Many diseases are caused by abnormal responses to ultraviolet radiation (UVR) and visible light exposure. This textbook includes separate chapters on other idiopathic (usually presumed immune-mediated) photodermatoses, including polymorphic light eruption/polymorphous light eruption (PLE/PMLE), actinic prurigo, hydroa vacciniforme (HV), and solar urticaria, and photodermatoses as a manifestation of metabolic diseases such as the cutaneous porphyrias. This chapter discusses conditions with a dermatitis on exposed sites, whether or not covered sites are also affected. These conditions include chronic actinic dermatitis, photoallergic contact dermatitis, drug-induced photosensitivity, and manifest as a dermatitis (eg, caused by thiazides) and photoaggravation of other dermatitides (atopic eczema, seborrheic dermatitis, and, often when caused by an airborne allergen, allergic contact dermatitis). Frequently, clinical assessment alone is insufficient to distinguish between true abnormal cutaneous photosensitivity (as in chronic actinic dermatitis) and photoaggravation, not true photosensitivity, of another dermatitis, and investigation with some form of phototesting can be necessary for definitive diagnosis, with important implications for management.
CHRONIC ACTINIC DERMATITIS
Chronic actinic dermatitis is a rare, acquired, persistent eczematous eruption of exposed skin, sometimes having pseudolymphomatous (reticuloid) features.
It commonly affects older men, but is increasingly recognized in women and in younger people, including children.
Histologic features are eczematous, but pseudolymphomatous forms may be virtually indistinguishable from cutaneous T-cell lymphoma.
It usually involves severe ultraviolet B sensitivity but often also involves ultraviolet A sensitivity and sometimes sensitivity to visible light.
Persistent light reaction, actinic reticuloid, photosensitive eczema, and photosensitivity dermatitis are all considered either clinical variants or old diagnostic terms.
It is likely the result of a delayed-type hypersensitivity reaction against an endogenous photoinduced epidermal antigen(s).
Therapy consists of strict avoidance of the relevant ultraviolet and visible rays, along with topical and intermittent oral steroids, and topical calcineurin inhibitors. Occasionally, phototherapy (ultraviolet B, broadband ultraviolet A, ultraviolet A1, or psoralen-ultraviolet A photochemotherapy) can be used, guided by the findings of investigation, particularly phototesting. If these measures are insufficient, or cause too much disruption to quality of life, then systemic immunosuppression (such as azathioprine or methotrexate) is required.
Chronic actinic dermatitis (CAD),1 formerly called the photosensitivity dermatitis/actinic reticuloid syndrome,2 occurs across the world.3-5 As it is frequently impossible to definitively diagnose CAD without some form of phototesting, it is likely that some persons with this condition are being labeled as having photoaggravated atopic eczema. CAD is possibly more common in people of darker-skin phototypes, but can be found in all peoples.4,6 Perhaps, melanin plays a part in causing this condition. CAD has not been reported in people with albinism.
ETIOLOGY AND PATHOGENESIS
Studies of the clinical, histologic, and immunohistochemical features of CAD all show it to resemble the delayed-type hypersensitivity reaction of allergic contact dermatitis,7,8 even in its severe pseudolymphomatous form (formerly called actinic reticuloid), in which the clinical and ...