Pemphigus can be induced by topical phenol as well as by foods and drugs that contain phenols or thiols.

Pemphigus is an autoimmune disease that results from the interaction between predisposing genetic factors and exogenous factors, the most common environmental factors being drugs and food. Topical phenol has induced pemphigus in one patient. Drugs and foods that induce pemphigus are divided into three main groups according to their chemical structure: thiols (containing a sulfhydryl group), phenol, nonthiol nonphenol.

A possible mechanism for phenol-induced pemphigus.

A possible mechanism for phenol-induced pemphigus lesions in genetically predisposed individuals is proposed that accounts for in vitro observations and cases of biochemical acantholysis, as well as the in vivo acantholysis in pemphigus induced by phenols. The mechanism involves the induction of interleukin-1a and tumor necrosis factor-a release by keratinocytes. These cytokines in turn have been shown to be involved in the regulation and synthesis of complement and proteases like plasminogen activator, which have been implicated in the pathogenesis of acantholysis in pemphigus vulgaris.

Pemphigus vulgaris triggered by glibenclamide and cilazapril.

A case of pemphigus triggered by glibenclamide and cilazapril is described. The suspicion of drug induction was confirmed in a laboratory study in which a pemphigus-like effect was induced by glibenclamide in cultured human skin explants. Withdrawal of the drugs and their replacement by hydrochlorothiazide and metformin resulted in subsidence of the lesions and no appearance of new lesions.

Liver failure and transplantation after itraconazole treatment for toenail onychomycosis.

Three weeks after completing a 4-pulse course of itraconazole for toenail onychomycosis, a 25-year-old woman patient developed severe liver crisis and required an emergency liver transplant. We report the case and discuss the use of itraconazole in onychomycosis and dermatomycoses.

Suspected induction of a pyoderma gangrenosum-like eruption due to sulpiride treatment.

A case of a pyoderma gangrenosum (PG)-like eruption due to the antipsychotic drug sulpiride, a form of risperidone, is described. The contribution of sulpiride to the etiology of the PG-like lesion is based on the reduction and healing of the ulcer upon cessation of the drug and the formation of a bulla following the drug's re-administration. The literature on drug-induced PG or PG-like eruptions is discussed.