Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.
Appearance of Non-Rheumatoid Arthralgia after Tocilizumab Treatment in RA Patients with High Disease Activity.
Saiki2, Osamu, Uda1, Hiroshi
Tocilizumab, IL-6 receptor antagonist, is one of essential biologics to treat RA patients and several side reactions have been reported, but appearance of non-rheumatoid arthralgia after tocilizumab injection has not been discussed. We experienced several RA patients who developed additional non-rheumatoid somatic arthralgia after tocilizumab treatment. We conducted this study to examine which patients develop non-rheumatoid arthralgia and to clarify how the pain is appeared and how we should take care of these patients.
Patients and Method:
We treated RA patients with tocilizumab who had not responded to MTX and/or TNF inhibitors. When we treated RA patients with tocilizumab, we examined CRP and other blood tests in addition to clinical symptoms. Serum levels of IL-6 and TNF-a were also examined before and after tocilizumab treatment.
Sixty-eight RA patients were treated with 8mg/kg tocilizumab every 4 week. Among 68 RA patients, 25 patients developed non-rheumatoid arthralgia. They suffered from severe pains of large joints such as shoulder pain and lumbago, and the quality and the site of pain was quite different from those of RA. The pain started one day after receiving tocilizumab injection and lasted for one week or longer. The magnitude of pain reduced time by time. When the non-rheumatoid arthralgia was appeared, the levels of CRP had fallen down from high levels (more than 50 mg/L) to low levels (under 5mg/L). In the patients experienced non-rheumatoid arthralgia, the serum CRP levels before tocilizumab therapy were significantly higher (113 ± 57 mg/L) than those in patients without non-rheumatoid arthralgia (31 ± 18 mg/L) and the serum levels of IL-6 were very high at 28 days after first tocilizumab treatment and they were significantly higher than in those without non-rheumatoid arthralgia. But the serum levels of high sensitive TNF-a were less than 2.8 pg/mL in both patients.
In tocilizumab treatment, RA patients with high disease activity develop non-rheumatoid arthralgia more frequently than those with low disease activity. In the patients who developed non-rheumatoid arthralgia, the levels of IL-6 but not CRP or TNF-a were selectively high suggesting that the pain would preferentially relate to IL-6 rather than CRP or TNF-a. The elevation of IL-6 levels is due to blocking of IL-6 receptor by tocilizumab treatment. However, the relationships between appearance of non-rheumatoid arthralgia and the high levels of IL-6 were remained to uncertain.
To cite this abstract, please use the following information:
Saiki, Osamu, Uda, Hiroshi; Appearance of Non-Rheumatoid Arthralgia after Tocilizumab Treatment in RA Patients with High Disease Activity. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :373