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

Photosensitivity and Other Reactions to Light Part 6 Table 57-4 Photoallergic Drugs Topical Systemic 6-Methylcoumarin + Aminobenzoic acid and esters + Bithionol + Chlorpromazine +...

Chapter 057 Photosensitivity and Other Reactions to Light

(Part 6)

Table 57-4 Photoallergic Drugs

Topical Systemic

6-Methylcoumarin +

Aminobenzoic acid and esters +

Bithionol +

Chlorpromazine +

Diclofenac +

Fluoroquinolones +

Halogenated salicylanilides +

Hypericin (St John's Wort) + +

Musk ambrette +

Promethazine +

Sulfonylureas +

A very uncommon type of persistent photosensitivity is known as chronic

actinic dermatitis These patients are typically elderly men with a long history of

preexisting 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 In patients with suspected phototoxicity, determining the minimal erythema dose (MED) while the patient is exposed to a suspected agent and then repeating the MED after discontinuation of the agent may provide a clue to the causative drug or chemical Photopatch testing can be performed to confirm the diagnosis of photoallergy This is a simple variant of ordinary patch testing in which a series of known photoallergens is applied to the skin 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 a positive result The characteristic abnormality in patients with persistent light reaction is a diminished threshold to erythema evoked by UV-B Patients with chronic actinic dermatitis usually manifest a broad spectrum of UV hyperresponsiveness and require meticulous photoprotection including avoiding sun exposure, high (>30) SPF sunscreens, and in severe cases systemic immunosuppression, preferably with azathioprine (1–2 mg/kg per day)

The management of drug photosensitivity involves first and foremost the elimination of exposure to the chemical agents responsible for the reaction and minimization of sun exposure The acute symptoms of phototoxicity may be ameliorated by cool, moist compresses, topical glucocorticoids, and systemically

administered NSAIDs In severely affected individuals, a rapidly tapered course of systemic glucocorticoids may be useful Judicious use of analgesics may be necessary

Photoallergic reactions require a similar management approach Furthermore, patients with persistent light reaction and chronic actinic dermatitis must be meticulously protected against light exposure In selected patients in whom chronic systemic high-dose glucocorticoids pose unacceptable risks, it may

be 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 common inherited or acquired derangements in the synthesis of heme Heme is an iron-chelated tetrapyrrole or porphyrin, and the nonmetal iron-chelated porphyrins are potent 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 the two body compartments with the largest capacity for its production are the bone marrow and the liver Accordingly, the porphyrias originate in one or the other of these organs, with the end result of excessive endogenous production of potent photosensitizing porphyrins The porphyrins circulate in the bloodstream and

diffuse into the skin, where they absorb solar energy, become photoexcited, generate ROS, and evoke cutaneous photosensitivity The mechanism of porphyrin photosensitization is known to be photodynamic, or oxygen-dependent, and is mediated by ROS such as singlet oxygen and superoxide anions