Disparate effects of anti-TNF-A therapies on measures of disease activity and mediators of endothelial damage in ankylosing spondylitis

Background: asymmetric dimethylarginine (adma) is associated with endothelial injury. increased adma levels are found in rheumatoid arthritis (ra) and ankylosing spondylitis (as). we set out to assess the adma and symmetric dimethylarginine (sdma) levels in as,ra,and healthy controls,and in the anti-tnf treated patients with active as. methods: in 78as patients and 29 rapatientswho were anti-tnf treatment naive at baseline,along with 23 healthy control subjects,we assessed erythrocyte sedimentation rate (esr),high-sensitivity c-reactive protein (hscrp),adma,and sdma. for as patients,the bath ankylosing spondylitis disease activity index (basdai),back pain vas and patient's global activity of disease were calculated. after 6 months,we repeated the assessment in 30 out of the 78 as patients in whom the anti-tnf treatment was initiated. results: the baseline mean (sd) plasma admaconcentration of as patients was 0.64 (0.19) ?mol/l and did not differ from controls (0.65 [0.19] ?mol/l,p > 0.05). in the ra group,adma concentration was higher than in controls (0.77 vs. 0.65 ?mol/l,p < 0.05). both at baseline and at follow-up,adma levels correlated positively with basdai (r = 0.52,p = 0.02,and r = 0.47,p = 0.04,baseline and follow-up,respectively). six months of anti-tnf treatment did not influence admaconcentration (0.51 [0.12] vs. 0.51 [0.11] ?mol/l,p = 0.70). conclusion: an absence of changes in plasma admalevels in the anti-tnf treated as group despite the improvement in disease activity (basdai) and inflammation (esr,crp) may suggest either a lack of effect,or,even if such an effect were to take place,it needs not imply measurable changes in blood adma.