Cerebrospinal fluid and serum antiphospholipid antibodies in multiple sclerosis, Guillain-Barré syndrome and systemic lupus arythematosus

Marchiorji, Paulo E.; Reis, Marisa dos; Quevedo, Maria Eugenia; Callegaro, D.; Hirata, Motoe; Scaff, Milberto; Oliveira, Ricardo Manoel de

doi:10.1590/s0004-282x1990000400010

Cited by 20 publications

(18 citation statements)

References 7 publications

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“…One study has been done in Behçet's disease [26] and three studies in SLE [4,27,28]. Fields et al [4] did not detect aCL in the CSF of five SLE patients (in four patients aCL was present in sera).…”

Section: Discussionmentioning

confidence: 99%

“…Fields et al [4] did not detect aCL in the CSF of five SLE patients (in four patients aCL was present in sera). Marchiori et al [27] detected aCL in CSF in 15 of 30 SLE patients, whereas Martinez-Cordero et al [28] detected aCL in CSF in 10 of 16 acute NP-SLE patients (in eight patients aCL was present in sera) and in two of 16 SLE patients with headaches (in no cases was aCL present simultaneously in the serum). In our study aCL was not detected in any patient, neither in the six seropositive for aCL nor in the nine who were seronegative.…”

Section: Discussionmentioning

confidence: 99%

“…In Fields et al's. study [4] both CSF and sera were diluted 1:100; Marchiori et al [27] gave no information on the dilution of the CSF used. In our study the sera were diluted 1:50 (according to the original Gharavi method [18]) and the CSF was not diluted.…”

Section: Discussionmentioning

confidence: 99%

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Evaluation of Cerebrospinal Fluid for the Presence of Anticardiolipin Antibodies (aCL) in NP-SLE Patients

Jędryka-Góral

Ząbek

Wojciechowska

et al. 2000

Clinical Rheumatology

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Many neurological or psychiatric manifestations of SLE (NP-SLE) are related to the presence of anticardiolipin antibodies (aCL) in the patient's sera. The aim of this study was to evaluate the presence of aCL in cerebrospinal fluid (CSF) in SLE patients with NP features. Fifteen SLE patients were studied, all with NP features. CSF was evaluated for intrathecal IgG synthesis, oligoclonal IgG, and blood-brain barrier impairment. Sera and CSF were tested by ELISA for the presence of aCL-IgG and aCL-IgM with and without beta2 glycoprotein (beta2 GPI) cofactor. CSF and sera of 50 low back pain patients served as controls. Six patients were aCL(+) and nine aCL(-). In all patients the general CSF examination was normal. In all patients the value of indices of intrathecal IgG synthesis were normal but oligoclonal protein was present in the CSF of three patients. In none of the patients was the blood-brain barrier impaired. Neither aCL-IgG nor aCL-IgM was detected in the CSF of any NP-SLE patient. Mean levels of aCL in patients without cofactor beta2 GPI and with cofactor were as follows: for IgG class 0.005 and 0.057 OD (negative); for IgM class 0.004 and 0.024 OD (negative). We could not detect aCL in the CSF of patients with NP-SLE, even if sera were positive for aCL.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Evaluation of Cerebrospinal Fluid for the Presence of Anticardiolipin Antibodies (aCL) in NP-SLE Patients

Jędryka-Góral

Ząbek

Wojciechowska

et al. 2000

Clinical Rheumatology

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“…Although there are some studies which associated a high CSF total protein or leukocyte cell count with a worse prognosis [13], most authors agree that routine CSF findings are of no value for improving prognostic accuracy in GBS [18,38,66,78]. [40]. These findings were demonstrated to be unspecific of GBS, as similar antibody levels were observed in MS, and to a lower extent in SLE.…”

Section: ■ Csf Basic Findingsmentioning

confidence: 99%

Cerebrospinal fluid biomarkers in Guillain-Barré syndrome – Where do we stand?

Brettschneider

Petzold²,

Süßmuth

et al. 2009

J Neurol

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Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy affecting the myelin-protein sheathing and the axons themselves to various degrees. Damage to these structures causes biomarkers to be released into the adjacent body fluid compartment. In case of the proximal nerve roots these biomarkers diffuse into the cerebrospinal fluid (CSF). Here we review the literature on CSF biomarkers in GBS, including a discussion of CSF basic findings, myelin sheath-associated markers (myelin basic protein), axonal damage markers (neurofilaments, tau, anti-ganglioside antibodies), glial and neuronal markers (neuron specific enolase, 14-3-3 proteins, S100B, hypocretin-1), immunological markers (different chemokines and complement factors, cystatin C, tumor necrosis factor-alpha) as well as recent advances in the field of CSF proteome analysis in GBS. Second, the different pathophysiological mechanisms reflected by these biomarkers are discussed. Finally, candidate biomarkers are reviewed with regard to their clinical relevance to act as a surrogate for the disease process, their value for improving prognostic accuracy and their potential to be used as predictors of treatment response.

