What are the approach considerations in the diagnosis of CNS lupus?

Updated: May 04, 2021
  • Author: Pradeep C Bollu, MD; Chief Editor: Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM  more...
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Conventional blood studies have varying utility in diagnosing systemic lupus erythematosus (SLE), depending on the associated conditions and manifestations. With systemic or other organ system involvement suggestive of autoimmune dysfunction (e.g., low-grade fevers, fatigue, arthralgias or arthritis, renal dysfunction, malar or other skin rashes) laboratory evaluation should include at minimum antinuclear antibody (ANA) testing and anti-DNA binding to confirm a positive ANA result. Other autoantibody testing is dependent on clinical judgment and test availability.

In the patient with SLE who has risk factors for conventional small-vessel cerebrovascular disease (e.g., diabetes, hypertension), the clinical distinction between SLE and atherosclerotic (lipohyalinoid) disease as a cause of a given stroke may be difficult. Under these circumstances, additional studies such as lumbar puncture for evidence of central nervous system (CNS) inflammation, antinuclear antibodies (ANAs), or intrathecal immunoglobulin (IgG) synthesis may support a diagnosis of SLE over atherosclerotic small vessel disease. Clinical–radiologic correlations are not always obvious; more importantly, magnetic resonance imaging (MRI) lesions may resolve completely within days in keeping with clinical improvement or persist despite clear remission.

The complete blood cell (CBC) count in SLE may demonstrate a hemolytic anemia with reticulocytosis or reductions of neutrophils, lymphocytes, or platelets.

Although Fcgamma receptor genes have been suggested to play an important role in the pathogenesis of SLE and lupus nephritis, Yuan et al's study results suggested that FcgammaRIIIb polymorphism might not be a susceptibility gene for SLE and lupus nephritis. [24]

AlSaleh et al reported a high prevalence of positive anti-Ro antibodies (52.3%) among their Arab patients, which they felt probably reflected a common characteristic in SLE patients of Middle East origin. [25]

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