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Drug-induced photosensitivity
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Drug-induced photosensitivity

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Author: Dr. Simona Stiuriuc

Pathogenesis of drug photosensitivity
Signs and symptoms
Treatment

Causes and risk factors

Diagnosis
Suffering from a dermatologic al?

Drug-induced
photosensitivity
refers
to
the
development of cutaneous manifestations as a result of
the combined effects of chemicals and light. exposure
to chemicals or only just light is not sufficient to induce
disease, however photoactivation occurs when chemicals
may occur one or more events . Such events include
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phototoxic and photoallergic reactions, lichen planus ,
protoporfirie and lupus erythematosus subacute
Stop & Reverse Effects of
cutaneous. photosensitivity reactions may result from
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ultraviolet A range, so that particular product are more
likely to cause induced photosensitivity reactions,
although occasionally ultraviolet B may be responsible for
such effects. Ultraviolet B frequently cause sunburn and
skin
cancer
nonmelenomic.
In
patients
with
photosensitivity is difficult to differentiate from those
photoallergic phototoxic reactions . phototoxic reactions are due to the destructive effects of components by
activated by light in cell membranes and in some cases DNA. In contrast, photoallergic reactions are immunemediated activation of the light component. Typically appear as exaggerated sunburn. Photoallergic reactions
include contact dermatitis with a distribution limited to sun-exposed areas of the body. When these reactions are
severe or prolonged it may extend to the areas covered. photoallergic reactions develops only in a minority of
people exposed to composite and light. Are less prevalent than phototoxic reactions. The amount of drug
required to trigger a photoallergic reaction is considerably lower than that required for phototoxic reactions. In
addition, photoallergic reactions are a form of cell-mediated immunity, their onset is late, up to 24-72 hours
after exposure to the drug and light. In contrast, phototoxic response occurs in a few minutes or hours after
exposure to light. based therapy is the DENTIFICATION and avoid these drugs, use sunscreen and
symptomatic measures. Use topical corticosteroids, cold compresses painkillers. drug-induced
photosensitivity is associated with death only in rare cases, people who are exposed to large amounts of sunlight
after taking a significant dose of psoralen. Although mortality is rare, drug-induced photosensitivity can cause
significant morbidity in some people who have to limit their exposure to natural or artificial light. Carcinogenic
potential by prolonged exposure to these drugs has been suggested and its clinical relevance remains to be
determined.

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Pathogenesis of drug photosensitivity

Phototoxic reactions
Phototoxic reactions result from direct tissue destruction caused by photoactivated compound. Numerous
compounds have the potential to cause phototoxicity. Most have at least one double bond or an aromatic ring
that can absorb radiant energy. Most compounds are activated by UV-A, although some have a maximum
absorption in the visible range of ultraviolet B. Most times photoactivation of a compound determine the
excitation of electrons in stable form in one excited. As the electrons are returning to a more stable
configuration, they transfer their energy oxygen leading to the formation of reactive oxygen intermediates.

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12/8/13

Drug-induced photosensitivity

These compounds such as superoxide anion, hydrogen peroxide, injure cell membranes and DNA. Cotokine can
lead to the formation of arachidonic acid and activation. The result is an inflammatory response that has the
clinical appearance of an exaggerated sunburn. exception to this mechanism is mediamentos induced
phototoxicity phototoxicity induced by psoralen. Psoralenii intercalates DNA forming mono-functional way.
Exposure to ultraviolet radiation causes DNA bidirectional pathways.

Photoallergic reactions
Photoallergic reactions are mediated cellular immune responses to the antigen is a drug activated by light.
Photoactivation rise to a metabolite that can bind to protein carriers in the skin to form a complete antigen.
reaction then proceed as any inflammatory cell-mediated response. Langerhans cells take up antigen and migrate
to regional lymph nodes. This T cell antigens are presented showing specific receptors. T cell becomes activated
and proliferate Returning to the place photoallergenic deposits. T lymphocytes in the skin cause an inflammatory
response if photoallergenic eczematous morphology applied topically or characteristics of a drug eruption if
photoallergenic administered systemically.

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Causes and risk factors

Most photoallergic reactions result from systemic administration of drugs. photosensitizing drugs include: tetracyclines (doxycycline, tetracycline) - fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin) - NSAIDs
(ketoprofen, naproxen, celecoxib) - diuretics (furosemide, bumetanide, hydrochlorothiazide ) - retinoids
(isotretinoin, acitretin) - hypoglycaemic agents (sulphonylurea 5 aminolevulinic acid) - neuroleptics
(chlorpromazine, fluphenazine, piperazine, thioridazine) - antifungals (terbinafine, itraconazole, voriconazole) paraaminobenzoic acid, 5 fluorouracil, amiodarone, diltiazem, quinidine - hydroxychloroquine, coal, enalapril,
dapsone, oral contraceptives - solar screens (salicylates, benzophenones, cinnamates) - perfume (musk, 6
metilcoumarina).

