PHOTODERMATOLOGIC

DISORDERS
(PHOTODERMATOSES)
Mikias woldetensay
Mikiaswoletensay@gmail.com
Dermatology & venereology
Oct 2021
 OUTLINE

• INTRODUCTION
• CUTANEOUS UVR RESPONSES
– SUNBURN
– SOLAR LENTIGO
– PHOTOAGING
• DRUG/CHEMICAL INDUCED
PHOTOERMATOSES
– PHOTOALLERGIC CONTACT DERMATITIS
– PHOTOTOXIC DERMATITIS
• DNA REPAIR DEFECTS
– XERODERMA PIGMENTOSUM
 INTRODUCTION
• Photodermatology
– Photo=light.
– Photodermatology is a branch of
dermatology that deals with the
interaction of solar radiation with the
skin, as well as the various skin diseases
related to or caused by sunlight.
 INTRODUCTION
• Photodermatoses
• (Photodermatologic diseases )
– Refer to cutaneous disorders where solar
radiation (mainly Ultraviolet ray & visible
light) plays the main pathogenetic role.
 INTRODUCTION
• Sunlight [mainly UVR (ultraviolet
radiation)], is a portion of the entire solar
spectrum known as electromagnetic
radiation.
 INTRODUCTION
• The main culprit of solar radiation–induced
skin pathology is the ultraviolet portion of
the solar spectrum.
• The UVR based on wave lengths is divided
in to:
– UVA…315-400 nm.
• UVA I…340-400 nm.
• UVA II…315-340 nm.
– UVB…290-315 nm.
– UVC…200-290 nm.
 INTRODUCTION
• Only UVA & UVB
reach the skin surface.
• UVC is reflected by
the ozone layer.
• UVA
– Penetrates up to the
deep dermis.
• UVB
– Penetrates up to the
upper dermis.
 INTRODUCTION
• Light energy (UVR) travels in packed energy
forms known as photons.
• Light energy (UVR) (photons)/ after
reaching the skin, absorbed by
molecules/compounds known as
chromophores.
 INTRODUCTION
• Chromophores
– A compound/molecule that absorbs
radiation or light energy.
– Chromophores may be endogenous ,
exogenous or a combination of both.
– Endogenous chromophores
• Mostly present in the skin or produced
in the body by abnormal metabolism.
• Melanin, hemoglobin, porphyrins, DNA.
 INTRODUCTION
• Exogenous chromophores
– Topically applied medications or systemic
drug molecules.
• After light energy is absorbed by
chromophores, it is either:
– Re-emitted harmlessly as biologically
inactive radiation, or
– Diverted to driving thermochemical
reactions, leading to molecular, cellular,
tissue, and clinical changes.
 INTRODUCTION
• These biochemical reactions result in
biologic responses to light (UVR).
• The biologic responses are usually
protective & physiologic.
– Vit D production, photoaging.
• The biologic responses could also be
pathological.
– E.g. Photocarcinogenesis, Sunburn
 INTRODUCTION
• Cutaneous UVR responses.
– Acute
• Sunburn
• Tanning
• VIT D synthesis
• Immunosuppression
– Chronic
• Photoaging
• Photocarcinogenesis
 INTRODUCTION
• Immunosuppression
– An acute cutaneous UVR response.
– UVR diminishes the antigen presenting
ability of dendritic antigen presenting
cells.
– Impaired antigen presentation to effector
T cells leading to suppressed T-cell
responses.
 INTRODUCTION
• Photodermatoses
– Skin diseases resulting from an abnormal
interaction of sunlight (mostly UVR) and
the skin.
– Affect the photoexposed (sunlight
exposed) sites of the skin.
– Spare the photoprotected (cloth covered)
sites of the skin.
 INTRODUCTION
• Photodermatoses
– Photo-exposed sites:
• Face, v-area of the neck, extensor
forearms, dorsal hands.
– Photoprotected sites.
• Trunk, proximal extremities, palms &
soles, flexor sites of the forearms.
• Folds (nasolabial, retroauricular,
eyelid).
 INTRODUCTION

