Photosensitivity / Photodermatoses

Meet the patient

A 24-year-old woman returns from a sunny spring weekend with itchy papules and tiny vesicles across her forearms, neck and the V of her chest — every site the sun reached, every site spared beneath her bra straps and watch. She had the same rash last May, and by July it had quietly stopped.[3][4]

The two questions that frame every photosensitivity case are sitting on her skin: how long after sun did the rash appear? and what does the distribution spare? Hold those two and the four buckets below sort themselves.[2]

One spectrum, four buckets

Photosensitivity is not one disease — it is four mechanisms read through two bedside clues. The four buckets every fellow must separate at the viva:[2][11]

[2] [11] [19] [20]

The classic trap: a photo-distributed rash is not "an allergy to the sun" until you have excluded lupus, a drug, and a porphyria. The distribution is given; the cause is your job.[2]

The UV spectrum — what penetrates, what burns

Learn three wavelength bands and the disease each drives, and most of this topic follows.[1][2]

[1] [2]

Two facts that win viva marks: UVC is filtered by ozone and is irrelevant to natural disease, and UVA passes through window glass while UVB does not — which is why the lupus or PCT patient flares sitting by the car window, not just on the beach.[1][23]

Read the distribution — the sparing tells you more than the rash

A photo-distributed rash hits sun-exposed skin and, just as importantly, spares the shadows. The affected sites are the face, neck, V of the chest, dorsa of the forearms and hands.[2][11]

The spared sites are the exam answer: submental triangle, retroauricular fold, upper eyelids, nasolabial folds, beneath spectacle frames, under watchstraps and bra straps, and the webbed finger spaces. That pattern of sparing is what separates a true photodermatosis from a generalised eczema. Morphology then narrows it further — wheals mean urticaria, vesicles mean hydroa or PLE, fragility and milia mean porphyria, scarring means lupus or XP.[2]

The timing face-off — minutes, hours, days

Latency from sun to rash is the single most powerful discriminator, and the centrepiece of this topic. Get the timing right and the diagnosis narrows to two or three possibilities.[1]

[1] [3] [9] [18] [20]

The number rule to memorise: minutes is urticaria or EPP; hours-to-a-day is PLE or phototoxicity; one-to-three days is photoallergy; forever is lupus, porphyria or XP.[1]

Polymorphic light eruption — the commonest, and the spring arrival

PLE is the commonest photodermatosis by a distance — up to 10–20 percent of temperate-climate populations — and the diagnosis is in its calendar. Itchy papules, papulovesicles or plaques appear hours to a day or two after sun, on exposed sites, in a young adult woman, in spring, resolving without scarring over days.[3][4]

The two features that earn marks: the morphology is polymorphous between patients but monomorphic in the same patient (her rash looks identical every year), and the "hardening" phenomenon — reactivity dampens as summer progresses, so she improves by July without treatment.[3][4]

The action spectrum is usually UVA, sometimes UVB. Diagnosis is clinical; provocation phototesting reproduces lesions and excludes mimics. Management is a graded ladder:[3]

[3] [4]

The classic trap: PLE mimics lupus photosensitivity, and the two can coexist. Lupus gives persistent scaly plaques with systemic features and a positive ANA and anti-Ro; PLE clears without a trace and has no serology. If a "PLE" scars or comes with arthralgia, test for lupus.[3]

Actinic prurigo — the childhood one that stays all year

Actinic prurigo is PLE's stubborn cousin: it starts in childhood, persists year-round, and involves the lips and conjunctiva. It is strongly associated with HLA-DRB1*04:07 and is commonest in Indigenous American populations.[5][6]

Excoriated papules, nodules and lichenified plaques sit on sun-exposed sites but extend to covered areas and to the lips (cheilitis) and conjunctiva. There is no hardening — it does not fade through the summer. The HLA tie is close enough that HLA-DRB1*04:07 typing supports the diagnosis.[5][6]

Thalidomide is the most effective systemic agent — 50–100 mg at night, under a strict pregnancy-prevention programme and with nerve conduction surveillance for neuropathy. Photoprotection, topical corticosteroids, calcineurin inhibitors, ciclosporin, mycophenolate and omalizumab are alternatives or adjuncts.[5][6]

Chronic actinic dermatitis — the eczema of older men

CAD is a chronic eczematous photodermatosis of older men, often atop a background of contact or atopic dermatitis, exquisitely sensitive across a broad spectrum — UVB, UVA, and frequently visible light.[7][8]

Clinically it looks like a persistent eczema confined to exposed skin, sometimes generalising to erythroderma; histology shows chronic eczema, occasionally with a CD8-positive T-cell pseudolymphomatous infiltrate. The defining investigation is a markedly reduced minimal erythema dose to UVB and UVA, often with abnormal visible-light responses on monochromator phototesting.[7][8]

