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

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 +
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 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 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.