pancreatitis and dogs with nonpancreatic disease, which clinically or biochemically resembled pancreatitis. This last group was further subdivided into dogs with renal and those with nonrenal disease. The plasma and urinary TAP concentration was determined by a competitive enzyme immunoassay. Clinical cases additionally had serum trypsin-like immunoreactivity concentration measured, as well as radiography and ultrasound of the abdomen and further diagnostic procedures. Nonparametric analysis of variance (Kruskal-Wallis test) was performed using Statistix 4.0 program. There was a wide range of urinary TAP concentration in healthy dogs (mean 52.30 nmol/L, standard deviation 55.25) that made interpretation of urinary TAP concentrations difficult in the other groups. There was a narrow reference range for plasma TAP (mean 2.67 nmol/L, standard deviation 0.93). Plasma and urinary TAP concentrations, as well as urinary TAP to creatinine ratio, were all increased in dogs that died with necrotising pancreatitis. Values were not increased in mild, interstitial pancreatitis. Increased plasma TAP concentrations were also present in dogs with severe renal disease. Plasma TAP concentration is a good prognostic indicator in naturally occurring pancreatitis in dogs. The failure of TAP to increase in mild pancreatitis, and the increase present in severe renal disease, suggests its measurement has limited application as a sole diagnostic tool for canine pancreatitis. Further investigations are required in order to explain the large variability of urinary TAP concentration and the presence of circulating TAP in healthy dogs.

Early prediction of severity in acute pancreatitis by urinary trypsinogen activation peptide: a multicentre study

There is a pressing clinical requirement for an early simple test of severity in acute pancreatitis. We investigated the use of an assay of trypsinogen activation peptide (TAP). We undertook a multicentre study in 246 patients (172 with acute pancreatitis [35 with severe disease], 74 controls). We assessed the predictive value of urinary TAP concentrations measured by a validated competitive immunoassay. We compared the results with those for plasma C-reactive protein and three clinicobiochemical scoring systems. TAP and C-reactive protein concentrations were analysed at set times after symptom onset and compared with the clinicobiochemical systems scores at key times during hospital stay. At 24 h after symptom onset, the median urinary TAP concentration was 37 nmol/L (IQR 17-110) for severe and 15 nmol/L (5-35) for mild disease (p<0.001). The respective values for plasma C-reactive protein were 24 mg/L (3-34) and 25 mg/L (6-75; p=0.208). The sensitivity, specificity, positive predictive, and negative predictive values of the test to show severe acute pancreatitis compared with mild acute pancreatitis at 24 h were: for TAP (>35 nmol/L), 58%, 73%, 39%, and 86%, respectively, and for C-reactive protein (>150 mg/L), 0%, 90%, 0%, and 75%. 48 h after admission the values for the clinicobiochemical scoring systems were: APACHE II (> or =8), 56%, 64%, 30%, and 85%; Ranson score (> or =3), 89%, 64%, 38%, and 96%; and Glasgow score (> or =3), 77%, 75%, 44%, and 93%. At 48 h, the values for C-reactive protein were 86%, 61%, 37%, and 94% and for TAP were 83%, 72%, 44%, and 94%. Combined testing of C-reactive protein and TAP was not superior to TAP alone for accuracy. Urinary TAP provided accurate severity prediction 24 h after onset of symptoms. This single marker of severity in acute pancreatitis deserves routine clinical application.

