Photosensitivity Dermatoses
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Direct answer
Eruptions confined to, or worst on, sun-exposed skin define the photosensitivity dermatoses — forehead, nose, malar cheeks, rims of ears, nape, V of chest, forearms and dorsal hands, with striking sparing of submental, retro-auricular and inner canthal skin. The commonest idiopathic disorder is polymorphic light eruption (PLE), itchy papules, plaques or vesicles appearing hours after the first strong sun exposure of the season and settling without scarring. Drug photosensitivity divides into phototoxic reactions (dose-related, sunburn-like, within hours — doxycycline, thiazides, fluoroquinolones, amiodarone) and photoallergic reactions (eczematous, delayed, immunological — quinine, sulfonamides, ketoprofen). Chronic actinic dermatitis, actinic prurigo, solar urticaria and the cutaneous porphyrias complete the list; phototesting with a monochromator and photopatch testing separate them.
What you must remember
- The exposed-site map: involvement of the forehead, nose, ears, malar area, nape, chest V and dorsal forearms with sparing of the upper eyelids, submental region and flexors is itself the diagnosis-defining sign.
- Polymorphic light eruption: the commonest primary photosensitivity; itchy papules or plaques hours after sun, first exposure of summer worst, improves as the season progresses (natural hardening); antimalarials and prophylactic narrowband UVB before summer are options.
- Phototoxic versus photoallergic: phototoxic is immediate, sunburn-like, dose-dependent and occurs in everyone given enough drug and light; photoallergic is eczematous, delayed-type hypersensitivity, spreads beyond exposed sites and persists after drug withdrawal.
- Classic drug list: doxycycline, thiazides, amiodarone (slate-grey facial pigmentation with long use), fluoroquinolones, voriconazole (aggressive squamous carcinomas in transplant patients), quinine, ketoprofen (photoallergic).
- Chronic actinic dermatitis: thickened, lichenified, light-exposed eczema in older men; histology can mimic mycosis fungoides; monochromator phototesting shows abnormal responses to UVB, UVA and often visible light.
- Actinic prurigo: childhood onset, papules on sun-exposed face and, distinctively, the lips and conjunctiva; strong association with HLA-DR4 in American Indian populations.
- Solar urticaria: wheals within minutes of sun and settle within an hour — the only photosensitivity that starts and stops that fast.
- Do not miss porphyria cutanea tarda: fragility and blisters on dorsal hands with hypertrichosis and hyperpigmentation; check urine porphyrins, and in Indian clinics remember the frequent association with hepatitis C and alcohol.
Building the diagnosis from timing and morphology
Suppose three patients attend the same phototherapy clinic. The first is a 24-year-old woman with itchy papules on forearms and V of the neck after a beach weekend, clearing in a week and leaving nothing — she has PLE, and her management is broad-spectrum sunscreen, sun behaviour and, for severe cases, hardening with graduated narrowband UVB or short-course antimalarials before the sunny season. The second is a 68-year-old farmer with thickened, excoriated, lichenified skin of face, neck and hands that never fully clears; monochromator phototesting confirms chronic actinic dermatitis, and he needs sun avoidance, emollients, topical steroids, and often systemic immunosuppression such as azathioprine 1-3 mg/kg/day (after thiopurine methyltransferase testing). The third developed tense blisters and milia on the dorsal hands with facial hypertrichosis — the pattern points away from an immunological photosensitivity and toward porphyria cutanea tarda, confirmed by fluorescent urine under Wood's lamp and plasma/urine porphyrin assay.
Timing refines morphology: minutes suggest solar urticaria, hours suggest PLE or phototoxicity, a day or two suggests photoallergy, and relentless chronicity with thickening suggests chronic actinic dermatitis. When a drug is suspected, stopping it and re-challenging light (never the drug) settles the issue; photopatch testing formally confirms photoallergy.
Where students slip in exams
The most common error is diagnosing "sun allergy" without naming the pattern — NEET-PG stems reward the specific disorder, and the discriminating clues are timing (minutes, hours, days) and morphology (wheal, papule, eczema, blister). The second slip is forgetting the porphyrias in the differential of hand blisters: PCT is the one photosensitivity that causes fragility, milia and hypertrichosis rather than itch. Candidates also mix up amiodarone's slate-grey pigmentation (a phototoxic distribution on face) with true phototoxic eczema. Finally, remember that photoprotection advice must specify broad-spectrum UVA-plus-UVB cover, since most drug photosensitivity in Indian conditions is UVA-driven and ordinary SPF-15 UVB screens fail.
Frequently asked questions
What is the most common primary photosensitivity disorder?
Polymorphic light eruption — itchy papules, plaques or vesicles on covered-then-exposed skin hours after strong sun, improving through the summer by natural hardening.
How do phototoxic and photoallergic drug reactions differ?
Phototoxicity is dose-dependent, sunburn-like and occurs within hours in anyone; photoallergy is eczematous, cell-mediated, spreads beyond exposed skin and persists after stopping the drug.
Which investigation separates chronic actinic dermatitis from eczema?
Monochromator phototesting demonstrates lowered erythema thresholds to UVB, UVA and often visible light, confirming the photosensitive basis.
Which photosensitivity disorder affects the lips prominently?
Actinic prurigo — paediatric papules on sun-exposed face with characteristic cheilitis and conjunctival involvement.
Why is porphyria cutanea tarda suspected in hand blisters?
Fragility, tense blisters, milia, hypertrichosis and hyperpigmentation on the dorsal hands distinguish PCT from immunological photosensitivities.