Fot. Akenami et al., CEREBROSPINAL-FLUID PLASMINOGEN-ACTIVATOR INHIBITOR-1 IN PATIENTS WITH NEUROLOGICAL DISEASE, Journal of Clinical Pathology, 50(2), 1997, pp. 157-160
Aim--To study cerebrospinal fluid (CSF) concentrations of plasminogen
activator inhibitor type-1 (PAI-1) in patients with neurological disea
se. Methods-CSF PAI-1 concentrations were measured in 51 patients with
neurological disease and 20 reference subjects using an ELISA. The pa
tient group comprised three patients with viral meningitis, 20 with en
cephalitis, nine with acute lymphoblastic (n = 7) and myeloid (n = 2)
leukaemia (with central nervous system involvement), and 19 with multi
ple sclerosis. Results-Raised PAI-1 concentrations were observed in pa
tients with leukaemia, encephalitis and multiple sclerosis. There was
no difference in the mean concentrations of PAI-1 in patients with men
ingitis when compared with the reference subjects. The highest mean (S
EM) PAI-1 concentration was found in patients with leukaemia (1.28 (0.
36) ng/ml), and the next highest in those with encephalitis (1.19 (0.2
0) ng/ml). These values were much higher than those in patients with v
iral meningitis. In a previous report, raised CSF tissue-type plasmino
gen activator (tPA) activities were detected in patients with multiple
sclerosis, leukaemia and encephalitis, with mean activities in decrea
sing order. PAI-1 concentrations in the same patients were the reverse
of their corresponding tPA activities, being higher in those with leu
kaemia and encephalitis, than in patients with multiple sclerosis. The
re was no association between CSF PAI-1 concentrations and age in eith
er patients or controls. Similarly, there was no association between C
SF PAI-1 concentrations and urokinase-type plasminogen activator (uPA)
. Conclusions--Raised CSF PAI-1 concentrations may be used as a non-sp
ecific marker of neurological disease. Moreover, PAI-1 may play an imp
ortant role in regulating the functions of tPA, and probably uPA, in C
SF.