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January 1982

Griseofulvin-Resistant Dermatophytosis-Reply

Arch Dermatol. 1982;118(1):3. doi:10.1001/archderm.1982.01650130006005

In Reply.—  We agree with Jorizzo et al that inadequate host defense is frequently associated with the therapeutic failure of griseofulvin. In our recent study of griseofulvinresistant dermatophytosis, many of the patients providing fungal isolates for minimal inhibitory concentration studies had chronic, widespread infections with minimal inflammation. Such a stabilized host-parasite relationship certainly suggests an inadequate host defense. Thus, any therapy that can be devised to restore partially or improve host defense would be expected to augment a less than optimal response to any therapy, including griseofulvin. In this respect, cimetidine may be useful.The host's cutaneous inflammatory response to dermatophyte infection ranges from minimally inflammatory to highly inflammatory. Each person typically exhibits one pattern of inflammation but not both. Most evidence indicates that cell-mediated immunity to trichophytin causes the highly inflammatory response. The mechanism leading to minimal inflammation is unknown. Minimal inflammation correlates with chronic widespread infection.Evidence accumulated

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