PHOTODERMATOSES

A group of skin diseases initiated or aggravated by

solar radiation

50%5% 45%

Photodermatoses

I. Normal photodermatoses

● erythema solare (sunburn, acute reaction)

● chronic changes due to UV radiation (degenerative r.)

II. Pathological photodermatoses

● phototoxic and photoallergic reactions ● idiopatic photodermatoses (unknown

etiopathogenesis)

III. Other types of photodermatoses● genodermatoses

● skin disorders aggravated by sun-light

erythema solare = sunburn (acute reaction)

Erythema appears within minutes and persist for days, desquamation occurs within a week.

In the second stage → edema, blisters.

Therapy: cool wet compresses, topical corticosteroids

• atrophy of the skin, wrinkles

• solar elastosis (thickened, yellowish, wrinkled skin)

• reddish-brown pigmentation

• angiectasis (dilatation of vessels)

• actinic keratosis, basal cell ca, squamous cell carcinoma

Chronic changes induced by sunlight

(photoaging)

phototoxic (more frequent)

A photosensitizer (plants, drugs…) is absorbed into skin (topically or systemically), skin must be exposed to sunlight → skin absorbs bigger amount of UV-light (quantitative photosesitivity).

Higher concentration of a photosensitizer and more UV-light.

Clinical findings: occur in minutes or hours… …sharply bordered erythema…

UV-light initiates changes of chemicals or drugs, after

reaction between changed agents and skin protein forms a new antigen

(= immunologic reaction, qualitative increased

photosensitivity).

Less alergen, less UV-light.

Clinical findings: occur in days (immunization is

in progress), eczematous inflammation spreads on the skin non-

exposed to UV light.

photoallergic

II. Pathological photodermatoses

Phototoxic Photodermatoses

A photosensitizer (plants – root celery, carrot, figs, coal tar, drugs – ATB…) is absorbed into skin (topically or systemically), skin must be exposed to sunlight → skin absorbs bigger amount of UV-light (quantitative photosesitivity).

More frequent than photoallergic reactions.

Necessary appropriate (higher) concentration of a photosensitizer and adequate amount (more) of UV-light.

Clinical findings: occur in minutes or hours… …sharply bordered erythema, blistering,… ...postinflammatory hyperpigmentation for a long time…

Berloque Dermatitis

It is due to psoralens (photosensitizer) contained in

bergamot oil, in some perfumes and

exposure UV-light.

exogenous phototoxic reaction

Dermatitis Bullosa Pratensis (phytophotodermatitis, meadow grass

dermatitis)

Exposure to plants (celery, parsley, meadow grass…) containing light-sensitizing compounds (so-called

furocoumarins) and UV-light occur erythema, burning edema,

vesiculation in linear streak, only in the place of contact with plants.

exogenous phototoxic reaction

endogenous phototoxic reaction

Porphyria Cutanea Tarda It is caused by enzymatic defect in the heme

biosynthetic pathway. Accumulation of porphyrins in the skin leads to photosenzitivity and skin fragility (a slight

trauma damages skin). Clinical features: blistering in sun-exposed areas (the

back of hands, cheeks, temples, top of the head), hyperpigmentation… (+ massive increased urine

porfyrins)

inherited or acquired (more often) usually in men (alcoholic intake)

Idiopathic photodermatoses (unknow trigger)

• Polymorphic light eruption (UVA) = reaction after exposure to UV-light without additional drug.

• Solar urticaria (UVA, UVB, visible light)

• Hydroa vacciniformia

Polymorphic Light Eruption

o frequent, middle age, more in women (4:1), most people have excerbations each spring for many years

o several clinical types – papular, eczematous…

Solar Urticaria

o caused by UVA, UVB, visible light

o in sun-exposed sites – itching urticaria

Hydroa Vacciniforme

o uncommen

o childhood, in spring

o blisters, crusts, scars…

Other types of photodermatoses (uncommen)

Enzymatic defects: xeroderma pigmentosum, fenylketonurie…Other genodermatoses: Bloom´s syndroma, ataxia teleangictatica…

Xeroderma Pigmentosum

defect in DNA repairing enzymes, with extremely photosensitivity, erythema, pigmentation, 2000x greater risk of skin cancer, 20-fold risk of internal malignancy then of the general population

herpes simplex

lupus erythematodes

dyskeratosis follicularis

rosacea

vitiligo

perioral dermatitis

bullous pemfigoid

photosensitive psoriasis…

Skin Disorders Aggravated by Sun-light

DIAGNOSTICS

• History of the photodermatosis• Clinical features• Phototests• Skin biopsy • Laboratory findings

• Corticosteroids• Antimalarial agents (PCT)• Surgical intervention (XP)

Therapy

Prevention

Photoprotection (sunscreens, clothes,

sunglasses…), antimalarial agents,

betacarotens…

Dermatoses of Physical Dermatoses of Physical (external) Origin (external) Origin

Thermal injuryThermal injury

Burn (combustio) = acute tissue damage

caused by heat (flame, fume, hot liguid or

solids), electricity, chemicals, radiation,

friction...

Burns are described according to the depth of

injury to the dermis and are

loosely classified into first, second, third

and fourth degrees.

I. degree - affects epidermis,

clinical picture: redness (erythema), dry, painful,

time to healing: 1wk or less without complication

Thermal injury – burn (combustio)

II. degree (superficial partial thickness), extends into superficial (papillary) dermis,

clinical picture: redness with clear blisters,

blanches with pressure, moist

surface, painful,

time to healing: 2-3wks,

complication: local

(bacterial) infection

Thermal injury – burn (combustio)

II. degree (deep partial thickness), extends into deep (reticular) dermis

clinically: red-and-white with bloody blisters, moist, painful,

time to healing: weeks - may progress to third

degree, complication: scarring,

contractures

(may require excision

and skin grafting)

Thermal injury – burn (combustio)

III. degree (full thickness) extends

through entire dermis

clinically: white/brown, necrotic tissue, dry,

leathery, painless

healing: requires excision

complication: scarring,

contractures,

(amputation in some cases)

IV. degree extends through skin, subcutaneous

tissue and into underlying muscle and bone

clinically: black; charred with eschar, dry,

painless

healing: requires excision

complication: amputation,

significant functional

impairment

Thermal injury – burn (combustio)

Cold injury – Frostbite (congelation) Direct tissue injury that results when skin temperature drops below 0°C. Skin damage depends on the intensity of the cold, wind, type of clothing, the presence of the peripheral vascular abnormalitis, the use of alcohol…Appearance: four phases – erythema, blisters,

spf. necrosis, deeper necrosis (either dry necrosis = mumification or wet necrosis with infection = gangrene)Therapy: rewarming, debridement of necrotic tissue

Cold injury – chilblains (pernio, perniones) Pernio is associated with prolonged

exposure to above-freezing temperature. People who work in cold dump places (butcher shop, meat peacking plants…) + tight shoes and gloves, thin socks, peripheral vascular insuficiency.

Appearance: lesions are typically located on the dorsal aspects of the fingers or toes, they are blue-red, edematous, sharply bordered, flat patches or nodules, painful, itchingTherapy: symptomatic (warm area, vasodilatation)