Systemic Lupus Erythematosus (SLE)

• Definition
• Incidence
• Etiology
• Symptoms
• Diagnosis
• Treatment
• Recent Advances
• Conclusion

DIAGNOSIS

The diagnosis of lupus can be difficult. It may take months or even years for physicians to piece together the symptoms to diagnose this complex disease accurately.

No single test can determine whether a person has lupus, but several laboratory tests may aid in the diagnosis. Most persons with lupus test positive for ANA. However, there are a number of other causes of positive ANA results, including infections and other rheumatic or immune diseases-occasionally they even are found in healthy adults. The ANA test simply provides another clue for the physician to consider in making a diagnosis.

In addition, blood tests for individual types of autoantibodies exist that are more specific to persons with lupus, though not all persons with lupus test positive for these, and not all persons with these antibodies have lupus. These antibodies include anti-DNA, anti-Sm, anti-RNP, anti-Ro (SSA), and anti-La (SSB). These antibody tests may help in the diagnosis of lupus.

Some tests are used less frequently but may be helpful if the cause of a person's symptoms remains unclear. A biopsy of the skin or kidneys may be indicated if those body systems are affected. A test for syphilis or the anticardiolipin antibody may also be useful. Positive test results do not mean that a person has syphilis; however, the presence of this antibody may increase the risk of blood clotting and can increase the risk of miscarriages in pregnant women with lupus. Again, all these tests merely serve as tools in making a diagnosis.

Other laboratory tests are used to monitor the progress of the disease once it has been diagnosed. A complete blood count, urinalysis, blood chemistries, and erythrocyte sedimentation rate test can provide valuable information. Another common test measures the blood level of a group of substances called complement. Persons with lupus often have increased erythrocyte sedimentation rates and low complement levels, especially during flares of the disease.

Persons diagnosed with systemic lupus erythematosus (SLE) have autoantibodies in their blood years before any symptoms appear, according to an article in the October 16, 2003, issue of The New England Journal of Medicine.

The early detection of autoantibodies may facilitate the recognition of those persons who will develop SLE and may allow physicians to monitor them before the disease might otherwise be noticed.

THINK ABOUT THESE 
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Full Source Title:American Journal of Medicine 
   
 Abstract
 
  PURPOSE:We sought to assess the nephritogenic antibody profile of patients with systemic lupus erythematosus (SLE), and to determine which antibodies were most useful in identifying patients at risk of nephritis. METHODS: We studied 199 patients with SLE, 78 of whom had lupus nephritis.

We assayed serum samples for antibodies against chromatin components (double-stranded deoxyribonucleic acid [dsDNA], nucleosome, and histone), C1q, basement membrane components (laminin, fibronectin, and type IV collagen), ribonucleoprotein, and phospholipids. Correlations of these antibodies with disease activity (SLE Disease Activity Index) and nephropathy were assessed. Patients with no initial evidence of nephropathy were followed prospectively for 6 years. RESULTS: Antibodies against dsDNA, nucleosomes, histone, C1q, and basement membrane components were associated with disease activity (P <0.05). In a multivariate analysis, anti-dsDNA antibodies (odds ratio [OR] = 6; 95% confidence interval [CI]: 2 to 24) and antihistone antibodies (OR = 9.4; 95% CI: 4 to 26) were associated with the presence of proliferative glomerulonephritis. In the prospective study, 7 (6%) of the 121 patients developed proliferative lupus glomerulonephritis after a mean of 6 years of follow-up. Patients with initial antihistone (26% [5/19] vs. 2% [2/95], P = 0.0004) and anti-dsDNA reactivity (6% [2/33] vs. 0% [0/67], P = 0.048) had a greater risk of developing proliferative glomerulonephritis than patients without these autoantibodies.

CONCLUSION: In addition to routine anti-dsDNA antibody assay, antihistone antibody measurement may be useful for identifying patients at increased risk of proliferative glomerulonephritis. 

Full Source Title:Arthritis and Rheumatism

Abstract:

OBJECTIVE: To determine the degree to which changes in C3 and C4 precede or coincide with changes in systemic lupus erythematosus (SLE) activity, as measured by 5 global activity indices, the physician's global assessment (PGA), modified SLE Disease Activity Index (M-SLEDAI), modified Lupus Activity Index (M-LAI), Systemic Lupus Activity Measure (SLAM), and the modified British Isles Lupus Assessment Group (M-BILAG), and to evaluate the association between changes in C3 and C4 levels and SLE activity in individual organ systems. RESULTS: Lupus flares occurred at 12% of visits based on the PGA, 19% based on the M-SLEDAI, 25% based on the M-LAI, 13% based on the SLAM, and 12% based on the M-BILAG. Recent changes in C3 and C4 levels were not associated with flares based on 3 of the 5 activity indices. Flares defined by the M-LAI were more frequent when there was a concurrent decrease in C3 (odds ratio [OR] 1.9, 95% confidence interval [95% CI] 1.1-3.1) or C4 (OR 2.1, 95% CI 1.3-3.6). Higher flare rates, as defined by the SLAM, were associated with previous increases in C3 (OR 1.6, 95% CI 1.0-2.6) and C4 (OR 2.2, 95% CI 1.2-3.9). When individual organ systems were analyzed, decreases in C3 and C4 were associated with a concurrent increase in renal disease activity (OR 2.2, 95% CI 1.4-3.5 and OR 1.9, 95% CI 1.1-3.4, respectively). Decreases in C3 were also associated with concurrent decreases in the hematocrit (OR 4.6, 95% CI 1.7-12.3), platelet (OR 2.5, 95% CI 1.5-4.1), and white blood cell (OR 2.2, 95% CI 1.3-3.6) counts. Previous increases in C3 levels were associated with a decrease in platelets (OR 1.7, 95% CI 1.1-2.7). A decrease in C4 was associated with a concurrent decrease in the hematocrit level (OR 3.2, 95% CI 1.3-7.5) and platelet count (OR 1.6, 95% CI 1.0-2.5).

CONCLUSION: Decreases in complement levels were not consistently associated with SLE flares, as defined by global measures of disease activity. However, decreasing complement was associated with a concurrent increase in renal and hematologic SLE activity