Treatment of ankylosing spondylitis with TNFa inhibitors does not affect serum levels of tryptophan metabolites

The imbalance between the kynurenine and serotonin pathways can have serious consequences, e.g., depression. One of the factors leading to the imbalance between the pathways of tryptophan metabolism is inflammation. The aim of our study was to assess the impact of treatment with tumor necrosis factor-alpha (TNFa)-inhibitors on tryptophan metabolism in patients with ankylosing spondylitis (AS). Forty patients with AS (twenty-eight males, twelve females; mean age 40 & PLUSMN; 11 years), qualified to receive anti-TNF-a treatment, were prospectively assessed. As a control group, 20 healthy volunteers (7 males and 13 females, mean age 38 & PLUSMN; 5 years) were recruited from the general population. Patients underwent full clinical and biochemical assessment before and after 6 months of therapy. Disease activity was assessed by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). The presence of depressive disorders was assessed with Beck's Depression Inventory (BDI) scale. Serum concentrations of tryptophan, serotonin, kynurenine, and quinolinic acid were measured. The predominance of the kynurenine pathway in AS patients (compared to the control group) was demonstrated (p < 0.001). Surprisingly, no significant changes in serum levels of tryptophan and its metabolites in AS patients after treatment were found, despite clinical improvement. Moreover, the components of tryptophan metabolism did not correlate significantly with the clinical activity of AS, depression nor laboratory inflammatory markers. Probably some other factors influence the pathways of tryptophan metabolism in patients with ankylosing spondylitis.