Successful Treatment of Rheumatoid Vasculitis-Associated Foot-drop with Infliximab
To the Editor:
We read with interest of the experience of Richette and colleagues in the use of infliximab in rheumatoid arthritis (RA)1, in which they describe the development of necrotizing vasculitis-associated sensory neuropathy in one patient and the deterioration of rheumatoid vasculitis-associated mononeuritis multiplex in another. This contrasts with our own recent experience of a patient with rheumatoid vasculitis who developed a mononeuritis of the left common peroneal nerve with foot-drop, resistant to 6 infusions of cyclophosphamide and high dose oral steroid, but resolving entirely after 6 doses of infliximab.
The patient was a 52-year-old woman with a 20 year history of erosive seropositive RA, which had been resistant to treatment with a range of disease modifying antirheumatic drugs over the years, including methotrexate, myocrisine, and D-penicillamine; she was then maintained on leflunomide 10 mg and prednisolone 20 mg daily. Her drug therapy had been unchanged for over a year, except for a gradual increase in her dose of steroid. She had a history of rheumatoid vasculitis, treated successfully with intravenous cyclophosphamide, but leaving her with a peripheral sensory neuropathy in both feet, with reduced sensation from mid-shin distally.
She presented 4 months before commencing infliximab therapy with left-side foot-drop that had developed over a few days. On examination, there was complete loss of power on dorsiflexion of the left foot. Nerve conduction studies revealed marked distal delay in the left common peroneal nerve (6.2 ms) and undetectable motor response. The rest of the neurological examination was unchanged. She received 6 infusions of 500 mg cyclophosphamide over 12 weeks, with 40 mg prednisolone daily and cotrimoxazole prophylaxis, without any improvement in her foot-drop.
Four months after her presentation she commenced infliximab (3 mg/kg), stopped leflunomide, and restarted methotrexate at a dose of 7.5 mg/week. The steroid dose was initially unchanged, but was gradually reduced to 5 mg daily once she reported significant clinical improvement in pain and stiffness with infliximab infusions. After the third infliximab infusion, there was a gradual return of left ankle dorsiflexion, and after the sixth infusion, power had returned to normal.
Despite the negative experience of Richette and colleagues, and other reports of the development of optic neuritis with infliximab treatment in RA2, we suggest that the drug can offer benefits to at least some patients with rheumatoid vasculitis-associated mononeuritis.
DAVID J. ARMSTRONG, MD; MAURA T. McCARRON, MD; GARY D. WRIGHT, MD, Department of Rheumatology, Musgrave Park Hospital, Belfast, UK.
REFERENCES1. Richette P, Dieude P, Damiano J, et al. Sensory neuropathy revealing necrotizing vasculitis during infliximab therapy for rheumatoid arthritis. J Rheumatol 2004;31:2079-81.
2. Ten Tusscher MPM, Jacobs PJC, Busch MJWM, de Graff L, Diemont WL. Bilateral anterior optic neuropathy and the use of infliximab. BMJ 2003;326:579.