Chloracne: histopathologic findings in one case

Pastor, María Antonia; Carrasco, Loreto; Izquierdo, M J; Fariña, M C; Martín, Lucía; Renedo, G; Requena, Luís

doi:10.1034/j.1600-0560.2002.290401.x

Cited by 19 publications

(19 citation statements)

References 17 publications

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“…TCDD increases the quantity of cornified envelopes in monolayer cultures and organotypic cultures of keratinocytes [43]. TCDD also enhances filaggrin, involucrin, transglutaminase, and IL-1β expression [42, 63, 77]. In addition, TCDD exposure significantly augments the mRNA expression of other epidermal differentiation complex genes [38]: repetin, hornerin, late cornified envelope (LCE) 3E, LCE3A, LCE2B, LCE2A, LCE1C, small proline-rich protein (SPRR) 1A, SPRR2A, SPRR2B, S100A9, S100A12, and S100A7 [77].…”

Section: Role Of Ahr/arnt In Epidermal Barrier Functionmentioning

confidence: 99%

Role of AhR/ARNT system in skin homeostasis

et al. 2014

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Aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that binds to structurally diverse synthetic and naturally occurring chemicals including dioxins, flavonoids, tryptophan photoproducts, and Malassezia metabolites. Upon binding to its ligands, cytoplasmic AhR translocates to the nucleus, heterodimerizes with aryl hydrocarbon receptor nuclear translocator (ARNT), and mediates numerous biological and toxicological effects by inducing the transcription of various AhR-responsive genes. AhR ligation controls oxidation/antioxidation, epidermal barrier function, photo-induced response, melanogenesis, and innate immunity. This review summarizes recent advances in the understanding of the regulatory mechanisms of skin homeostasis mediated by the AhR/ARNT system.

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Section: Role Of Ahr/arnt In Epidermal Barrier Functionmentioning

confidence: 99%

Role of AhR/ARNT system in skin homeostasis

et al. 2014

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“…The external dose needed to induce chloracne is much lower than that for inducing systemic toxicity. Clinically, and in part also histologically [14,15,16], chloracne includes a wide differential diagnosis: acne vulgaris, nodular elastosis with cysts and comedones (Favre-Racouchot syndrome), rosacea, pilar keratosis, planopilar lichen and chronic discoid lupus erythematosus. While ordinary acne is associated with inflammation, chloracne manifests itself with inflammation late in the course of the disease and is characterized histologically by the absence of sebaceous glands and hyperpigmented stratum corneum, which represents its two salient characteristics, as well as follicular orthokeratotic hyperkeratosis, infundibular dilatation (open orifices) and infundibular cysts (closed orifices).…”

Section: Discussionmentioning

confidence: 99%

Chloracne: Still Cause for Concern

Passarini

Infusino

Kasapi³

2010

Dermatology

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Chloracne, first described by Herxheimer in 1899, is a dermatosis consisting of more or less diffuse acneiform lesions distributed prevalently on the face and on body areas not usually affected by acne and caused by chronic or acute exposure to halogenated chemical compounds. Dioxin is the common name for dibenzo-p-dioxins and dibenzofurans, contaminants nearly ubiquitous in the environment and highly resistant to chemical and biological degradation. These compounds can survive for decades in the environment and accumulate in the human and animal food chains. Chloracne is characterized by the onset of numerous comedo-like lesions and yellowish cysts on the face, particularly on the cheeks, that can spread to the trunk and other body regions not usually affected by acne vulgaris, with diffuse grayish skin pigmentation and sometimes associated with hypertrichosis and areas of folliculitis. The lesions may occasionally be accompanied by skin or systemic manifestations. We report 9 cases of chloracne, 8 of them with rapid onset in patients residing in the same building, and 1 in a patient occupationally exposed to halogenated compounds. In our series, the doses of dioxin and polychlorinated biphenyls in the soil, water and plant material, and the serum titer of dioxin were within the normal range. This consideration raises the issue of the need to revise the serum threshold for dioxin poisoning and the environmental threshold. We wish also to underline the value of dermatopathology in the differential diagnosis of chloracne.

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“…The maximum infundibular dilatation occurred proximally, resulting in either bottle-shaped formations, with the neck near the surface, or columnar funnels along the entire length of the infundibular structure. [19][20][21] Chloracne is easy to be diagnosed by history of exposure to chloracnegens, characteristic clinical manifestations and histopathology, and high serum concentration of chloracnegens. Chloracne has acneiform comedo and cyst, but different from acne vulgaris in etiology, pathogenesis, clinical features, histopathology and treatment (Table 1).…”

Section: Histopathology Of Chloracnementioning

confidence: 99%

Environmental pollution and acne-chloracne

Qiang

Zouboulis

Xia

2009

Dermato-Endocrinology

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Environmental pollutants can result in a variant of acne called 'chloracne'. Chloracne is caused by systemic exposure to certain halogenated aromatic hydrocarbons 'chloracnegens', and is considered to be one of the most sensitive indicators of systemic poisoning by these compounds. Dioxin is the most potent environmental chloracnegen. Most cases of chloracne have resulted from occupational and non-occupational exposures, non-occupational chloracne mainly resulted from contaminated industrial wastes and contaminated food products. Non-inflammatory comedones and straw-colored cysts are the primary clinical manifestation of chloracne. Increasing of cysts in number is a signal of aggravation of chloracne. Generalized lesions can appear on the face, neck, trunk, exterimities, genitalia, axillary and other areas. Course of chloracne is chronic. Severity of chloracne is related to dosage of exposed chloracnegens, chloracnegenic potency and individual susceptibility. Histopathology of chloracne is characterized mainly by hyperplasia of epidermal cell, while follicular and sebaceous gland are taken placed by keratinized epidermal cell. The pathogenesis of chloracne maybe related to the imbalance of epidermal stem cell. Chloracne appears to be resistant to all tested forms of treatment. The only way to control chloracne is to prevent exposure to chloracnegens.

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Chloracne: histopathologic findings in one case

Abstract: Our findings support the notion that tiny infundibular cysts rather than comedones represent the basic lesions of chloracne.

Cited by 19 publications

References 17 publications

Role of AhR/ARNT system in skin homeostasis

Role of AhR/ARNT system in skin homeostasis

Chloracne: Still Cause for Concern

Environmental pollution and acne-chloracne

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