Affiliations: Kyoto Prefectural University of Medicine
Hamamatsu University School of Medicine
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: firstname.lastname@example.org
To the Editor:
We read with great interest the recent case report (February
2001)1of 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
animals2and in humans,3and some studies
have reported the reduction of T-suppressor cell activity by rifampicin
in both humans4and mice.5Indeed, prolonged
allograft rejection in experimental animals treated with rifampicin has
been demonstrated,6and the prophylactic activity of this
drug against adjuvant arthritis in rats has been
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.8In 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
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
We were pleased to read the commentary by Inoue and colleagues
regarding our article (February 2001).1The
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.
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