SSA/Ro Ab in serum

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Etiology

Reference interval

  • Normal: Negative

Principle

Highly purified SSA antigen is bound to microwells & stabilized for extended shelf life. Diluted patient sera are placed in the microwells & incubated. If anti-SSA antibodies are present, they will bind to the antigen in the microwell. The microwells are then washed to remove residual sample & a second incubation with anti-human IgG conjugated to alkaline phosphatase is carried out. The conjugate will bind immunologically to the anti-SSA IgG antigen-antibody complex, forming a 'sandwich' consisting of:

Conjugate (Enzyme-labeled Anti-human IgG)

Human anti-SSA (IgG)

Well Coated with SSA antigen

Unbound conjugate is removed in the subsequent washing step. Enzyme substrate is then added to the microwell & if bound conjugate is present, the colorless substrate (p-nitrophenyl phosphate), will be hydrolyzed to form a yellow end product, (p-nitrophenol). The reaction is then stopped & the color fixed. The intensity of the color is measured photometrically at 405 nm & is proportional to the concentration of anti-SSA present in the patients sample.

Clinical significance

The presence of antibody to the SSA antigen strongly correlates with distinguishable subsets of SLE & Sjogren's Syndrome. Antibody to SSA (Ro) occurs in 62% of patients with 'ANA negative' SLE, 63% to > 85% of patients with subacute cutaneous lupus erythematosus, 75% of the homozygous C2-deficient patients with SLE-like picture, & in 80% of patients with Sjogren's Syndrome who have vasculitis. The existence of the autoantibody in pregnant mothers has been closely associated with the development of neonatal congenital heart block and neonatal lupus: thus the screening of pregnant SLE patients for anti-SSA antibodies is recommended.

SLE patients who have anti-SSA antibodies alone can be distinguised clinically & serologically from those who produce both anti-SSA & SSB antibodies. For example, nephritis occurs much more frequently in the former group than the latter. In addition, the incidence & levels of anti-DNA antibodies are significantly greater in patients with SSA antibodies alone compared to those with SSA & SSB antibodies. Patients producing anti-SSA alone never have been observed to produce anti-SSB whereas those producing both antibodies have not thus far been observed to cease having one or the other antibody in their sera. Fluctuating titers of anti-SSA antibodies in some SLE patients have been reported. In this case the changes in anti-SSA levels often correlated with disease activity & anti-DNA antibody levels.

Specimen

Serum is separated from the clot & refrigerated, 2-8 degrees C for short term storage or stored frozen, -20 degrees C, for long term storage. Avoid freeze-thaw cycles. CAUTION: Serum samples should not be heat inactivated, as this may cause false positive results.

No special patient preparation required.

Interpretation

More general terms

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Additional terms

Component of

References

  1. Henry, John Bernard, Clinical Diagnosis amd Management by Labortory Methods, W. B. Saunders Co., Philadelphia, 1991. pp 891-892.
  2. The Physicians Guide to Anti-DNA Antibody Testing, Diamedix Corporation, Miami, Aug. 1989. pp 1-6.
  3. Summary of Procedure. DiaMedix Corporation, Miami, June 1991. pp 1-8
  4. 4.0 4.1 4.2 4.3 Medical Knowledge Self Assessment Program (MKSAP) 11, 17, 19. American College of Physicians, Philadelphia 1998, 2015, 2022