Chapter 057. Photosensitivity and Other Reactions to Light (Part 6)

TopicalSystemic6-Methylcoumarin+Aminobenzoic acid and esters+Bithionol+Chlorpromazine+Diclofenac+Fluoroquinolones+Halogenated salicylanilides+Hypericin (St Johns Wort)++Musk ambrette+Piroxicam+Promethazine+Sulfonamides+Sulfonylureas+A very uncommon type of persistent photosensitivity is known as chronic actinic dermatitis. These patients are typically elderly men with a long history ofpreexisting allergic contact dermatitis or photosensitivity. They are usually exquisitely sensitive to UV-B, UV-A, and visible wavelengths.Diagnostic confirmation of phototoxicity and photoallergy can often be obtained using phototest procedures. ...
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Chapter 057. Photosensitivity and Other Reactions to Light (Part 6) Chapter 057. Photosensitivity and Other Reactions to Light (Part 6)Table 57-4 Photoallergic Drugs Topical Systemic6-Methylcoumarin +Aminobenzoic acid and esters +Bithionol +Chlorpromazine + Diclofenac + Fluoroquinolones + Halogenated salicylanilides + Hypericin (St Johns Wort) + + Musk ambrette + Piroxicam + Promethazine + Sulfonamides + Sulfonylureas + A very uncommon type of persistent photosensitivity is known as chronicactinic dermatitis. These patients are typically elderly men with a long history ofpreexisting allergic contact dermatitis or photosensitivity. They are usuallyexquisitely sensitive to UV-B, UV-A, and visible wavelengths. Diagnostic confirmation of phototoxicity and photoallergy can often beobtained using phototest procedures. In patients with suspected phototoxicity,determining the minimal erythema dose (MED) while the patient is exposed to asuspected agent and then repeating the MED after discontinuation of the agentmay provide a clue to the causative drug or chemical. Photopatch testing can beperformed to confirm the diagnosis of photoallergy. This is a simple variant ofordinary patch testing in which a series of known photoallergens is applied to theskin in duplicate and one set is irradiated with a suberythema dose of UV-A.Development of eczematous changes at sites exposed to sensitizer and light is apositive result. The characteristic abnormality in patients with persistent lightreaction is a diminished threshold to erythema evoked by UV-B. Patients withchronic actinic dermatitis usually manifest a broad spectrum of UVhyperresponsiveness and require meticulous photoprotection including avoidingsun exposure, high (>30) SPF sunscreens, and in severe cases systemicimmunosuppression, preferably with azathioprine (1–2 mg/kg per day). The management of drug photosensitivity involves first and foremost theelimination of exposure to the chemical agents responsible for the reaction andminimization of sun exposure. The acute symptoms of phototoxicity may beameliorated by cool, moist compresses, topical glucocorticoids, and systemicallyadministered NSAIDs. In severely affected individuals, a rapidly tapered course ofsystemic glucocorticoids may be useful. Judicious use of analgesics may benecessary. Photoallergic reactions require a similar management approach.Furthermore, patients with persistent light reaction and chronic actinic dermatitismust be meticulously protected against light exposure. In selected patients inwhom chronic systemic high-dose glucocorticoids pose unacceptable risks, it maybe necessary to employ immunosuppressive drugs such as azathioprine,cyclophosphamide, cyclosporine, or mycophenolate mofetil. Porphyria The porphyrias (Chap. 352) are a group of diseases that have in commoninherited or acquired derangements in the synthesis of heme. Heme is an iron-chelated tetrapyrrole or porphyrin, and the nonmetal chelated porphyrins arepotent photosensitizers that absorb light intensely in both the short (400–410 nm)and the long (580–650 nm) portions of the visible spectrum. Heme cannot be reutilized and must be continuously synthesized, and thetwo body compartments with the largest capacity for its production are the bonemarrow and the liver. Accordingly, the porphyrias originate in one or the other ofthese organs, with the end result of excessive endogenous production of potentphotosensitizing porphyrins. The porphyrins circulate in the bloodstream anddiffuse into the skin, where they absorb solar energy, become photoexcited,generate ROS, and evoke cutaneous photosensitivity. The mechanism of porphyrinphotosensitization is known to be photodynamic, or oxygen-dependent, and ismediated by ROS such as singlet oxygen and superoxide anions.