Search for prognostic markers for acute pancreatitis

The clinician is poor at predicting the severity of acute pancreatitis at the bedside. 1 Wilson C Heath D Imrie C Prediction of outcome in acute pancreatitis: a comparative study of APACHE II, clinical assessment and multiple factor scoring systems. Br J Surg. 1990; 77: 1260-1264 Crossref PubMed Scopus (415) Google Scholar Consequently there are numerous markers of severity, which have been based on the notion that early prediction improves clinical outcome. There is some evidence for the value of accurately identifying the patient who has or will develop severe pancreatitis in that some patients with severe pancreatitis will benefit from prophylactic antibiotics, 2 Johnson C Antibiotic prophylaxis in severe acute pancreatitis. Br J Surg. 1996; 83: 883-884 Crossref PubMed Scopus (36) Google Scholar enteral nutrition, 3 Windsor A Kanwar S Li A et al. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. Gut. 1998; 42: 431-435 Crossref PubMed Scopus (615) Google Scholar and early endoscopic retrograde cholangio-pancreatography. 4 Fan S Lai E Mok F Lo C Zheng S Wong J Early treatment of acute biliary pancreatitis by endoscopic papillotomy. N Engl J Med. 1993; 328: 228-232 Crossref PubMed Scopus (719) Google Scholar Other reasons for the early prediction of severity of pancreatitis are to identify patients who might benefit from transfer to a specialist centre, to select patients for clinical trials, and to compare results between centres. Early prediction of severity in acute pancreatitis by urinary trypsinogen activation peptide: a multicentre studyUrinary TAP provided accurate severity prediction 24 h after onset of symptoms. This single marker of severity in acute pancreatitis deserves routine clinical application. Full-Text PDF

Do plasma and urine trypsinogen activation peptides (TAP) really increase in trypsin-taurocholate-induced pancreatitis?

Plasma and urine levels of trypsinogen activation peptides (TAP) reflect the severity of acute pancreatitis in experimental and clinical acute pancreatitis. In trypsin-taurocholate-induced pancreatitis in rats, the extrinsic bovine trypsin used for the induction of pancreatitis might influence on the TAP levels after induction of pancreatitis. The aim of the present study was to elucidate whether infused trypsin itself affects TAP levels in trypsin-taurocholate-induced pancreatitis. Rats were divided into three groups. In the pancreatitis group, acute pancreatitis was induced by a retrograde infusion of bovine trypsin and sodium taurocholate into the pancreatic duct. In the duct infusion group and peritoneal injection group, a mixture of bovine trypsin and trypsin inhibitor, ONO-3403, was infused into the pancreatic duct or the peritoneal cavity. Plasma and urine TAP concentration significantly increased in trypsin-taurocholate-induced pancreatitis but not in the duct infusion and peritoneal injection groups for 6 hours after the infusion of trypsin. Serum rat immunoreactive trypsin (IRT) and amylase significantly increased in the pancreatitis and duct infusion groups but not in the peritoneal injection group. Serum levels of bovine IRT in the pancreatitis group was significantly lower than those in duct infusion and peritoneal injection groups. In conclusion, an intraductal infusion of bovine trypsin itself into pancreatic duct does not influence the levels of plasma and urine TAP in trypsin-taurocholate-induced pancreatitis.

Comparison of urine trypsinogen-2 test strip with serum lipase in the diagnosis of acute pancreatitis

Comparison of urine trypsinogen-2 test strip with serum lipase in the diagnosis of acute pancreatitis

Time course and clinical value of Urine trypsinogen-2 in acute pancreatitis

Time course and clinical value of Urine trypsinogen-2 in acute pancreatitis

A multicentre study of early prediction of severity in acute pancreatitis by urinary trypsinogen activation peptide

A multicentre study of early prediction of severity in acute pancreatitis by urinary trypsinogen activation peptide

Bradykinin B2-receptor antagonism attenuates fatal cardiocirculatory breakdown induced by severe experimental pancreatitis.

