Related Experiment Videos
Neuropsychiatric lupus erythematosus, cerebral infarctions, and anticardiolipin antibodies
R A Fields1, W L Sibbitt, H Toubbeh
1Department of Medicine, University of New Mexico School of Medicine, Albuquerque 87131.
Insights
Anticardiolipin antibody (aCL) may correlate with cerebral infarcts in systemic lupus erythematosus (SLE) patients. However, aCL is unlikely to directly cause diffuse encephalopathy in central nervous system lupus.
Area of Science:
- Neurology
- Immunology
- Rheumatology
Background:
- Systemic lupus erythematosus (SLE) is an autoimmune disease with diverse clinical manifestations.
- Anticardiolipin antibody (aCL) is linked to thromboembolic events in SLE patients.
- The role of aCL in central nervous system (CNS) manifestations of SLE remains unclear.
Observation:
- Serum and cerebrospinal fluid samples were analyzed from five SLE patients with acute CNS symptoms.
- Anticardiolipin antibody (aCL) was detected in the serum of four out of five patients.
- No aCL was found in the cerebrospinal fluid of any patient.
Findings:
- Nuclear magnetic resonance imaging revealed "infarct-like" lesions in the brains of the four patients with detectable serum aCL.
- A potential correlation between serum aCL and cerebral infarcts in CNS lupus is suggested.
- The study indicates aCL may not have a direct pathogenic role in diffuse encephalopathy associated with acute CNS lupus.
Implications:
- This research highlights a possible association between serum aCL and ischemic stroke in SLE.
- Further investigation is warranted to elucidate the precise mechanisms linking aCL to CNS involvement in SLE.
- Findings suggest focusing on systemic rather than direct CNS pathogenic roles for aCL in SLE-related encephalopathy.
Abstract:
Anticardiolipin antibody (aCL) has been associated with thromboembolic phenomena, including stroke, in certain patients with systemic lupus erythematosus (SLE); however, the relation between this antibody and the central nervous system manifestations of SLE is unknown. Serum samples and cerebrospinal fluid from five patients with SLE and acute central nervous system manifestations were assayed for the presence of aCL. Anticardiolipin antibody was identified in sera from four of the five patients but in none of the cerebrospinal fluid samples. Nuclear magnetic resonance imaging showed 'infarct-like' lesions in these four patients. This preliminary study suggests that a correlation between serum aCL and cerebral infarcts in central nervous system lupus may potentially exist. From this limited study it seems unlikely that aCL has a direct pathogenic role in the diffuse encephalopathy of acute central nervous system lupus.