Management combines strict photoprotection, topical corticosteroids and calcineurin inhibitors, systemic immunosuppression for severe disease, and — paradoxically — low-dose phototherapy to induce tolerance.[7]

Everyone forgets: CAD patients react to visible light, which standard sunscreens do not block. They need tinted iron-oxide sunscreens and behavioural avoidance, not just SPF.[7][23]

Solar urticaria — wheals in minutes, anaphylaxis in the severe

Solar urticaria is an inducible (physical) urticaria in which UV or visible light triggers wheals within minutes, resolving within an hour. Sheer speed separates it from every other photodermatosis.[9]

It can be debilitating, and on large-body-surface exposure it can become systemic and anaphylactic — the one photodermatosis that may need adrenaline in the bag. The action spectrum is variable (UVB, UVA or visible light).[9]

Management is photoprotection, up-dosed second-generation H1 antihistamines (two- to fourfold standard), omalizumab in refractory cases, phototherapy-induced tolerance, and ciclosporin or IVIG in the severe.[9]

Hydroa vacciniforme — vesicles that scar

Hydroa vacciniforme is a rare childhood-onset photodermatosis of recurrent vesiculobullous lesions on exposed skin that heal with varioliform (vacciniform) scarring. Most cases remit by adolescence.[10]

The trap that earns consultant marks: severe, persistent adult disease with systemic features — fever, hepatosplenomegaly, lymphadenopathy — is associated with an EBV-driven T/NK-cell lymphoproliferative disorder and needs haematology referral and EBV monitoring, not just a sunscreen.[10]

Photoprotection is the mainstay; the scarring and the lymphoproliferative tie are the exam points.[10]

The phototoxic vs photoallergic split — examiners love this

If you learn one distinction in drug photosensitivity, learn this: phototoxic is dose-related and affects everyone; photoallergic is cell-mediated and needs a sensitised patient. It is the most-examined single fact in the topic.[11][12][13]

[11] [12] [13] [15]

The classic trap: photoallergy can persist as a chronic actinic dermatitis ("persistent light reaction") for years after the drug is stopped, because the immune memory remains. A "drug rash that will not go" in a sun-exposed distribution is photoallergy until photopatch testing proves otherwise.[13][15]

The culprit drug list — CAPTAINS

The high-yield photosensitising drug classes are the single most-examined list in the topic. Most are UVA-driven phototoxic; a few — topical NSAIDs, sulphonamides, dapsone — are characteristically photoallergic.[11][12]

[11] [12] [13] [14]

Phytophotodermatitis is the psoralen exemplar: plant contact (citrus, celery, parsnip, fig) plus UVA produces painful linear bullae with striking post-inflammatory hyperpigmentation — the streaked forearm after strimming or squeezing limes at a barbecue. It is phototoxic, not allergic; anyone exposed to enough psoralen and enough UVA reacts.[14]

Photoaggravated dermatoses — light worsens a disease that exists anyway

Several dermatoses are worsened, not caused, by sunlight, and recognising the underlying disease redirects the whole work-up.[2][24]

• Lupus erythematosus — photosensitivity is a classification criterion; subacute cutaneous lupus gives annular or papulosquamous photo-distributed plaques (anti-Ro/SSA positive), discoid lupus scarring plaques, systemic lupus the malar rash that spares the nasolabial folds.
• Dermatomyositis — the shawl and V-sign, heliotrope eyelids, Gottron papules over the knuckles.
• Pellagra — niacin (B3) deficiency, classically from isoniazid, malabsorption, anorexia or Hartnup disease; the Casal necklace with the dermatitis–diarrhoea–dementia triad; treated with niacin.[24]

The light-reactive dermatosis sends you to autoantibodies (ANA, anti-Ro/SSA, anti-dsDNA) and biopsy with immunofluorescence for lupus, and to niacin replacement for pellagra.[2][24]

Xeroderma pigmentosum — the trap no child should miss

Severe sunburn on minimal exposure in a child is xeroderma pigmentosum until excluded. XP is an autosomal recessive defect in nucleotide excision repair, producing catastrophic failure to fix UV-induced DNA damage.[20]

The phenotype declares itself in early childhood: severe sunburn on trivial exposure, freckle-like lentiginosis and poikiloderma on exposed skin, and a more than 10,000-fold increased risk of basal cell carcinoma, squamous cell carcinoma and melanoma at a young age. Ocular (keratitis, lid cancers) and neurological involvement (sensorineural deafness, ataxia, cognitive decline) feature in some complementation groups.[20]

Management is absolute, lifelong photoprotection — UV-filtered home, school and car windows, UPF 50+ clothing, mineral SPF 50+ sunscreens — plus intensive cancer surveillance and tissue-sparing excision. Median survival without aggressive protection is bleak; a dedicated XP clinic changes outcomes.[20]