• The photodermatoses include various

disorders, grouped in to 4 major categories:
– Idiopathic (probably immune-mediated)
photodermatoses. E.g chronic actinic
dermatitis.
– Drug/chemical induced
photodermatoses.
• Photoallergic contact dermatitis
• Phototoxic dermatitis
 INTRODUCTION
• Photoaggravated dermatoses
– Most diseases affecting the skin primarily,
but get aggravated & worsen during UVR
exposure.
– E.g acne, rosacea, etc.
• DNA repair defects.
– E.g xeroderma pigmentosum
CUTANEOUS UVR RESPONSES
• SUNBURN
• SOLAR LENTIGO
• PHOTOAGING
 SUNBURN
• An acute and transient inflammatory
response of normal skin after exposure to
UVR.
• Mostly UVB.
• Characterized by pain, tenderness,
erythema, edema, vesicles, bullae &
erosions in severe cases.
 SUNBURN
• The initiating event is thought to be
damage to DNA.
• Exposed keratinocytes with UV-induced
DNA damage switch on a variety of damage
response pathways in which they secrete
various inflammatory mediators.
– Serotonin, TNF, prostaglandins, nitric
oxide, neuropeptides.
 SUNBURN
• The development of sunburn depends on
– The amount of UVR energy delivered.
• UVR intensity is highest around midday,
with decreasing latitude, increasing
altitude.
– The susceptibility of the individual (SPT).
• Susceptible skin phototypes.
– Fair/white colored..(SPT I individual).
 SUNBURN
• With these requirements fulfilled, a
phototoxic reaction occurs on the skin.
• Sunburn is a phototoxic reaction where
there is a direct keratinocyte toxicity.
• Keratinocyte necrosis is the pathologic
event leading to clinical lesions.
 SUNBURN
• Onset of symptoms depends on intensity of
exposure.
• Erythema develops after 6 hours of intense
sun exposure and peaks after 24 hours.
• Followed by tanning and desquamation.
 SUNBURN
• Pruritus
– Could be seen in both mild & severe
sunburn.
• Pain/burning sensation and tenderness
– Seen in severe sunburn.
 SUNBURN
• Mild sunburn
– Erythema of the skin sharply confined to
photoexposed sites, sparing covered sites.
– Sharply marginated at the border
between exposed and covered skin.
 SUNBURN
• Severe sunburn
– Pain, tenderness.
– Oedema, vesicles, bullae, erosions.
– Constitutional symptoms.
• Fever, chills, headaches, athralgia, malaise.
• Tachycardia.
 SUNBURN
• RX
– Mild sunburn
• Avoid exposure at high intensity UVR
periods.
• Photoprotection (both physical &
chemical protection).
–Physical…umbrellas, wide brimmed
hats, protective clothing.
–Chemical…Sunscreens.
 SUNBURN
• Rx
– Mild sunburn
• Topical Cool wet dressings.
• Topical glucocorticosteroids.
• Analgesics..,NSAIDs.
 SUNBURN
• Rx
– Severe Sunburn
• If very severe, a “toxic” patient may
require hospitalization for fluid
replacement, treatment of infections,
etc.
• Topical Cool wet dressings.
• Topical glucocorticoids.
• Systemic glucocorticoids..prednisolone
 SOLAR LENTIGO
• A circumscribed brown macule resulting
from a localized proliferation of
melanocytes due to chronic exposure to
sunlight.
• More common in fair skinned individuals.
• Cryosurgery and laser are effective means of
treatment
SOLAR LENTIGO
 PHOTOAGING
• A chronic normal cutaneous response to
cummulative UVR exposure.
• UVA reaches the dermis and causes
cumulative damage to the collagen & elastin
in the deep dermis.
• Features of aging like wrinkling. wizened,
leathery appearance.
 PHOTOAGING
• More severe in fair skin individuals.
 DRUG & CHEMICAL INDUCED
PHOTODERMATOSES
• Due to the interaction of UVR with a
chemical/ drug within the skin which acts
as a chromophore absorbing UVR.
• Two mechanisms are recognized:
– Phototoxic reactions
– Photoallergic reactions
 DRUG & CHEMICAL INDUCED
PHOTODERMATOSES
• Phototoxic reactions
– Photochemical reactions leading to direct
keratinocyte necrosis.
• Photoallergic reactions
– A photoallergen is formed & initiates an
immunologic response (delayed type 4
hypersensitivity reaction).
 DRUG/CHEMICAL INDUCED
PHOTODERMATOSIS
• The main clinical difference between
phototoxic and photoallergic eruptions is
that the former manifests like an irritant
(toxic) contact dermatitis or sunburn and
the latter like an allergic eczematous
contact dermatitis.
 PHOTOALLERGIC CONTACT
DERMATITIS
• In sensitized individuals exposure to a
photoallergen and sunlight results in a
pruritic eczematous eruption confined to
exposed sites.
• In most patients the eliciting drug/chemical
is topically applied.
– Disinfectants, antimicrobials, agents in
sunscreens, perfumes in aftershaves, or
whiteners.
 PHOTOALLERGIC CONTACT
DERMATITIS
• Less commonly, systemic drugs are
incriminated.
• The chemical agent present in the skin
absorbs photons and forms a photoproduct.
• This then binds to a soluble or membrane-
bound protein to form an antigen to which a
type IV immune response is elicited.
 PHOTOALLERGIC CONTACT
DERMATITIS
• Pruritus on sunexposed sites.
• Eczematous lesions appear on sunexposed
sites.
– Erythema, oedema, papules, vesicles,
oozing, erosions.
– Papules & scales.
– Lichenification.
 PHOTOXIC DERMATITIS
• An adverse reaction of the skin that results
from simultaneous exposure to certain
drugs (via ingestion, injection, or topical
application) and to UVR or visible light.
• Systemic agents (drugs) are the commonest
causes.
• Less commonly, the causes are topical
agents.
 PHOTOXIC DERMATITIS
• Photochemical reactions result in direct
keratinocyte toxicity….(sunburn like clinical
picture).
• Presents as an exaggerated sunburn
response.
– Pain & tenderness.
– Erythema, edema, vesicles, and/or bullae.
• Lesions occur on photoexposed sites.
 Rx of Photoallergic & phototoxic dermatitis

