Transcript Light-Related Disorders

Light-Related
Disorders
By
Omar Y. Abdullah
• Sunlight has profound effects on the skin and is
associated with a variety of diseases.
• Ultraviolet (UV) light causes most photobiologic
skin reactions and diseases.
• UV light is divided into UVA (320 to 400 nm), UVB
(290 to 320 nm), and UVC (100 to 290 nm).
• UVA is further subdivided into UVA I (long wave)
and UVA II.
• The ratio of UVA to UVB is 20:1, and two thirds of
this UVA is UVA I.
• More than 90% of UV radiation may penetrate
clouds!!!
• UV radiation generates reactive oxygen species
that damage skin.
UVA
• UVA causes immediate and delayed tanning and
contributes little to erythema and burning.
• Constant throughout the day and throughout the year.
• The longer wavelengths of UVA can penetrate more
deeply, reaching the dermis and subcutaneous fat.
• Chronic exposure causes connective tissue
degeneration (photoaging), photocarcinogenesis, and
immunosuppression.
• UVA augments the carcinogenic effects of UVB
• UVA penetrates window glass and interacts with topical
and systemic chemicals and medications.
• It produces photoallergic and phototoxic reactions.
UVB
• UVB produces the most harmful effects and is greatest during
the summer.
• Snow and ice reflect UVB radiation.
• UVB delivers a high amount of energy to the stratum corneum
and superficial layers of the epidermis.
• It is primarily responsible for sunburn, suntan, inflammation,
delayed erythema, and pigmentation changes.
• Chronic effects include photoaging, immunosuppression, and
photocarcinogenesis.
• It is most intense when the sun is directly overhead between
10 am and 2 pm.
• UVB is absorbed by window glass.
• Prior exposure to UVA enhances the sunburn reaction from UVB.
UVC
• UVC is almost completely absorbed by the ozone layer and is
transmitted only by artificial sources such as germicidal lamps.
So what happens?
• DNA is mutated by UVB.
• Absorption of UVA leads to the release of
reactive oxygen species.
• These reactive oxygen species cause oxidation
of lipids and proteins that affect DNA repair,
produce dyspigmentation, and cause
photoaging and carcinogenesis.
NORMAL AGING
• The skin begins to show signs of aging by ages 30 to 35.
• Aged skin is thin, fragile, and inelastic. The epidermis
becomes thin.
• There is a gradual loss of blood vessels, dermal
collagen, subcutaneous fat, and the number of elastic
fibers.
• There is a reduction in the density of hair follicles,
sweat ducts, and sebaceous glands, resulting in a
reduction in perspiration and sebum production.
• The skin becomes atrophic and fragile when
subcutaneous tissue is lost.
• Loss of elastic fibers results in fine wrinkles that
disappear by stretching. The skin is easily distorted, but
it recoils slowly.
• Potent steroids should not be used on aged skin.
PHOTOAGING
• Photoaging refers to those skin changes
superimposed on intrinsic aging by chronic
sun exposure.
• Unprotected, chronically exposed children can
acquire significant actinic damage by the time
they reach 15.
• Sun-damaged skin is characterized by elastosis
(a coarsening and yellow discoloration of the
skin), irregular pigmentation, roughness or
dryness, telangiectasia, deep wrinkling,
follicular plugging, and a variety of benign and
malignant neoplasms. The epidermis thickens.
Solar Elastosis
• Is a sign highly characteristic of severe sun
damage.
• There is massive deposition in the upper
dermis of an abnormal, yellow, amorphous
elastotic material that does not form
functional elastic fibers.
• This altered connective tissue does not have
the resilient properties of elastic tissue.
Wrinkling becomes coarse and deep rather than fine,
and the skin is thickened. These wrinkles do not
disappear by stretching.
Sun-induced
wrinkling on the
back of the neck
shows a series of
crisscrossed lines
that form a
rhomboidal
pattern (cutis
rhomboidalis
nuchae).
Reddish-brown, reticulate pigmentation with
atrophy and telangiectasia is seen on the sides
of the neck (poikiloderma of Civatte).
Slightly elevated seborrheic keratoses occur on
the back of the hands and may be misdiagnosed
as solar lentigines.
Blood vessels diminish in number, and the walls of the remaining
vessels become thin. Bleeding occurs with the slightest trauma
to the sun-damaged surfaces of the forearms and hands but not
to the unexposed surfaces. Fragile sun-damaged skin is easily
torn and heals with haphazard scars called stellate pseudoscars.
