Tissue plasminogen activator and plasminogen activator inhibitor-1 in human choledochal bile

Fibrinolytic properties have been detected in animal and human gallbladder (GB) bile. Plasminogen activator inhibitor-1 (PAI-1) has been reported in g reater concentration in GB stone bile and may be a nucleating factor in the pathogenesis of GB stone formation. it is unknown whether or not human cho ledochal bile has similar properties, which could have a role in choledocho lithiasis. The aims of this study were to determine the presence of fibrino lytic properties of human choledochal bite and to compare those properties among normal, acalculous, and calculous-infected choledochal bile. Tissue p lasminogen activator (t-PA) and PAI-1 of choledochal bile were measured by enzyme linked immunosorbent assay in patients with cholangitis due to acalc ulous bile duct obstructions (n=9), choledocholithiasis with cholangitis (n =20), and normal bile (n=7). The t-PA concentration of choledochal bile was no different among the three groups (acalculous-infected bile, median 4.61 ng/ml, and calculous-infected bile, 4.61 ng/ml, versus normal bile, 7.33 n g/ml). PAI-1 was detected in choledochal bile in significantly greater conc entrations in patients with acalculous cholangitis due to bile duct obstruc tions and choledocholithiasis with cholangitis (acalculous-infected bile, m edian 0.36 ng/ml, and calculous-infected bile, 0.1 ng/ml, versus normal bil e, 0.02 ng/ml, p<0.05), but the bile concentration of PAI-1 was no differen t between the acalculous and calculous-infected choledochal bile. Human cho ledochal bile possesses t-PA and PAI-1. PAI-1 was present in greater concen trations in both acalculous and calculous-infected choledochal bile. Increa sed levels of PAI-1 may be an epiphenomenon of cholangitis rather than a fa ctor in the pathogenesis of choledocholithiasis.