Transcript photodermatoses

PHOTODERMATOSES
A group of skin diseases initiated
or aggravated by solar radiation
5%
45%
50%
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
Chronic changes
induced by sunlight
(photoaging)
• 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
II. Pathological photodermatoses
phototoxic
photoallergic
(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.
 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
 Clinical findings: occur
in days (immunization is
in minutes or hours…
in progress), eczematous
…sharply bordered erythema… inflammation spreads on the
skin non-exposed to UV light.
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…
exogenous phototoxic reaction
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.
endogenous phototoxic reaction
 inherited or acquired (more often)
 usually in men (alcoholic intake)
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)
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
Skin Disorders Aggravated by Sun-light
 herpes simplex
 lupus erythematodes
 dyskeratosis follicularis
 rosacea
 vitiligo
 perioral dermatitis
 bullous pemfigoid
 photosensitive psoriasis…
DIAGNOSTICS
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History of the photodermatosis
Clinical features
Phototests
Skin biopsy
Laboratory findings
Therapy
• Corticosteroids
• Antimalarial agents
(PCT)
• Surgical intervention
(XP)
Prevention
Photoprotection
(sunscreens, clothes,
sunglasses…),
antimalarial agents,
betacarotens…
Dermatoses of Physical
(external) Origin
Thermal 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.
Thermal injury – burn (combustio)
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)
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)
Thermal injury – burn (combustio)
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
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, itching
Therapy: symptomatic (warm area, vasodilatation)