PubMed · 7555098
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D L Shriner, R A Schwartz, C K Janniger. 1995. Impetigo.. https://pubmed.ncbi.nlm.nih.gov/7555098/
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The occurrence of erosions on the mucous membranes and (or) blisters on the skin usually indicates the seriousness of an adverse drug reaction. This paper will review the clinical and histological presentation, drug causes, and prognosis of blistering drug eruptions, with special focus on the most severe: Stevens-Johnson syndrome and Toxic epidermal necrolysis.
Hypersensitivity to the constituents of dental amalgam is uncommon. When it occurs it typically manifests itself as a lichenoid reaction involving a delayed, type IV, cell-mediated hypersensitivity response. Rarely, a more acute and generalised response can occur involving both the oral mucosa and skin. We describe two cases that illustrate the presentation and management of these two types of reaction.
A wide spectrum of diseases of the skin are manifested as a blistering process. Blistering may occur as a secondary event associated with viral or bacterial infections of the skin, eg, herpes simplex and impetigo, or with local injury of the skin, eg, burns, ischemia, and dermatitis. In other diseases, blistering of the skin occurs as a primary event and is associated with tissue injury and fluid accumulation within a specific layer of the skin: intraepidermal, dermal-epidermal junction, or subepidermal. Blister formation in this latter group of diseases is due to either genetic mutation or an autoimmune response. Genodermatoses associated with blisters are typically manifested in the neonate, whereas the autoimmune blistering disorders are acquired and usually expressed later in life. Recent advances have uncovered the relevance of the keratinocyte cytoskeleton, the desmosome, the hemidesmosome, and extracellular matrix proteins in blister formation. A pathogenetic classification of blistering diseases is presented.