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“…A stronger association between aPL and neurological disorders might be easier to establish if aPL are sought and detected in the cerebral spinal fluid (CSF) of patients experiencing neurologic symptoms. Historically, scarce reports of aPL in CSF are limited mostly to IgG and IgM anticardiolipin (aCL) detection (Marchiorri, 1990;Lolli et al, 1991;Wang et al, 1992;Gallo et al, 1994;Yeh et al, 1994;Martinez-Cordero, 1997;Jedryka-Goral et al, 2000;Lai and Lan, 2000;Baraczka et al, 2002). Rarely are IgA aCL sought (Wang et al, 1992).…”

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confidence: 99%

Testing for Antiphospholipid Antibody (aPL) Specificities in Retrospective “Normal” Cerebral Spinal Fluid (CSF)

Sokol

Wagenknecht

McIntyre

2004

Journal of Immunology Research

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Antiphospholipid antibodies (aPL) have been found in the blood of patients with systemic and neurological disease. The rare reports of aPL in cerebral spinal fluid (CSF) have been limited mostly to IgG and IgM anticardiolipin (aCL). Our published finding of IgA aPE in the CSF of a young stroke victim prompted us to establish "normal" CSF aPL values for a panel of aPL, which included aCL, antiphosphatidylserine (aPS), antiphosphatidylethanolamine (aPE) and antiphosphatidylcholine (aPC). CSF samples were tested by ELISA for IgG, IgM and IgA aPL. In addition, the CSF samples were tested for activity in the presence and absence of phospholipid (PL) binding plasma-proteins. A total of 24 data points were obtained for each CSF sample. We tested 59 CSF samples obtained from 59 patients who were undergoing evaluation for systemic or neurologic diseases. All CSF samples had normal protein, glucose and cell counts. Ten of the 59 CSF samples (17%) had elevated aPL optical density (OD) values an order of magnitude higher than the other 49 CSF samples for one or more aPL specificity and/or isotype. One CSF sample had both PL-binding protein dependent and independent IgG aPE activity. Another CSF sample showed both IgG aPE and aPC reactivity. The remaining eight CSF samples showed single aPL findings; IgG aPE (5), IgG aPC (1), IgG aCL (1) and IgM aPC (1). Seven of 10 patients with elevated CSF values were females. As expected, most "normal" aPL OD values were substantially lower in CSF than those we have reported in blood samples from volunteer blood donors. Jacobson et al., 1999). The associations of aPL with neurologic conditions other than thromboocclusive events have been considered "weak" and attributable to an "epiphenomenon" rather than to pathophysiologic mechanisms (Brey, 2000). A stronger association between aPL and neurological disorders might be easier to establish if aPL are sought and detected in the cerebral spinal fluid (CSF) of patients experiencing neurologic symptoms. Historically, scarce reports of aPL in CSF are limited mostly to IgG and IgM anticardiolipin (aCL) detection (Marchiorri, 1990;Lolli et al., 1991;Wang et al., 1992;Gallo et al., 1994;Yeh et al., 1994;Martinez-Cordero, 1997;Jedryka-Goral et al., 2000;Lai and Lan, 2000;Baraczka et al., 2002). Rarely are IgA aCL sought (Wang et al., 1992). To our knowledge only one report included testing for IgG and IgM antiphosphatidylserine (aPS) and antiphosphatidylethanolamine (aPE) in CSF; the results were negative (Gallo et al., 1994). Our finding of IgA aPE in the CSF of a young stroke victim (Sokol et al., 2000), together with our intent to continue testing additional CSF samples, prompted us to undertake and establish "normal" aPL values for CSF. Our findings form the basis of this report. PATIENTS AND METHODSBecause of the potential risks associated with spinal taps to healthy individuals we were unable to obtain CSF samples from random donors. We opted to perform a retrospective analysis using residual CSF that was collected for diagnostic purposes a...

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Cerebrospinal fluid and serum antiphospholipid antibodies in multiple sclerosis, Guillain-Barré syndrome and systemic lupus arythematosus

Cited by 20 publications

References 7 publications

Evaluation of Cerebrospinal Fluid for the Presence of Anticardiolipin Antibodies (aCL) in NP-SLE Patients

Evaluation of Cerebrospinal Fluid for the Presence of Anticardiolipin Antibodies (aCL) in NP-SLE Patients

Cerebrospinal fluid biomarkers in Guillain-Barré syndrome – Where do we stand?

Testing for Antiphospholipid Antibody (aPL) Specificities in Retrospective “Normal” Cerebral Spinal Fluid (CSF)

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