A Case of Phenol-Related Contact Pemphigus

Goldberg, Ilan; Sasson, Oshrat; Brenner, Sarah

doi:10.1159/000051793

Cited by 14 publications

(5 citation statements)

References 9 publications

(15 reference statements)

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“…17 The objectives of this article are to report the clinical, histological and immunological characteristics of a series of 22 dogs that exhibited a unique acantholytic pustular dermatitis arising first at the site of PD application. Laboratory investigations provided evidence suggesting that these PD-associated pemphigus-like reactions (PAPLR) most probably represent a unique contact drug-triggered PF, a phenomenon rarely reported in the medical literature [18][19][20][21][22][23] but never before described in veterinary dermatology.…”

Section: Introductionmentioning

confidence: 99%

Metaflumizone–amitraz (Promeris)‐associated pustular acantholytic dermatitis in 22 dogs: evidence suggests contact drug‐triggered pemphigus foliaceus

Oberkirchner¹,

Linder

Dunston³

et al. 2011

Veterinary Dermatology

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Promeris Duo (PD) is a novel topical flea and tick preventative for dogs, which is also licensed for treatment of canine demodicosis. In this article, we present 22 dogs that all developed pemphigus foliaceus (PF)-like cutaneous drug reactions at the site of PD application. In eight dogs, the lesions were restricted to the application site (localized group). Signs of systemic illness were reported in three dogs, and four required immunosuppressive treatment. Direct immunofluorescence for IgG was positive in four dogs, although circulating antikeratinocyte IgG could not be detected in any tested sera. Complete remission was achieved in all dogs, with one patient still remaining on treatment. Fourteen dogs developed skin lesions at the application site as well as other noncontiguous areas (distant group). Systemic signs were reported in 11 dogs, and immunosuppression was required in 10 cases. Direct and indirect immunofluorescence tests were positive for antikeratinocyte autoantibodies in 10 of 13 and six of 10 patients with distant disease, respectively. Complete remission was achieved in 10 of 13 dogs with distant disease; one-third are still on treatment. Histological changes were similar to canine PF. Desmosomal architectural changes, assessed by desmoglein-1 immunostaining, were also similar to those of dogs with spontaneous autoimmune PF. Apoptosis did not appear to contribute to lesion formation, in either autoimmune or PD-associated PF. In conclusion, PD has the potential of triggering a variant of PF that resembles spontaneously occurring autoimmune PF at clinical, morphological, immunological and treatment outcome levels.

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Section: Introductionmentioning

confidence: 99%

Metaflumizone–amitraz (Promeris)‐associated pustular acantholytic dermatitis in 22 dogs: evidence suggests contact drug‐triggered pemphigus foliaceus

Oberkirchner¹,

Linder

Dunston³

et al. 2011

Veterinary Dermatology

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“…Pemphigus developed in a 66-years-old woman after a cosmetic skin procedure in which phenol-containing chemical peels were used ( 74 ). In a more recent case report, pemphigus developed in a 32-years-old woman as a result of exposure to a nonyl phenol containing cleaning agent ( 75 ). The authors reported also several other studies with cases of pemphigus induced by contact with various substances such as garlic, benzoin tincture, basochrome, diclofenac.…”

Section: Trigger Factorsmentioning

confidence: 99%

Pemphigus: trigger and predisposing factors

Moro,

Sinagra,

Salemme

et al. 2023

Front. Med.

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Pemphigus is a life-threatening autoimmune blistering disease affecting skin and mucous membranes. Despite its etiopathogenesis remains largely unknown, several trigger and predisposing factors have been reported. Pemphigus is caused by autoantibodies that target desmoglein 1 and desmoglein 3, impacting desmosome function. However, circulating autoantibodies are often the consequence of a precipitating factor that occurs in predisposed individuals. This review aims to describe and discuss almost all trigger and predisposing factors reported as possible or probable cause of the disease. Among the reported trigger factors that may induce or exacerbate pemphigus, we have found of particular interest: drug intake (especially thiol- and phenol-containing compounds), vaccines, infections, as well as some reports about pregnancy, radiations, emotional stress, pesticides and physical trauma. Moreover, we discuss the possible role of food intake in pemphigus onset and particular attention is given to dietary factors containing thiol, phenol and tannin compounds. A trigger factor is “the straw that breaks the camel’s back,” and often acts together with predisposing factors. Here we discuss how pemphigus onset may be influenced by genetic susceptibility and comorbidities like thyroid diseases, malignancies and other autoimmune disorders.To identify other hitherto unknown trigger and predisposing factors, well designed prospective studies are needed. In this context, future research should explore their connection with the aim to advance our understanding of pemphigus pathogenesis.

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“…Studies on phenol‐containing drugs and compounds that induced pemphigus were subsequently reported 9–11 …”

Section: Drugs and Pemphigusmentioning

confidence: 99%

“…Studies on phenol-containing drugs and compounds that induced pemphigus were subsequently reported. [9][10][11] Diet and pemphigus Some nutritional components are chemically similar to known causative drugs. The large amounts of thiols, phenols, and polyphenolic compounds like tannins in certain foods ( Table 2) led the authors to postulate that these foods may also induce and promote pemphigus.…”

Section: Drugs and Pemphigusmentioning

confidence: 99%

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

Brenner

Srebrnik

Goldberg

2003

J of Cosmetic Dermatology

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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. Thiol and phenol compounds can induce acantholysis in tissue cultures in vitro. The suggested mechanisms for thiol acantholysis include direct biochemical impairment of cell adhesion, protease activation and immunological reaction with the formation of a neoantigen. Possible mechanisms of phenol-induced pemphigus include the induction of IL-1alpha and TNF-alpha release by keratinocytes. These cytokines have been shown to be relevant in the regulation and synthesis of complement and proteases, like plasminogen activator, which has been implicated in the pathogenesis of acantholysis in pemphigus vulgaris. Avoiding exposure of genetically predisposed individuals to these factors is important in treating and preventing this disease.

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A Case of Phenol-Related Contact Pemphigus

Cited by 14 publications

References 9 publications

Metaflumizone–amitraz (Promeris)‐associated pustular acantholytic dermatitis in 22 dogs: evidence suggests contact drug‐triggered pemphigus foliaceus

Metaflumizone–amitraz (Promeris)‐associated pustular acantholytic dermatitis in 22 dogs: evidence suggests contact drug‐triggered pemphigus foliaceus

Pemphigus: trigger and predisposing factors

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

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