The classic trap: a "badly sunburnt child" sent home from the emergency department with paracetamol. A first severe burn in an infant demands a DNA-repair work-up, not reassurance.[20]

The cutaneous porphyrias — PCT and EPP

The porphyrias are defects of haem biosynthesis; the cutaneous forms accumulate phototoxic porphyrins that absorb UVA and visible light and generate reactive oxygen species. Two dominate the exam.[19][25]

[16] [17] [18] [19]

The preventable death in this topic: EPP causes acute burning pain on sun in a child, and in a minority the accumulated protoporphyrin obstructs the biliary tree and precipitates cholestatic liver failure. Afamelanotide controls the skin but not the liver — these patients need hepatology follow-up forever.[18][26]

One honest mimic to cite: the sun-distributed petechiae and purpura of EPP can superficially resemble anticoagulant-related purpura. Covert vitamin K antagonist (difenacoum) poisoning produces a similar photo-distributed petechial pattern and is excluded by a coagulation screen.[29]

The diagnostic ladder — MED, monochromator, photopatch, porphyrins

Diagnosis combines bedside pattern recognition with a structured laboratory ladder, and every fellow must name the rungs.[2][15]

• Minimal erythema dose (MED) — the lowest UV dose producing perceptible erythema at 24 hours; a reduced MED to UVB or UVA marks abnormal sensitivity and is the hallmark of CAD.
• Monochromator phototesting — defines the action spectrum across UVB, UVA and visible light; essential for CAD and solar urticaria.
• Provocation phototesting — repeated sub-erythemogenic UVA or UVB reproduces PLE or solar urticaria.
• Photopatch testing — allergens applied then irradiated with UVA; the diagnostic test for photoallergy.
• Porphyrin studies — plasma, urine and faecal porphyrins plus free erythrocyte protoporphyrin; the screen for cutaneous porphyria.
• Autoantibodies and biopsy with immunofluorescence — ANA, anti-Ro/SSA, anti-dsDNA for lupus and dermatomyositis.[15]

Sunscreen science — SPF, UVA, broad-spectrum, filters

Photoprotection is the foundation of management in every photodermatosis, and the sunscreen vocabulary is directly examinable.[1][21]

• SPF (sun protection factor) quantifies UVB protection — the ratio of MED with and without sunscreen. Real-world protection is far lower than labelled, because users apply roughly a quarter of the tested thickness.
• UVA protection is measured by PPD (persistent pigment darkening) and the EU UVA circle (UVA protection at least one-third of SPF). Broad-spectrum (UVB plus UVA) is mandatory for photosensitivity patients.
• Organic (chemical) filters — avobenzone, octocrylene, Tinosorb, mexoryl — absorb UV. Inorganic (physical or mineral) filters — zinc oxide, titanium dioxide — reflect and absorb, and are preferred for sensitive and paediatric skin.
• Visible-light protection needs iron-oxide tinted sunscreens, essential for hyperpigmentation in skin of colour and for the visible-light photodermatoses (CAD, solar urticaria).[23]
• Sunscreen and vitamin D — routine use does not cause vitamin D deficiency in the general population; high-risk photosensitivity patients may need oral supplementation.[22]

Everyone forgets: SPF is a UVB number only. A high SPF with no UVA cover will not protect a PLE or drug-photosensitivity patient, whose action spectrum is usually UVA. Always prescribe broad-spectrum with strong UVA cover.[1][21]

Drug doses that win marks

The systemic therapies in photosensitivity are few enough to memorise, and the doses are examinable. Two non-negotiables recur: hydroxychloroquine has two different doses for two different diseases, and thalidomide has two monitoring obligations.[5][17][18][26][27]

[17] [5] [6] [18] [26] [27]

The trials and guidelines that set practice

The evidence base for photodermatology is thin in places, but four anchor studies define modern practice.[26][27][28]

[26] [27] [28]

Special populations — presentation and risk both shift

Skin of colour. Erythema is masked, so hyperpigmentation is often the presenting sign in PLE, discoid lupus, lichen planus actinicus and pellagra. Visible light drives this hyperpigmentation and is not blocked by standard sunscreens — tinted iron-oxide sunscreens are essential, not optional. Lupus photosensitivity in skin of colour carries greater disease damage and scarring alopecia.[2][23]

Pregnancy. Hydroxychloroquine is safe and should be continued for lupus — flare risk on stopping outweighs drug risk. Thalidomide is absolutely contraindicated, with a pregnancy-prevention programme in place before prescribing. Tetracyclines, voriconazole and isotretinoin are contraindicated.[5][6]

Children. Actinic prurigo, hydroa vacciniforme, xeroderma pigmentosum and erythropoietic protoporphyria all declare themselves in childhood. EPP in particular drives school avoidance — the school must allow broad-brimmed hats, long sleeves and shaded play. XP demands filtered lighting throughout the school environment.[10][18][20]

