Abstract
Systemic lupus erythematosus (SLE) and antiphospholipid syndrome have an increased risk to develop cognitive impairment. A possible role for antiphospholipid antibodies (aPL) and antiglutamate receptor (anti-NMDA) antibodies in the pathogenesis of neurological manifestations of these two conditions, have been suggested. In particular, the role of anti-NMDA antibodies in the pathogenesis of neuropsychiatric SLE is supported by several experimental studies in animal models and by the finding of a correlation between anti-NMDA positivity in cerebrospinal fluid and neurological manifestations of SLE. However, data from the literature are controversial, as several studies have reported a correlation of these antibodies with mild cognitive impairment in SLE, but more recent studies have not confirmed this finding. The synergism between anti-NMDA and other concomitant autoantibodies, such as aPL, can be hypothesized to play a role in inducing the tissue damage and eventually the functional abnormalities. In line with this hypothesis, we have found a high incidence of at least one impaired cognitive domain in a small cohort of patients with primary APS (PAPS) and SLE. Interestingly, aPL were associated with low scoring for language ability and attention while anti-NMDA titers and mini-mental state examination scoring were inversely correlated. However, when patients were stratified according to the presence/absence of aPL, the correlation was confirmed in aPL positive patients only. Should those findings be confirmed, the etiology of the prevalent defects found in PAPS patients as well as the synergism between aPL and anti-NMDA antibodies would need to be explored.
Highlights
Systemic lupus erythematosus (SLE) is a chronic disease characterized by antibodies directed to different components of the cell nucleus in association with a variety of clinical manifestations, including skin rash, arthritis, serositis, nephritis, hematological cytopenias, and neurological manifestations
Treatment of SLE largely depends on the type of clinical manifestations: antimalarial agents in association with low-dose steroids represent the first choice in mild disease, while immunosuppressant agents, such as azathioprine, methotrexate, cyclophosphamide, and mycophenolate mofetil are used in more severe manifestations
The formal classification of Antiphospholipid syndrome (APS) requires the persistent presence of medium to high titers of antiphospholipid antibodies, namely anti-β2 glycoprotein I, anticardiolipin, and lupus anticoagulant (LA) (2)
Summary
Systemic lupus erythematosus (SLE) is a chronic disease characterized by antibodies directed to different components of the cell nucleus in association with a variety of clinical manifestations, including skin rash, arthritis, serositis, nephritis, hematological cytopenias, and neurological manifestations. The prevalence ranges from 15 to 50 cases per 100,000 persons and the incidence is around 2–8 new cases per 100,000 persons per year. Antiphospholipid syndrome (APS) is a systemic autoimmune disease close to SLE with significant overlap of serological and clinical characteristics (2). It is mainly characterized by pregnancy complications and thrombotic events, involving both the venous and the arterial district (2). Hydroxychloroquine, statins, rituximab, and eculizumab can be considered in refractory cases (3)
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