CEREBROSPINAL-FLUID PLASMINOGEN-ACTIVATOR INHIBITOR-1 IN PATIENTS WITH NEUROLOGICAL DISEASE

Citation
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
Citations number
33
Categorie Soggetti
Pathology
ISSN journal
00219746
Volume
50
Issue
2
Year of publication
1997
Pages
157 - 160
Database
ISI
SICI code
0021-9746(1997)50:2<157:CPIIPW>2.0.ZU;2-0
Abstract
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.