Trypsinogen activation peptides (TAP) in peritoneal fluid as predictors oflate histopathologic injury in necrotizing pancreatitis of the rat

Citation
J. Schmidt et al., Trypsinogen activation peptides (TAP) in peritoneal fluid as predictors oflate histopathologic injury in necrotizing pancreatitis of the rat, DIG DIS SCI, 44(4), 1999, pp. 823-829
Citations number
39
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTIVE DISEASES AND SCIENCES
ISSN journal
01632116 → ACNP
Volume
44
Issue
4
Year of publication
1999
Pages
823 - 829
Database
ISI
SICI code
0163-2116(199904)44:4<823:TAP(IP>2.0.ZU;2-3
Abstract
The levels of trypsinogen activation peptides (TAP) were quantified by ELIS A immunoassay in acute pancreatitis of the rat and compared to the degree o f late histopathological sequelae and exocrine functional impairment 4 and 12 weeks after the acute phase of the disease. For this purpose acute pancr eatitis of different severity was induced using a suitable rat model recent ly described. Forty five surviving animals were studied. The level of TAP i n peritoneal exudate measured 3 and 6 hr after pancreatitis induction corre lated well with the amount of the late histopathological injury at the end of the corresponding observation period (at 4 weeks after 3 hr: r = 0.75, P = 0.003, after 6 hr: r = 0.72, P = 0.005, Pearson; and at 12 weeks after 3 hr: r = 0.86, P = 0.0001, after 6 hr: r = 0.84, P = 0.0001, Pearson). A ne gative correlation of TAP with the impairment of exocrine function was foun d only at 4 weeks for the secretion of total protein (r = -0.76 after 3 hr; r = -0.62 after 6 hr) and for exocrine function (r = -0.67 after 3 hr, r = -0.57 after 6 hr), but not at 12 weeks after acute pancreatitis. No correl ation with plasma amylase and lipase was found. We conclude that quantitati on of TAP in ascites provides an accurate prediction of late histopathologi c sequelae. Pancreatic exocrine function could be predicted by TAP assay on ly in the early stage after pancreatitis induction leg, four weeks). In lat er stages of the disease leg, 12 weeks) remaining pancreatic tissue seems t o compensate for any exocrine deficits that have occurred.