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Kyoto Prefectural University of Medicine Kyoto, Japan
Correspondence to: Ken-ichiro Inoue, MD, Department of Internal Medicine, Naka Central Hospital, 1733-1, Iida, Naka-cho, Naka-gun, Ibaraki Prefecture, 311-0134, Japan; e-mail: keni{at}kk.iij4u.or.jp
To the Editor:
We read with great interest the recent case report (February 2001)1 of a patient with Wegener’s granulomatosis (WG) who responded to antituberculous drugs. In their discussion, however, Toyoshima and colleagues failed to refer to the possibility of immunosuppressive effects by one of the antituberculous drugs used. Rifampicin is an antimicrobial agent that was recently found to exhibit immunosuppressive activity in both animal and human studies. Rifampicin decreases both humoral and cellular responses to various antigens in animals2 and in humans,3 and some studies have reported the reduction of T-suppressor cell activity by rifampicin in both humans4 and mice.5 Indeed, prolonged allograft rejection in experimental animals treated with rifampicin has been demonstrated,6 and the prophylactic activity of this drug against adjuvant arthritis in rats has been reported.7
However, in regard to clinical studies, the efficacy of rifampicin as an immunosuppressive agent for patients with rheumatic disease is still controversial. Borg et al8 reported that rifampicin may be useful in the treatment of rheumatoid arthritis (RA) in the early stages.8 In contrast, Cox and colleagues9 did not agree with the beneficial effect of antituberculous drugs (rifampicin and isoniazid) for even the early stages of RA. They demonstrated no significant improvement in the mean values of the clinical and laboratory parameters measured except for the erythrocyte sedimentation rate and the serum concentrations of C-reactive protein after treatment with the drugs for 6 months in 21 patients with early-stage RA.
As Toyoshima and colleagues discussed, neither the identity of the antituberculous drug that was effective nor the mechanism of its effects in their patient was clear. However, we believe it can also be speculated that rifampicin ameliorates WG through immunosuppressive activity. Further accumulation of similar case reports is needed to clarify the efficacy of antituberculous drugs for collagen vascular diseases.
References
Hamamatsu University School of Medicine Hamamatsu, Japan
Correspondence to: Mikio Toyoshima, MD, Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3192 Japan 
To the Editor:
We were pleased to read the commentary by Inoue and colleagues regarding our article (February 2001).1 The immunosuppressive activity of rifampicin has been reported.2 3 However, as they discussed in their letter, the efficacy of rifampicin as an immunosuppressive agent in humans has not been established. We think that its immunosuppressive power is too weak to modify a clinical course of Wegener’s granulomatosis (WG) because adverse effects such as opportunistic infections, which are caused by the immunosuppressive activity of rifampicin, have never been reported in the treatment of tuberculosis. Although the possible involvement of the immunosuppressive activity of rifampicin cannot be completely excluded, we believe that the major effect of rifampicin in our case depended on its antimicrobial activity against Staphylococcus aureus, which has been reported as a precipitating factor of this WG.4 It is reasonable to assume that rifampicin ameliorates WG by the elimination of S aureus rather than through immunosuppressive activity in our case. To clarify this point, further investigation involving a large number of similar cases will be needed.
References
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