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Absence of antineutrophil cytoplasmic antibodies in giant cell arteritis
T A Baranger1, M A Audrain, A Castagne
1Laboratoire d'Immunologie, Centre Hospitalier Universitaire de Nantes, France.
Insights
Antineutrophil cytoplasmic antibodies (ANCA) were not typically detected in patients with active giant cell arteritis (GCA) using validated assays. Careful laboratory controls are essential for interpreting potential ANCA positivity in GCA.
Area of Science:
- Rheumatology
- Immunology
- Vasculitis Research
Background:
- Giant cell arteritis (GCA) is a large-vessel vasculitis.
- The role of antineutrophil cytoplasmic antibodies (ANCA) in GCA is not well-established.
Purpose of the Study:
- To determine the prevalence of ANCA in patients with active GCA.
- To assess the diagnostic utility of ANCA testing in GCA.
Main Methods:
- 23 patients with active GCA were enrolled.
- Sera were tested for ANCA using indirect immunofluorescence (IIF) and enzyme-linked immunosorbent assay (ELISA).
- Antigen specificity was determined using proteinase 3 (PR3), lactoferrin (LF), and myeloperoxidase (MPO) ELISA.
Main Results:
- Only one patient showed borderline anti-MPO reactivity, which was not confirmed by further testing.
- No typical ANCA positivity was detected in the majority of patients with active GCA.
- Assays included IIF, ELISA, and Western blot analysis for ANCA detection.
Conclusions:
- Typical ANCA are not prevalent in patients with active GCA when using validated antigen-specific assays.
- Careful laboratory controls and clinical correlation are crucial for interpreting ANCA results in GCA.
- The findings suggest ANCA may not be a reliable biomarker for active GCA.
Objective:
To determine the prevalence of antineutrophil cytoplasmic antibodies (ANCA) in patients with active giant cell arteritis (GCA).
Methods:
23 patients with GCA were selected according to ACR 1990 criteria. Sera were harvested in all patients at an active stage of the disease and during followup (1 to 3 sera/patient for a total of 50 sera). ANCA positivity was searched for by indirect immunofluorescence (IIF) and enzyme linked immunosorbent assay (ELISA) using a neutrophil extract, and antigen specificity was determined by proteinase 3 (PR3), lactoferrin (LF) and myeloperoxidase (MPO) ELISA:
Results:
Only 1/23 patients exhibited reactivity in IgG ANCA ELISA and IIF, with borderline anti-MPO reactivity in ELISA which was not inhibited by preincubation with MPO in the liquid phase, and no reactivity in Western blot analysis. Specificity could not be demonstrated in another patient who had positive IgG ANCA ELISA but negative ANCA IIF and negative antigen specific ELISA: All other patients were ANCA negative.
Conclusion:
As our patients with GCA did not exhibit typical ANCA when validated antigen specific assays were used, careful laboratory controls and clinical evaluation would seem essential in cases of apparent ANCA positivity.
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