Lack of association between anticardiolipin antibodies and migraine in systemic lupus erythematosus

Montalbán, J; Cervera, Ricard; Font, Josep; Ordi, J; Vianna, J. L.; Haga, Hans‐Jacob; Tintoré, Mar; Khamashta, M. A.; Hughes, G. R. V.

doi:10.1212/wnl.42.3.681

Cited by 68 publications

(48 citation statements)

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“…To further complicate matters, the high prevalence of migraine in healthy populations (6%-12%) 123 and its even higher prevalence in populations also prone to DIAM, such as patients with SLE, should be considered. 124,125 …”

Section: Underlying Conditions In Patients With Diammentioning

confidence: 99%

The Challenge of Drug-Induced Aseptic Meningitis

Morís¹,

1999

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Several drugs can induce the development of aseptic meningitis. Drug-induced aseptic meningitis (DIAM) can mimic an infectious process as well as meningitides that are secondary to systemic disorders for which these drugs are used. Thus, DIAM constitutes a diagnostic and patient management challenge. Cases of DIAM were reviewed through a MEDLINE literature search (up to June 1998) to identify possible clinical and laboratory characteristics that would be helpful in distinguishing DIAM from other forms of meningitis or in identifying a specific drug as the culprit of DIAM. Our review showed that nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, intravenous immunoglobulins, and OKT3 antibodies (monoclonal antibodies against the T3 receptor) are the most frequent cause of DIAM. Resolution occurs several days after drug discontinuation and the clinical and cerebrospinal fluid profile (neutrophilic pleocytosis) do not allow DIAM to be distinguished from infectious meningitis. Nor are there any specific characteristics associated with a specific drug. Systemic lupus erythematosus seems to predispose to NSAID-related meningitis. We conclude that a thorough history on prior drug intake must be conducted in every case of meningitis, with special focus on those aforementioned drugs. If there is a suspicion of DIAM, a third-generation cephalosporin seems a reasonable treatment option until cerebrospinal fluid cultures are available.

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Section: Underlying Conditions In Patients With Diammentioning

confidence: 99%

The Challenge of Drug-Induced Aseptic Meningitis

Morís¹,

1999

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“…Ocular disturbances (amaurosis fugax [2,13] and optic atrophy [2]), multiinfarct dementia, dementia of nonischemic origin (6,14,15), and chorea (16) have also been reported in patients with primary APS. Controversial reports exist regarding a similar association with nonspecific and migraine headaches (17,18), transverse myelitis (3,19), and Guillain-Barre syndrome (20).…”

Section: Introductionmentioning

confidence: 99%

Neurological dysfunction and hyperactive behavior associated with antiphospholipid antibodies. A mouse model.

Ziporen¹,

Shoenfeld²,

Levy³

et al. 1997

J. Clin. Invest.

117

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“…Some authors suggested that interaction between aPL and neurotransmitters might lead to a lower threshold for the development of epileptic crisis [13]. Whether migraine is associated with aPL is still controversial, with most studies failing to find any association [14,15]. In our experience, there is a higher prevalence of headache in patients with aPL than in the normal population, but aPL are not associated with any particular type of cephalea [16].…”

Section: Introductionmentioning

confidence: 90%

Antiphospholipid syndrome

Cuadrado

López‐Pedrera

2003

Clin Exp Med

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The antiphospholipid syndrome (APS) was reported in the early 1980s as the association of thrombosis, recurrent pregnancy loss in the presence of anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LA). Since then, many other clinical manifestations have been associated with aPL. Almost any organ and tissue may be involved in the disease, including the brain, the heart, the kidneys, the placenta and many more. aPL are a heterogeneous group of autoantibodies that are detected by immunoassays and functional coagulation tests. The antigenic targets are negatively charged phospholipids and serum phospholipid-binding proteins. Despite the strong association between aPL and thrombosis, the pathogenic role of aPL in the development of thrombosis has not been fully elucidated. Proposed mechanisms include antibody-mediated interference with coagulation homeostasis, activation of platelets and endothelial cells and a T-cell immune response to serum phospholipid-binding proteins. The mainstay of therapy is anticoagulation, whereas immunosuppression seems to be ineffective. Recommendations for the management of thrombosis in the antiphospholipid antibody syndrome have been based largely on retrospective case series. Several prospective clinical trials are currently underway and their results will probably lead to a more precise therapeutic approach of this problem.

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Lack of association between anticardiolipin antibodies and migraine in systemic lupus erythematosus

Cited by 68 publications

References 0 publications

The Challenge of Drug-Induced Aseptic Meningitis

The Challenge of Drug-Induced Aseptic Meningitis

Neurological dysfunction and hyperactive behavior associated with antiphospholipid antibodies. A mouse model.

Antiphospholipid syndrome

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