• General measures
– Avoid/discontinue culprit agent.
• Topical or systemic agents.
– Photoprotection (physical & sunscreens).
– Treat bacterial superinfections.
– Antihistamines for severe itching.
 Rx of Photoallergic & phototoxic dermatitis

• General measures….
– Analgesics for severe pain.
– Wet dressings for wet lesions/erosions.
• Specific Rx
– Mild cases….topical steroid
creams/ointments.
– Severe cases….systemic steroids.
XERODERMA PIGMENTOSUM

• An x-linked autosomal recessive disorder.

• Consanginuous marriage is a risk factor for
x-linked autosomal recessive disorders.
• Mutations in various different genes
involved in DNA repair after UV damage.
XERODERMA PIGMENTOSUM

• After UVR exposure, DNA damage on the

skin is repaired in normal states.
• In XP, failure of DNA repair mechanisms.
XERODERMA PIGMENTOSUM
• Photodisributed UVR induced lesions occur
at an early age.
• Early skin findings (onset before 2 years).
– Photosensitivity (exaggerated
erythematous response to sunlight
exposure)and
– Lentigines (UVR induced hyperpigmented
macules).
XERODERMA PIGMENTOSUM
• Multiple actinic keratoses (SCC in situ).
• Premature (before the age of 10 years)
development of various types of skin cancer.
– SCC, BCC.
• Early death from malignant skin cancer.
– Second decade.
XERODERMA PIGMENTOSUM
• Dx
– Clinical
• Rx
– Early dx and follow up for the
development of skin cancer & occular
complications is vital.
– No specific treatment.
– Strict Photoprotection.