Naresh Kumar Tripathy1, Nakul Sinha, Soniya Nityanand. 1. Departments of Immunology and Cardiology, Sanjay Gandhi Post-Graduate Institute of Medical Sciences (SGPGIMS), Raebareli Road, Lucknow 226014, India.
Abstract
OBJECTIVE: To investigate the prevalence of antimonocyte antibodies (AMA) in Takayasu's arteritis (TA) and their relationship with disease activity. METHODS: IgG-AMA were studied in the sera of 60 patients with TA (29 active disease, 31 inactive) and 43 controls by a cellular ELISA using glutaraldehyde fixed U-937 cells or peripheral blood monocytes as antigen. Relationship of AMA with disease activity was evaluated by measuring titers of these antibodies in followup sera of 15 AMA positive patients with active TA undergoing immunosuppressive therapy. RESULTS: Twenty-six of 60 TA patients (43%) compared to 4 of 43 controls (9%) (p < 0.001) and 20 of 29 patients with active disease (69%) compared to 6 of 31 patients with inactive disease (19%) (p < 0.001) were positive for AMA. The antibody titers were significantly higher in patients with active disease than those with inactive disease (0.396 +/- 0.172 vs 0.232 +/- 0.096; p < 0.001). In the followup study of 15 patients with active disease who received immunosuppressive therapy, we observed normalization of AMA titers in 6 of the 7 patients who became inactive, compared to only one of the 8 patients whose disease remained active during followup (p < 0.01). CONCLUSION: AMA are present in a significant proportion of patients with TA and correlate with disease activity, suggesting a possible pathogenic role of these antibodies in TA.
OBJECTIVE: To investigate the prevalence of antimonocyte antibodies (AMA) in Takayasu's arteritis (TA) and their relationship with disease activity. METHODS: IgG-AMA were studied in the sera of 60 patients with TA (29 active disease, 31 inactive) and 43 controls by a cellular ELISA using glutaraldehyde fixed U-937 cells or peripheral blood monocytes as antigen. Relationship of AMA with disease activity was evaluated by measuring titers of these antibodies in followup sera of 15 AMA positive patients with active TA undergoing immunosuppressive therapy. RESULTS: Twenty-six of 60 TA patients (43%) compared to 4 of 43 controls (9%) (p < 0.001) and 20 of 29 patients with active disease (69%) compared to 6 of 31 patients with inactive disease (19%) (p < 0.001) were positive for AMA. The antibody titers were significantly higher in patients with active disease than those with inactive disease (0.396 +/- 0.172 vs 0.232 +/- 0.096; p < 0.001). In the followup study of 15 patients with active disease who received immunosuppressive therapy, we observed normalization of AMA titers in 6 of the 7 patients who became inactive, compared to only one of the 8 patients whose disease remained active during followup (p < 0.01). CONCLUSION: AMA are present in a significant proportion of patients with TA and correlate with disease activity, suggesting a possible pathogenic role of these antibodies in TA.
Authors: Haner Direskeneli; Sibel Z Aydin; Tanaz A Kermani; Eric L Matteson; Maarten Boers; Karen Herlyn; Raashid A Luqmani; Tuhina Neogi; Philip Seo; Ravi Suppiah; Gunnar Tomasson; Peter A Merkel Journal: J Rheumatol Date: 2011-07 Impact factor: 4.666