SERUM PANCREATIC PHOSPHOLIPASE-A(2) AND PROPHOSPHOLIPASE-A(2) IN ACUTE-PANCREATITIS AND AFTER ENDOSCOPIC RETROGRADE PANCREATOGRAPHY

Citation
K. Yamamoto et al., SERUM PANCREATIC PHOSPHOLIPASE-A(2) AND PROPHOSPHOLIPASE-A(2) IN ACUTE-PANCREATITIS AND AFTER ENDOSCOPIC RETROGRADE PANCREATOGRAPHY, Gastroenterologia Japonica, 28(5), 1993, pp. 679-686
Citations number
NO
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
04351339
Volume
28
Issue
5
Year of publication
1993
Pages
679 - 686
Database
ISI
SICI code
0435-1339(1993)28:5<679:SPPAPI>2.0.ZU;2-6
Abstract
Serum immunoreactive pancreatic phospholipase A2 (IP-PLA2) levels and the proportion of active pancreatic PLA2 in the serum IP-PLA2 were det ermined by radioimmunoassay with an antibody directed against active h uman PLA2. The subjects of this study included eight patients who unde rwent endoscopic retrograde pancreatography (ERP), nine patients with acute pancreatitis, and six healthy controls. The serum IP-PLA2 levels were elevated after ERP and during acute pancreatitis. The amount of active pancreatic PLA2 in the serum was determined after its separatio n from pancreatic prophospholipase A2 using reverse-phase high-perform ance liquid chromatography (HPLC). The serum IP-PLA2 was separated int o two peaks on reverse-phase HPLC. The one which eluted faster contain ed the PLA2 activity; the other peak did not. The latter IP-PLA2 peak consisted of pancreatic prophospholipase A2 as judged by HPLC analysis and PLA2 activity determination of the products after treatment with trypsin. The proportion of active pancreatic PLA2 in the serum IP-PLA2 of patients after ERP (13.9+/-0.5%) increased slightly compared with that in fasting, healthy controls (8.0+/-1.1%). For those with acute p ancreatitis, the proportion of active pancreatic PLA2 within 48 hours of hospital admission increased more markedly (44.0+/-5.7%) than that after ERP. These findings demonstrate that the proportion of active pa ncreatic PLA2 in the serum IP-PLA2 markedly increases during the early atage of acute pancreatitis, and that an ERP-induced rise in the intr aductal pressure leads to the leakage of pancreatic PLA2 into the circ ulation, but not to a marked activation of the leaked enzyme.