Organ transplant recipients. Chronic immunosuppression plus photosensitising drugs (azathioprine, ciclosporin, voriconazole) gives a 50- to 65-fold increased risk of cutaneous squamous cell carcinoma. Aggressive photoprotection, regular skin surveillance, and switching azathioprine to an mTOR inhibitor (sirolimus, everolimus) reduce SCC risk.[11][12]

The preventable-harm list — where photosensitivity kills or maims

• A child's first severe sunburn on minimal exposure, dismissed as "just sunburn", who has xeroderma pigmentosum — the preventable cancer burden.[20]
• Acute burning pain on sun in a child with EPP, treated as behavioural, whose protoporphyrin accumulation proceeds to cholestatic liver failure.[18][26]
• A photo-distributed rash with arthralgia, labelled PLE, that is subacute cutaneous lupus with anti-Ro — the missed connective-tissue disease.[2]
• Skin fragility and bullae on the hands, treated as eczema, that is porphyria cutanea tarda with undiagnosed hepatitis C or haemochromatosis.[16][17]
• A persistent light reaction from ketoprofen photoallergy that becomes a chronic actinic dermatitis for years after the drug is stopped.[13][15]
• Anaphylaxis in severe solar urticaria on large-surface exposure, unequipped with adrenaline.[9]
• A voriconazole-treated transplant recipient whose chronic phototoxicity accelerates into invasive squamous cell carcinoma.[11][12]
• A photosensitive patient on standard SPF only, whose UVA-driven PLE or drug reaction persists because the sunscreen has no UVA cover.[1][21]

The mantra, and the etymology

The mantra: minutes is urticaria or EPP, hours is PLE or phototoxicity, days is photoallergy, forever is lupus, porphyria or XP — and photoprotection first, always.[1][2]

Etymology for viva gold: phototoxicity shares its root with photon — the drug literally turns light into poison at the skin. Vacciniforme in hydroa vacciniforme means "smallpox-like", from vaccinia, because the scars resemble old smallpox vaccination scars. Poikiloderma in XP is Greek for "varied skin" — the mottled mix of atrophy, telangiectasia and pigment that chronic UV damage paints.[20]

[1]

Ward-round test — four stems, thirty seconds each

Stem 1 — the spring weekend rash (answer)

A 24-year-old woman has itchy papules and tiny vesicles on her forearms, neck and chest V two days after a sunny spring weekend, sparing beneath her bra straps and watch. What is the diagnosis, and what is the first management step? Model: This is polymorphic light eruption — the commonest photodermatosis, onset hours to a day after sun, polymorphic between patients but monomorphic in this patient, sparing shadowed sites, clearing without scarring. Action spectrum usually UVA. First step is broad-spectrum photoprotection with strong UVA cover plus an oral antihistamine and a short potent topical corticosteroid for the flare; prophylactic narrowband UVB hardening before next spring if recurrent.[3][4]

Stem 2 — the burning child (answer)

A 5-year-old screams and cries within minutes of going into the sun, with erythema and swelling of the face and hands but no blister. What is the diagnosis, the confirmatory test, and the preventable complication? Model: This is erythropoietic protoporphyria — burning pain within minutes, no blister, in a child. Confirm with raised free erythrocyte protoporphyrin. The preventable complication is cholestatic liver failure from protoporphyrin biliary obstruction — these children need lifelong hepatology surveillance. Afamelanotide is the licensed therapy.[18][26]

Stem 3 — the severe sunburn in an infant (answer)

A 9-month-old has severe blistering sunburn after ten minutes outdoors, with freckle-like lentigines on the cheeks. What must you exclude, and how? Model: This is xeroderma pigmentosum until proven otherwise — defective nucleotide excision repair, catastrophic UV sensitivity, lentiginosis and a more than 10,000-fold skin-cancer risk. Arrange DNA-repair testing and genetic counselling, institute absolute photoprotection (filtered windows, UPF 50+ clothing, mineral SPF 50+), and refer to a dedicated XP clinic for cancer surveillance. Dismissing this as ordinary sunburn is the preventable error.[20]

Stem 4 — the photo-distributed eczema on doxycycline (answer)

A 55-year-old on doxycycline for rosacea develops an exaggerated sunburn confined to sun-exposed skin within hours of gardening. Phototoxic or photoallergic, and why does it matter? Model: This is phototoxicity — dose-related, non-immunological, exaggerated sunburn confined to the irradiated area, occurring in anyone on enough drug plus enough UVA. It resolves in days to weeks after stopping the doxycycline. Photoallergy, by contrast, is type IV, eczematous, delayed 24–72 hours, may spread beyond the irradiated skin, and is confirmed by photopatch testing. The distinction matters because photoallergy can persist as a chronic actinic dermatitis for years.[11][12][13][15]

References

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