To investigate the impact of the long-acting bradykinin B2 receptor antagonist HOE 140 (Icatibant) on survival time in a model of severe porcine pancreatitis. Randomized, controlled intervention trial. Thirty domestic pigs of either gender anesthetized by intravenous application of piritramide, midazolam, and pancuronium and mechanically ventilated. Pancreatitis was induced by an injection of sodium taurocholate (5%, 1 mL/kg body weight [BW]) and enterokinase (10 U/kg BW). Control animals (group 1, n = 10) underwent the spontaneous course of the disease. In two treatment groups, Icatibant was administered either in a low (100 nmol/kg BW; group 2, n = 10) or in a high dosage (5000 nmol/kg BW; group 3, n = 10). Mean survival time was significantly prolonged by Icatibant (controls, 6.6 hrs; group 2, 9.8 hrs; p = .022; group 3, 10.9 hrs; p = .007). Six hours postinduction, the decline of total peripheral resistance (52% of baseline) and cardiac index (92% of baseline) in controls was significantly improved by Icatibant, both in the low (16% and 44%; p < .05) and high (6% and 45%; p < .05) dosage. The concentrations of free, nonreceptor-bound kinin in plasma 6 hrs postinduction were significantly lower in controls than in groups 2 and 3 animals (111+/-50 vs. 208+/-40 and 237+/-52 fmol/mL, respectively). Six hours postinduction, the pretreatment with Icatibant was associated with significantly higher plasma concentrations of phospholipase A2 (controls, +1194%; group 2, +2000%; group 3, +2285% of baseline values) and interleukin-1 receptor antagonist (controls, 1900+/-800; group 2, 3100+/-800; group 3, 3600+/-800 pg/mL). In contrast, the increase of urinary trypsinogen activation peptides indicating local pancreatic damage (589+/-114 nmol/L in controls) was substantially attenuated by pretreatment with Icatibant (group 2, 467+/-102, NS; 352+/-91 nmol/L in group 3; p = .022 vs. controls). Systemic inflammatory reactions, however, as quantified by C-reactive protein and the extracellularly discharged neutrophil cytosolic inhibitor leukocyte neutral proteinase inhibitor were not influenced by the bradykinin B2-receptor antagonist. Pretreatment with the bradykinin B2 receptor antagonist Icatibant resulted in prolonged survival time and in delayed impairment of major macrocirculatory and pulmonary variables. Icatibant resulted in elevated concentrations of free, circulating kinin. This was associated with increased concentrations of phospholipase A2 and interleukin-1 receptor antagonist, suggesting that circulating kinins strengthen the activation of some mediator cascades, the association of which with the kinin metabolism requires further experimental clarification. Other variables indicating a systemic inflammatory response (C-reactive protein, leukocyte neutral proteinase inhibitor) remained unaffected by Icatibant. Bradykinin antagonism distinctly ameliorated the local pancreatic damage, indicated by increased urinary concentrations of trypsinogen activation peptides. It is concluded that the kinin metabolism plays an important role in the pathophysiology of systemic complications after severe experimental pancreatitis.

Reliable screening for acute pancreatitis with rapid urine trypsinogen-2 test strip.

This study was designed to evaluate the validity of a new rapid urinary trypsinogen-2 test strip (Actim Pancreatitis) for detection of acute pancreatitis in patients with acute abdominal pain. A total of 525 consecutive patients presenting with abdominal pain at two emergency units was included prospectively and tested with the Actim Pancreatitis test strip. Urine trypsinogen-2 concentrations were also determined by a quantitative method. The diagnosis and assessment of severity of acute pancreatitis was based on raised serum and urinary amylase levels, clinical features and findings on dynamic contrast-enhanced computed tomography. In 45 patients the diagnosis of acute pancreatitis could be established. The Actim Pancreatitis test strip result was positive in 43 of them resulting in a sensitivity of 96 per cent. Thirty-seven false-positive Actim Pancreatitis test strips were obtained in patients with non-pancreatic abdominal pain resulting in a specificity of 92 per cent. Nine patients with severe acute pancreatitis were all detected by the dipstick. A negative Actim Pancreatitis strip result excludes acute pancreatitis with high probability. Positive results indicate the need for further evaluation, i.e. other enzyme measurements and/or radiological examinations. The test is easy and rapid to perform, unequivocal in its interpretation and can be used in healthcare units lacking laboratory facilities.

Rapid Measurement of Urinary Trypsinogen-2 as a Screening Test for Acute Pancreatitis

Acute pancreatitis can be difficult to diagnose. We developed a rapid dipstick screening test for pancreatitis, based on the immunochromatographic measurement of urinary trypsinogen-2. We prospectively compared the urinary trypsinogen-2 dipstick test with a quantitative urinary trypsinogen-2 assay, a urinary dipstick test for amylase, and serum and urinary amylase assays in 500 consecutive patients with acute abdominal pain at two emergency departments. Acute pancreatitis was diagnosed according to standardized criteria. The urinary trypsinogen-2 dipstick test was positive in 50 of the 53 patients with acute pancreatitis (sensitivity, 94 percent), including all 7 with severe pancreatitis. Two patients with urinary trypsinogen-2 concentrations below the sensitivity threshold of the test (50 ng per milliliter) and one with a very high concentration had false negative results. The test was also positive in 21 of the 447 patients without pancreatitis (specificity, 95 percent), including 7 with abdominal cancers, 3 with cholangitis, and 2 with chronic pancreatitis. The sensitivity and specificity of the dipstick test were similar to those of the quantitative urinary trypsinogen-2 assay and higher than those of the urinary amylase dipstick test. The serum amylase assay had a sensitivity of 85 percent (with a cutoff value of 300 U per liter for the upper reference limit) and a specificity of 91 percent. The sensitivity and specificity of the urinary amylase assay (cutoff value, 2000 U per liter) were 83 and 88 percent, respectively. In patients with acute abdominal pain seen in the emergency department, a negative dipstick test for urinary trypsinogen-2 rules out acute pancreatitis with a high degree of probability. A positive test usually identifies patients in need of further evaluation.

