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Chapter 057. Photosensitivity and Other Reactions to Light (Part 5)

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Polymorphous Light Eruption After sunburn, the most common type of photosensitivity disease is polymorphous light eruption (PLE), the mechanism of which is unknown. Many affected individuals never seek medical attention because the condition is often transient, becoming manifest each spring with initial sun exposure but then subsiding spontaneously with continuing exposure, a phenomenon known as "hardening." The major manifestations of PLE include pruritic (often intensely so) erythematous papules that may coalesce into plaques in a patchy distribution on exposed areas of the trunk and forearms. The face is usually less seriously involved. The diagnosis can be confirmed by skin biopsy...

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Nội dung Text: Chapter 057. Photosensitivity and Other Reactions to Light (Part 5)

  1. Chapter 057. Photosensitivity and Other Reactions to Light (Part 5) Polymorphous Light Eruption After sunburn, the most common type of photosensitivity disease is polymorphous light eruption (PLE), the mechanism of which is unknown. Many affected individuals never seek medical attention because the condition is often transient, becoming manifest each spring with initial sun exposure but then subsiding spontaneously with continuing exposure, a phenomenon known as "hardening." The major manifestations of PLE include pruritic (often intensely so) erythematous papules that may coalesce into plaques in a patchy distribution on exposed areas of the trunk and forearms. The face is usually less seriously involved.
  2. The diagnosis can be confirmed by skin biopsy and by performing phototest procedures in which skin is exposed to multiple erythema doses of UV- A and UV-B. The action spectrum for PLE is usually within these portions of the solar spectrum. Treatment of this PLE includes the use of sunscreens and the induction of hardening by the cautious administration of artificial UV-B (broad-band or narrow-band) and/or UV-A radiation for 2–3 weeks prior to initial sun exposure. Phototoxicity and Photoallergy These photosensitivity disorders are related to the topical or systemic administration of drugs and other chemicals. Both reactions require the absorption of energy by a drug or chemical resulting in the production of an excited-state photosensitizer that can transfer its absorbed energy to a bystander molecule or to molecular oxygen, thereby generating tissue-destructive chemical species, including ROS. Phototoxicity is a nonimmunologic reaction caused by drugs and chemicals, a few of which are listed in Table 57-3. The usual clinical manifestations include erythema resembling a sunburn reaction that quickly desquamates, or "peels," within several days. In addition, edema, vesicles, and bullae may occur. Table 57-3 Phototoxic Drugs
  3. Topical Systemic Amiodarone + Dacarbazine + Fluoroquinolones + 5-Fluorouracil + + Furosemide + Nalidixic acid + Phenothiazines + Psoralens + + Retinoids +/– +
  4. Sulfonamides + Sulfonylureas + Tetracyclines + Thiazides + Vinblastine + Photoallergy is much less common and is distinct in that this is an immunopathologic process. The excited-state photosensitizer may create highly unstable haptenic free radicals that bind covalently to macromolecules to form a functional antigen capable of evoking a delayed hypersensitivity response. Some of the drugs and chemicals that produce photoallergy are listed in Table 57-4. The clinical manifestations typically differ from those of phototoxicity in that an intensely pruritic eczematous dermatitis tends to predominate and evolves into lichenified, thickened, "leathery" changes in sun-exposed areas. A small subset (perhaps 5–10%) of patients with photoallergy may develop a persistent exquisite hypersensitivity to light even when the offending drug or chemical is identified and eliminated, a condition known as persistent light reaction.
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