ARTICLE
Tinea manus was proven by KOH-preparations and a positive culture (Trichophyton
rubrum). The skin lesion responded gradually and effectively to treatment
with topical anti-fungal drugs, and disappeared within 14 days despite
continuing the IFN-alpha therapy.
Comments
IFN-alpha was originally described as a protein capable of inducing
antiviral activity in cells, and it has since been used to treat chronic
hepatitis C. A variety of side effects have been associated with its administration.
Such side effects as chills, fever, arthralgia and fatigue seem to be
inevitable during therapy. Because IFN-alpha is a potent immune modulator
that influences both cellular proliferation and differentiation, it is
plausible that its use could lead to skin changes. The reported skin changes
associated with IFN-alpha administration have included either an aggravation
of or an induction of psoriasis and lichen planus [1, 2]. In this report,
we presented a patient who developed tinea manus related to the administration
of IFN-alpha.
Dermatophytosis has only rarely been reported to be associated with
IFN-alpha therapy. To our knowledge there are at least two Japanese reports
of such an association [3, 4]. A worsening of tinea pedis and manus 5
days after IFN-beta therapy was reported [3], and three cases with the
onset of tinea unguium during IFN-alpha therapy were described [4]. Our
case is consistent with these reports, which therefore indicates the possibility
that IFN therapy may play an aggravating role in dermatophytosis. Concomitant
dermatophytosis still is rather weak proof for a pathogenic link to IFN-alpha
therapy. However, it should be noted that either an aggravation of, or
an induction of dermatophytosis may occur as one of the adverse side effects
of IFN-alpha therapy. Furthermore, these observations suggest the possibility
that IFN-alpha may also participate in the pathophysiology of dermatophytosis.
The exact mechanism through which this occurs is still unclear. Some
clinical manifestations of dermatophytosis may be attributed to a delayed-type
hypersensitivity (DTH) response against dermatophyte antigen. IFN-gamma-mediating
DTH (Th1 cytokine-mediated process) is responsible for producing the cutaneous
manifestation of dermatophytosis [5]. IFN-alpha appears to influence the
cytokine cascade towards an increased Th1 expression [6]. Since the clinical
signs of dermatophytosis are considered, in part, to consist of an immune
response of Th1 cytokine, IFN-alpha therapy may therefore influence the
cutaneous manifestation of dermatophytosis.
Article accepted on 18/07/00
REFERENCES
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the frequency of interferon-g-producing human CD4 T cells. J Exp Med
1993; 178: 1655-63.
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