Actinic comedones. Open and closed
comedones are present in the periorbital areas.
Acne-like inflammation does not occur.
Actinic comedones may become very large but
can easily be expressed with a comedone
extractor.
Treatment of photoaging
• Photoaging is treated with either topical
treatments (tretinoin cream) or resurfacing
through chemical peels, dermabrasion, or
lasers.
• Sun protection: Sunscreens are topical agents
that absorb, scatter, or reflect UV radiation
and visible light.
 SPF???
• Estrogen replacement
Skin phototypes
Type
Characteristic
Examples
I
Always burns easily, never tans
Celtic or Irish extraction; often blue
eyes, red hair, freckles
II
Burns easily, tans slightly
Fair-skinned individuals; often have
blond hair; many whites
III
Sometimes burns, then tans
gradually and moderately
Mediterraneans and some Hispanics
IV
Burns minimally, always tans well
Darker Hispanics and Asians
V
Burns rarely, tans deeply
Middle Easterners, Asians, some
blacks
VI
Almost never burns, deeply
pigmented
Some blacks
POLYMORPHOUS LIGHT ERUPTION
• Polymorphous light eruption (PLE) is the most
common light-induced skin disease.
• It is a long-standing, slowly ameliorating disease.
• It is simply an itchy rash caused by sun exposure in
people who have developed photosensitivity.
• Starts in spring and early summer when a person’s
exposure to the sun increases.
• There are several morphologic subtypes, but
individual patients tend to develop the same type
each year.
• The eruption appears first on limited areas but
becomes more extensive during subsequent
summers.
• Most people with PLE have exacerbations each
summer for many years; a few have temporary
remissions.
• The amount of light exposure needed to elicit an
eruption varies greatly from one patient to
another.
• Most patients have symptoms 2 hours after
exposure.
• Light sensitivity decreases with repeated sun
exposure; this phenomenon is referred to as
hardening. Therefore, the eruption may cease to
appear after days or weeks of repeated sun
exposure.
• Those exposed to sunlight all year rarely acquire
PLE.
• Women are affected more often than are
men. The mean age at onset is 34 years (5 to
82 years).
• The most common initial symptoms are
burning, itching, and erythema.
• The eruption usually lasts for 2 or 3 days, but
in some cases it does not clear until the end of
summer.
• Many patients experience malaise, chills,
headache, and nausea starting few hours after
exposure but lasting only 1 or 2 hours.
• The most commonly involved areas are the V
of the chest (the area exposed by opennecked shirts), the backs of the hands,
extensor aspects of the forearms, and the
lower legs of women.
• Lesions usually heal without scarring.
• Many patients react to UVB, others to UVA, or
some to both.
Papular type
The papular type is the most common form. Small papules are disseminated
or densely aggregated on a patchy erythema.
Plaque type
Is the second most common pattern.
Papulovesicular type
This type is less common. It occurs almost exclusively in women. Itching is
common.
OTHER TYPES INCLUDE:
• Eczematous type : Erythema, papules, scale,
and sometimes vesicles occur. It occurs almost
exclusively in men.
• Erythema multiforme-like type.
• Hemorrhagic type.
TREATMENT of PLE
Patients can become disease free by using
sunscreens and gradually increasing sun
exposure in the spring. Phototherapy and
photochemotherapy are most effective.
• TOPICAL AND ORAL STEROIDS
• SUN PROTECTION
• DESENSITIZATION WITH PHOTOTHERAPY (UVB
and/or UVA)
• PUVA
• ANTIMALARIAL DRUGS
• Cyclosporine or azathioprine may be used for
rare severe disabling cases.
PHOTOTOXIC REACTIONS
• Phototoxicity occurs when a photosensitizer is
absorbed into the skin either topically or
systemically in appropriate concentrations and
is exposed to adequate amounts of specific
wavelengths of light, usually UVA.
• There is a variety of topical and systemic
agents like perfumes, plants
{phytophotodermatitis} (eg., lime juice), and
drugs (eg., antibacterials, NSAIDs, diuretics,
retinoids, antifungals).
Feature
Phototoxic reaction
Photoallergic reaction
Incidence
High
Low
Amount of agent required
Large
Small
Onset of reaction
Minutes to hours
24-72 hours
More than one exposure
to agent required
No
Yes
Distribution
Sun-exposed skin only
Sun-exposed skin; may
spread to unexposed
areas
Clinical characteristics
Resembles exaggerated
sunburn or blisters
Dermatitis
Immunologically
mediated
No
Yes; type IV
Doxycycline-induced phototoxicity