Urinary trypsinogen activation peptide (TAP) predicts severity in patients with acute pancreatitis.

Urinary TAP obtained within the first 48 h of the onset of symptoms can distinguish patients with severe acute pancreatitis. Urinary trypsinogen activation peptide (TAP) has recently been described as an early marker of severity in acute pancreatitis. In a multicenter study, urine samples were collected for TAP concentration at 6-12, 24, and 48 h after admission from 139 patients with acute pancreatitis (99 with mild disease, 40 with severe disease) and from 50 control patients. Severity of acute pancreatitis was defined by the presence of organ failure and/ or pancreatic necrosis on dynamic contrast-enhanced computed tomography. Median urinary TAP in the 139 patients with acute pancreatitis compared to the 50 control patients was significantly higher at admission, 4.6 vs 0.8 ng/mL (p < 0.001), and 6-12 h, 1.9 vs 0.55 ng/mL (p = 0.04). Among patients who presented within 48 h of the onset of symptoms, the median urinary TAP for severe pancreatitis (9 patients) compared to mild pancreatitis (40 patients) was significantly higher at admission, 29.6 vs. 3.6 ng/mL (p = 0.001). Also, when obtained within 48 h of the onset of symptoms, all patients with severe pancreatitis had an admission urinary TAP level > 10 ng/mL. The sensitivity and specificity of an admission urinary TAP > or = 10 for severe pancreatitis was 100 and 85%, respectively. Given a cutoff of 10 ng/mL for an admission urinary TAP obtained within 48 h of the onset of symptoms, the negative predictive value was 100% for mild pancreatitis.

Urine trypsinogen-2 as marker of acute pancreatitis

We examined the clinical utility of urine trypsinogen-2 as a marker of acute pancreatitis (AP). Fifty-nine patients with AP, 42 with acute abdominal diseases of extrapancreatic origin, and 63 without evidence of acute abdominal disease were studied. Urine trypsinogen-2 was determined by a time-resolved immunofluorometric assay. As reference methods we used serum trypsinogen-2, urine amylase, and serum amylase. The diagnostic accuracy of the markers was evaluated by receiver-operating characteristic (ROC) analysis. At admission, urine trypsinogen-2 differentiated patients with AP from controls with high accuracy. The area under the ROC curve (AUC) was 0.978, which was equal to that of serum trypsinogen-2 (0.998) and serum amylase (0.969) and significantly larger than that of urine amylase. For differentiation between severe and mild AP, urine trypsinogen-2 (0.730) was equal to serum trypsinogen-2 (0.721), and clearly better than amylase in serum and urine. These results suggest that determination of urine trypsinogen-2 is a useful test to detect AP and to evaluate disease severity.

Urinary Trypsinogen Activation Peptides (TAP) Are Not Increased in Mild ERCP-Induced Pancreatitis

Acute pancreatitis following endoscopic retrograde cholangiopancreatography (ERCP) occurs in 3-18% of patients undergoing either diagnostic or therapeutic ERCP. We prospectively measured urinary trypsinogen activation peptides (TAP) by an automated anti-TAP enzyme-linked immunoassay among 107 patients 4 h after ERCP to determine whether this measurement helps in the early diagnosis of ERCP-induced pancreatitis. Pancreatitis was documented in 10 of 107 patients (9.3%). All episodes were graded as mild. Urinary TAP was not significantly increased. We conclude that measurement of urinary TAP 4 h after ERCP is not helpful in documenting mild ERCP-induced acute pancreatitis.