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Relationship between elevated cerebrospinal fluid levels of plasminogen activator inhibitor 1 and neuronal destruction in patients with neuropsychiatric systemic lupus erythematosus.

Artikel i vetenskaplig tidskrift
Författare Jakub Kwiecinski
Marcin Kłak
Estelle Trysberg
Kaj Blennow
Andrej Tarkowski
Tao Jin
Publicerad i Arthritis and rheumatism
Volym 60
Nummer/häfte 7
Sidor 2094-101
ISSN 0004-3591
Publiceringsår 2009
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 2094-101
Språk en
Länkar dx.doi.org/10.1002/art.24603
Ämnesord Adolescent, Adult, Aged, Case-Control Studies, Cross-Sectional Studies, Female, Fibrin Fibrinogen Degradation Products, cerebrospinal fluid, Humans, Lupus Vasculitis, Central Nervous System, cerebrospinal fluid, pathology, Magnetic Resonance Imaging, Male, Middle Aged, Nerve Degeneration, pathology, Neurons, pathology, Plasminogen Activator Inhibitor 1, cerebrospinal fluid, Tissue Polypeptide Antigen, cerebrospinal fluid, Urokinase-Type Plasminogen Activator, cerebrospinal fluid, Young Adult
Ämneskategorier Reumatologi och inflammation

Sammanfattning

OBJECTIVE: A homeostatic imbalance between coagulation and fibrinolysis might occur intrathecally in neuropsychiatric systemic lupus erythematosus (NPSLE). However, there are no published data on levels of fibrinolytic factors in the cerebrospinal fluid (CSF) of patients with NPSLE. The present study was undertaken to assess CSF levels of fibrinolytic molecules, including urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), D-dimer, and plasminogen activator inhibitor 1 (PAI-1), in SLE patients with clinically verified neuropsychiatric involvement and to compare these levels with those in SLE patients without neuropsychiatric involvement and in healthy subjects. METHODS: Levels of uPA, tPA, and PAI-1 were assessed in CSF from 94 patients with SLE (33 who had NPSLE, 56 who did not have NPSLE, and 5 who were positive for antiphospholipid antibody [not included in the NPSLE or non-NPSLE group]) and from 53 age-matched controls. Patients were evaluated clinically, with magnetic resonance imaging of the brain, analyses of neuronal/glial degradation products in CSF, and neuropsychiatric testing. RESULTS: In the group of patients with NPSLE, intrathecal PAI-1 levels were significantly elevated compared with levels in SLE patients without overt neuropsychiatric involvement (P < 0.05) and in healthy controls (P < 0.001). In contrast, intrathecal levels of uPA did not differ significantly. Intrathecal levels of PAI-1 correlated significantly with CSF levels of interleukin-6 (IL-6) (r = 0.34, P < 0.001) and IL-8 (r = 0.33, P < 0.001). Importantly, increased PAI-1 and D-dimer levels were observed in SLE patients who had pathologically elevated levels of glial fibrillary acidic protein, neurofilament triplet protein, and tau protein in CSF. CONCLUSION: Intrathecal release of PAI-1 is increased in patients with NPSLE. This results in impaired fibrinolysis, which might contribute to neuronal and astrocytic damage in NPSLE.

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