Eczema is a clinical term that embraces a number of conditions with varied underlying etiologies. New lesions take the form of erythematous papules, often with overlying vesicles, which ooze and become crusted. Pruritus is characteristic. With persistence, these lesions coalesce into raised, scaling plaques. The nature and degree of these changes vary among the clinical subtypes, which include the following:
Allergic contact dermatitis—stems from topical exposure to an allergen and is caused by delayed hypersensitivy reactions.
Atopic dermatitis—formerly attributed to allergen exposure, now thought to often stem from defects in keratinocyte barrier function, defined as skin with increased permeability to substances to which it is exposed, such as potential antigens
Drug-related eczematous dermatitis—hypersensitivity reaction to a drug
Photoeczematous dermatitis—appears as an abnormal reaction to UV or visible light
Primary irritant dermatitis—results from exposure to substances that chemically, physically, or mechanically damage the skin
While atopic dermatitis reflects a genetic predisposition and can persist for years or decades, other forms of eczematous dermatitis resolve completely when the offending stimulus is removed or exposure is limited, stressing the importance of investigating the underlying cause. Only the most common form, contact dermatitis, is considered here.
Allergic contact dermatitis is triggered by exposure to an environmental contact-sensitizing agent, such as poison ivy, that chemically reacts with self-proteins, creating neoantigens that can be recognized by the T cell http://ebooksmedicine.net arm of the adaptive immune system. The self-proteins modified by the agent are processed by epidermal Langerhans cells, which migrate to draining lymph nodes and present the antigen to naïve T cells. This sensitization event leads to acquisition of immunologic memory; on reexposure to the antigen, the activated memory CD4+ T lymphocytes migrate to the affected skin sites during the course of normal circulation. There they release cytokines that recruit additional inflammatory cells and also mediate epidermal damage, as in any delayed-type hypersensitivity reaction (Chapter 5).
MORPHOLOGYAsthenameimplies,skininvolvementincontactdermatitisislimitedtositesofdirectcontactwiththetriggeringagent(
Fig.24.1A ),whereasinotherformsofeczema,lesionsmaybewidelydistributed.Spongiosis, orepidermaledema,characterizesallformsofacuteeczematousdermatitis—hencethesynonymspongiotic dermatitis. Edemafluidseepsintotheepidermis,whereitsplaysapartkeratinocytes(
Fig.24.1B ).Inter-cellularbridgesarestretchedandbecomemoreprominentandareeasiertovisualize.Thischangeisaccompaniedbyasuperficialperivascularlymphocyticinfiltrate,edemaofdermalpapillae,andmastcelldegranulation.Eosinophilsmaybepresentandareespeciallyprominentinspongioticeruptionsprovokedbydrugs,butingeneralthehistologicfeaturesaresimilarregardlessofcause,emphasizingtheneedforcarefulclinicalcorrelation.
Lesions of acute eczematous dermatitis are pruritic, edematous, oozing plaques, often containing vesicles and bullae. With persistent antigen exposure, lesions may become scaly (hyperkeratotic) as the epidermis thickens (acanthosis). Some changes are produced or exacerbated by scratching of the lesion (see “ ”, discussed later). The clinical causes of eczema are sometimes divided into “inside jobs”—reaction to an internal circulating antigen (such as an ingested food or drug)— and “outside jobs”—disease resulting from contact with an external antigen (such as poison ivy).