Methotrexate: a useful steroid-sparing agent in recalcitrant chronic urticaria

Summary Background Reports of methotrexate for chronic urticaria are anecdotal. Objectives To assess the effectiveness of methotrexate in steroid‐dependent chronic urticaria, its impact on steroid reduction and any differences in response between patients with and without functional autoantibodies. Methods A retrospective case‐note review of 16 patients with steroid‐dependent chronic urticaria treated with methotrexate was carried out. Ten patients had chronic ordinary/spontaneous urticaria (CU), including three with associated delayed‐pressure urticaria; four patients had normocomplementaemic urticarial vasculitis (UV); and two patients had idiopathic angio‐oedema without weals. Median disease duration before methotrexate was 48·5 months (range 12–164). All were unresponsive to antihistamines and second‐line agents, except prednisolone. Eleven were assessed for autoimmune urticaria with the basophil histamine release assay (n = 5), autologous serum skin test (n = 5) or both (n = 1). Response to methotrexate was scored: no benefit; some benefit (fewer weals and symptomatic improvement but no steroid reduction); considerable benefit (improvement with steroid reduction); or clear (no symptoms, off steroids but on antihistamines). Results Twelve of 16 patients (eight CU, three UV, one idiopathic angio‐oedema) responded. Three showed some benefit, seven considerable benefit and two cleared. Four of eight responders and three out of three nonresponders showed evidence of functional autoantibodies. The dose to achieve a steroid‐sparing effect was 10–15 mg weekly (cumulative dose range 15–600 mg, median 135 mg). Methotrexate was well tolerated. Conclusions Methotrexate may be a useful treatment for steroid‐dependent chronic urticaria. Functional autoantibodies do not correlate with response. The beneficial effects of methotrexate may be anti‐inflammatory and immunosuppressive. It may therefore benefit chronic urticaria independently of the pathogenic mechanism, whether autoimmune or not.