Drug-induced photosensitivity

Drug-induced photosensitivity

    Introduction *
    * Signs and symptoms
    * Diagnosis
    * Treatment
Drug-induced photosensitivity refers to the development of cutaneous manifestations as a result of the combined effects of chemicals and light. Exposure to chemicals or simply just is not enough light to induce disease, however, occurs when chemicals fotoactivarea may occur one or more events. These events include phototoxic and photoallergic reactions, lichen planus, lupus erythematosus and subacute cutaneous protoporfirie. Photosensitivity reactions may result from systemic and topical drug administration.
The wavelengths of ultraviolet light so that specific product ranges are more likely to cause photosensitivity reactions induced by ultraviolet B although occasionally may be responsible for such effects. Ultraviolet B frequently cause sunburn and skin cancer nonmelenomic. In patients who have photosensitivity is difficult to distinguish from those photoallergic phototoxic reactions. Phototoxic reactions are due to the destructive effects of light components by activated by cell membranes and DNA in some cases. In contrast, photoallergic reactions are a component mediated immune activation by light. Typically appear as exaggerated sunburn. Photoallergic reactions include contact dermatitis with a distribution limited to sun-exposed areas of the body. When these reactions are severe or prolonged it may extend the areas covered.
Photoallergic reactions develop only a minority of people exposed to compounds and light. They are less prevalent than phototoxic reactions. The amount of drug required to trigger a reaction Photoallergic is considerably lower than that required for phototoxic reactions. In addition, photoallergic reactions are a form of cell-mediated immunity, their onset is delayed until 24-72 hours after exposure to the drug and light. In contrast, phototoxic response occurs in a few minutes or hours after exposure to light. Based therapy is to identify and avoid these medications, use sunscreen and symptomatic measures. Topical corticosteroids are used, soothing cold compresses.
Photosensitivity induced by drugs is associated with death only in rare cases, people who are exposed to higher amounts of sunlight after taking a significant dose of psoralen. Although mortality is rare, drug-induced photosensitivity may cause significant morbidity in some individuals, who must limit their exposure to natural or artificial light. Carcinogenic potential of prolonged exposure to these drugs has been suggested, and its clinical relevance remains to be determined. Pathogenesis of drug photosensitivity Phototoxic reactions. Phototoxic reactions result from direct tissue destruction caused by a compound fotoactivat. Many compounds have the potential to cause phototoxicity. Most have at least one double bond or an aromatic nucleus which can absorb radiant energy. Most compounds are activated by ultraviolet A, although some have a maximum absorption in the visible range of ultraviolet B.
Most times fotoactivarea cause excitation of electrons from a compound stable form invariably aroused. As the electrons return to a more stable configuration they transfer their energy oxygen leading to formation of reactive oxygen intermediates. These compounds such as superoxide anion, hydrogen peroxide, damaging cell membranes and DNA. May lead to the formation of arachidonic acid and activation cotokine. The result is an inflammatory response that has the clinical appearance of an exaggerated sunburn. The exception to this mechanism is mediamentos induced phototoxicity phototoxicity induced by psoralen. Psoralenii intercalate with DNA forming Single purpose horses. Exposure to ultraviolet radiation produces DNA bidirectional way.
Photoallergic reactions Photoallergic reactions are mediated cellular immune responses to antigen is a drug activated by light. Fotoactivarea rise to a metabolite that can bind to protein carriers in the skin to form a complete antigen. Continuing reaction to any cell-mediated inflammatory response. Langerhans cells acquire antigen and migrate to regional lymph nodes. T-cell antigens are presented here which shows the specific receptors. T cell becomes activated and proliferate at the site of the return photoallergen deposits. T lymphocytes in the skin cause an inflammatory response if photoallergen eczematoasa morphology or characteristics is a topically applied drug eruptions photoallergen if administered systemically.
Causes and Risk Factors
Most photoallergic reactions result from systemic administration of drugs.
Photosensitising drugs include: -Tetracyclines (doxycycline, tetracycline) -Fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin) -NSAIDs (ketoprofen, naproxen, celecoxib) -Diuretics (furosemide, bumetanide, hydrochlorothiazide) -Retinoids (isotretinoin, acitretin) -Hipoglicemiantele (sulfonylureas, 5 aminolevulinic acid) -Neuroleptics (chlorpromazine, flufenazina, perazina, thioridazine,) -Antifungals (terbinafine, itraconazole, voriconazole,) Paraaminobenzoic acid, 5 fluorouracil, amiodarone, diltiazem, quinidine -Hydroxychloroquine, coal, enalapril, dapsone, oral contraceptives Solar-screens (salicylates, benzofenonele, cinnamates) -Perfumes (musks, 6-metilcoumarina).