Laboratory Findings
Supportive laboratory studies are mandatory for the diagnosis.
ANA test is positive with high titers (1:160 or higher) in >98% of SLE patients during the course of disease. ANA staining pattern can be homogenous (common), rim (specific), speckled, or nucleolar. Rheumatoid diseases other than SLE may also be associated with a positive ANA, but usually in lower titers (e.g., Sjögren syndrome, scleroderma, rheumatoid arthritis). If ANA is repeatedly negative, SLE can be excluded in the vast majority of suspected patients.
Anti-double-stranded DNA (anti-dsDNA) antibodies are highly specific for SLE. They are present in 70% of SLE patients but in less than 0.5% of healthy population or patients with other autoimmune diseases. These antibodies have been found to be associated with renal involvement (lupus nephritis), and their titers fluctuate with the activity of SLE, allowing for following the course of disease.
Anti-Smith (anti-Sm) antibodies are very specific (96%) but lack sensitivity (25%). They are associated with renal disease and occur more frequently in African American and Asian patients than in Caucasians with SLE.
Antibodies to U1 ribonucleoprotein (anti-RNP) coexist with anti-Sm antibodies in patients with SLE, but they are less specific. These antibodies are associated with myositis, Raynaud phenomenon, and less severe lupus. They are also present in mixed connective tissue disease and systemic sclerosis.
Anti-SSA/Ro and, less frequently, anti-SSB/La antibodies are detected in some SLE patients. These antibodies are frequently detected in patients with Sjögren syndrome. Presence of anti-SSA/Ro antibodies in patients with SLE is associated with lymphopenia, photosensitivity, neonatal lupus, complement deficiency, and subacute cutaneous lupus. In addition, their presence with anti-SSB/La antibodies during pregnancy confers a 1–2% risk of congenital heart block in the offspring.
Anti–ribosomal P protein (anti-Ribo-P) antibodies have been reported in SLE patients with neuropsychiatric manifestations.
Antihistone antibodies are present in >95% of patients with drug-induced lupus, especially with the disease associated with procainamide, hydralazine, chlorpromazine, and quinidine, whereas other autoantibodies are uncommon. Antihistone antibodies are also present in up to 80% of patients with idiopathic SLE.
See Figure
2-1
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Antibodies associated with the antiphospholipid syndrome (anticardiolipin antibodies, anti-β2 glycoprotein 1 antibodies) and lupus anticoagulant are frequently positive in SLE patients and associated with venous or arterial thrombosis. Approximately one third of patients with antiphospholipid syndrome have SLE.
Although RF is not specific for SLE, its presence correlates with active inflammatory arthritis.
Anemia may be that of chronic inflammation or autoimmune hemolytic.
