Chapter 057. Photosensitivity and Other Reactions to Light (Part 4)

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Immunologic Effects Exposure to solar radiation causes local (inhibition of immune responses to antigens applied at the irradiated site) and systemic (inhibition of immune responses to antigens applied at remote unirradiated sites) immunosuppression. The action spectrum for UV-induced immunosuppression closely mimics the absorption spectrum of DNA. Pyrimidine dimers in LCs may inhibit antigen presentation. The absorption spectrum of epidermal urocanic acid closely mimics the action spectrum for UV-B-induced immunosuppression. Trans-cis isomerization of urocanic acid in the stratum corneum leads to its systemic absorption and consequent immunosuppressive effects. Furthermore administration of modest doses of UV-B to human skin reduces the degree of allergic...

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Nội dung Text: Chapter 057. Photosensitivity and Other Reactions to Light (Part 4)

Chapter 057. Photosensitivity and Other Reactions to Light (Part 4) Immunologic Effects Exposure to solar radiation causes local (inhibition of immune responses to antigens applied at the irradiated site) and systemic (inhibition of immune responses to antigens applied at remote unirradiated sites) immunosuppression. The action spectrum for UV-induced immunosuppression closely mimics the absorption spectrum of DNA. Pyrimidine dimers in LCs may inhibit antigen presentation. The absorption spectrum of epidermal urocanic acid closely mimics the action spectrum for UV-B-induced immunosuppression. Trans-cis isomerization of urocanic acid in the stratum corneum leads to its systemic absorption and consequent immunosuppressive effects. Furthermore administration of modest doses of UV-B to human skin reduces the degree of
allergic sensitization to the potent contact allergen, dinitrochlorobenzene. This is associated with ROS-induced depletion of epidermal LCs. Higher doses of UV-radiation evoke diminished immunologic responses to antigens introduced either epicutaneously or intracutaneously at sites distant from the irradiated site. These suppressed responses are also associated with the induction of antigen-specific suppressor T lymphocytes and may be mediated by as yet undefined factors that are released from epidermal cells at the irradiated site. One important consequence of chronic sun exposure and the concomitant immunosuppression is enhanced risk of skin cancer. Perhaps the most graphic demonstration of the role of immunosuppression in enhancing the risk of nonmelanoma skin cancer has come from studies of patients receiving organ transplantation who are on chronic immunosuppressive antirejection drug regimens. More than 50% of transplant patients develop BCCs and SCCs, and these cancers are the most common malignancy arising in immunosuppressed solid-organ transplant recipients. Human papilloma viruses (HPVs) may also play a role in the increased risk of SCCs in these patients since tumors display an HPV DNA carriage rate of almost 80%. These patients require close periodic monitoring and rigorous photoprotection using sunscreens, protective clothing, and sun avoidance. Photosensitivity Diseases
The diagnosis of photosensitivity requires a careful history to define the duration of the signs and symptoms, the length of time between exposure to sunlight and the development of subjective complaints, and visible changes in the skin. The age of onset can also be a helpful clue; for example, the acute photosensitivity of erythropoietic protoporphyria almost always begins in childhood, whereas the chronic photosensitivity of porphyria cutanea tarda (PCT) typically begins in the fourth and fifth decades. A history of exposure to topical and systemic drugs and chemicals may provide important clues. Many classes of drugs can cause photosensitivity on the basis of either phototoxicity or photoallergy. Fragrances such as musk ambrette that were previously present in numerous cosmetic products are also potent photosensitizers. Examination of the skin may also offer important clues. Anatomic areas that are naturally protected from direct sunlight such as the hairy scalp, the upper eyelids, the retroauricular areas, and the infranasal and submental regions may be spared, whereas exposed areas show characteristic features of the pathologic process. These anatomic localization patterns are often helpful, but not infallible, in making the diagnosis. For example, airborne contact sensitizers that are blown onto the skin may produce dermatitis that can be difficult to distinguish from photosensitivity, despite the fact that such material may trigger skin reactivity in areas shielded from direct sunlight.
Many dermatologic conditions may be caused or aggravated by sunlight (Table 57-2). The role of light in evoking these responses may be dependent on genetic abnormalities ranging from well-described defects in DNA repair that occur in XP to the inherited abnormalities in heme synthesis that characterize the porphyrias. In certain photosensitivity diseases, the chromophore has been identified, whereas in the majority, the energy-absorbing agent is unknown. Table 57-2 Classification of Photosensitivity Diseases Type Disease Genetic Erythropoietic porphyria Erythropoietic protoporphyria Porphyria cutanea tarda—familial Variegate porphyria Hepatoerythropoietic porphyria Albinism Xeroderma pigmentosum
Rothmund-Thompson disease Bloom syndrome Cockayne's disease Kindler syndrome Phenylketonuria Metabolic Porphyria cutanea tarda—sporadic Hartnup disease Kwashiorkor Pellagra Carcinoid syndrome Phototoxic Internal Drugs External Drugs, plants, food
Photoallergic Immediate Solar urticaria Delayed Drug photoallergy Persistent light reaction/chronic actinic dermatitis Neoplastic and Photoaging degenerative Actinic keratosis Melanoma and nonmelanoma skin cancer Idiopathic Polymorphous light eruption Hydroa aestivale Actinic prurigo Photoaggravated Lupus erythematosus Systemic
Subacute cutaneous Discoid Dermatomyositis Herpes simplex Lichen planus actinicus Acne vulgaris (aestivale) [newpage]