Signs and symptoms

Men are more likely than women to photoallergic reactions. Drug photosensitivity can occur at any age. Patients
with photosensitivity sometimes shows intolerance to the sun ( solar urticaria ). While most people can
tolerate minutes or hours sun exposure, patients with photosensitivity skin lesions. In most cases there is a
sunburn or dermatitis. photosensitivity may cause drug-induced phototoxicity, photoallergy, lichenoid
reactions, subacute cutaneous lupus or pseudoporphyria . pseudoporphyria may occur in some drugs, most
commonly is naproxen. Pseudoporphyria bullosa is characterized by a reaction that is clinically and histologically
similar to porphyria cutanea tarda. Hipertrichoza and scleroderma changes that are typically seen in porphyria
cutanea tarda are not present in pseudoporphyria. Results of the studies are normal porphyrin. reactions
lichemoide appearing in a fotodistributie are often difficult to differentiate from idiopathic lichen planus. These
reactions are characterized by erythematous papules and plaques that purplish or sometimes Wickham striae.
Hydrochlorothiazide and captopril hidroxicloroquina are known causes of lichenoid reactions. reactions lupus-like
lesions include cancellation psoreiforme that blistered. Hydrochlorothiazide is the drug most commonly associated
with this reaction, but calcium channel blockers, angiotensin converting enzyme inhibitors, griseofulvin and
terbinafine are other agents involved. The rate of reaction is small for these agents. Hydrochlorothiazide is used
mainly in combination with antihypertensive agents. Patients with drug-induced reactions usually have antibodies
antiRo. Photodynamic therapy is a treatment well known for actinic keratoses and nonmelanoma skin cancers.
Recognizing this is important-induced phototoxicity. 5 aminolevulinic acid is applied topically followed by the use
of red or blue lights. It is a prodrug that enters the heme synthesis pathway and is metabolized intracellularly to
form a photosensitive molecule - protoporphyrin IX. The light activates protoporphyrin to generate oxygen free
radicals that cause malignant and non-malignant hyperproliferative tissue destruction. Common side effects are
mild phototoxic reaction that resolves in a few days. Differentiation between photosensitivity and skin disease
exacerbations by heat is difficult. It will determine whether the photosensitivity can be triggered by exposure to
sunlight through glass. UV-B does not penetrate through glass, while A and visible light waves do. physical
examination. phototoxic and photoallergic reactions occur in sun-exposed areas, including the face, the V
neck, the back of hands and arms . Scalp, the postauriculara, periorbital and submental are avoided. A rash
suggests widespread exposure to a systemic photosensitizer, while a localized eruption indicate a reaction by
topical application of the drug. phototoxic reaction on the skin. acute phototoxicity start through a sunburn
erythema and edema excess that occurs in a few minutes, hours exposure to light. vesicles and bubbles may
develop severe reactions. lesions heal with hyperpigmentation that rzolva in a few weeks or months. Chronic
phototoxicity may also appear as an exaggerated sunburn. However lichenification develops through frequent
scratching of photosensitive area. Therefore differentiation of the phototoxic reactions photoallergic based
strictly on clinical appearance is difficult. Other less common skin manifestations include pigment changes. A
blue-gray pigmentation is associated with various agents, including amiodarone, chlorpromazine and tricyclic
antidepressants. Reactions to products containing psoralen (fitofotodermatita) and drugs solve a brownish
discoloration of the skin . Frequently changing pigmentosa is preceded by a typical sunburn reaction. If the
reaction is severe some patients may notice redness. photosensitizing drugs can cause a rash similar to lichen
planus in areas exposed to the sun. Drugs that cause this reaction are often demeclocycline, hydrochlorothiazide,
enalapril, Quinine, quinidine, Chloroquine, hidroxicloroquina. pseudoporphyria may occur after exposure to
naproxen, nalidixic acid, tetracycline, sulfonylureas, forosemid, dapsone, amiodarone, bemetanida, pyridoxine.

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Drug-induced photosensitivity

Renal failure and tanning beds are predisposing factors. phototoxic reactions nail. Photo- onycholysis , or
separation of the nail from the nail bed is another manifestation of phototoxicity. Photo-onycholysis was
reported administration of systemic drugs including tetracycline, psoralen, chloramphenicol, fluoroquinolones,
oral contraceptives, Quinine, mercaptopurine. Photo-onycholysis may be the only manifestation in patients with
highly pigmented skin. photoallergic skin reactions. They develop in susceptible individuals typically 24-48
hours after exposure. reaction manifests as an itchy eczematous eruption. Redness and veziculizarea are
present in the acute phase. A chronic exposure cause erythema, lichenification and scaling .
hyperpigmentation occurs not in photoallergic reactions.

Diagnosis
Education Laboratory
- porphyria cutanea tarda to exclude measured urine porphyrin levels, which is normal in pseudoporphyria and
raised in porphyria
- determine antinuclear and anti-Ro. diagnostic test fotoalergiei and contact dermatitis. Fotoalergenii suspect
are applied back in two sets. A set is removed after 24 hours and irradiated with UV A. Both sets are evaluated
for a possible 48-hour reaction. Redness, swelling and veziculizarea irradiated site indicates a positive reaction.
Positive reaction in both locations indicating photoallergic contact dermatitis. A positive reaction in place of the
non-irradiated and irradiated strong one must be interpreted as contact dermatitis and photoallergic contact
dermatitis to the same compound. Fototestarea UV-A, UV-B and visible light sometimes is helpful in the
diagnosis of photosensitisation. The test is carried out by treatment of small areas of skin on the back with
increasing doses of light. Minimum dose of light used to produce erythema evenly across the irradiated area in 24
hours is called erythema dose. Phototoxic reaction patients have a reduced erythema dose of UV-A or UV-B
sometimes. Differential diagnosis is made
with the following conditions: allergic contact dermatitis, irritant
contact dermatitis, drug eruption , bullous epidermolysis, chronic actinic dermatitis, lichen planus lupus
erythematosus, solar urticaria.

Treatment
The main treatment is to identify and avoid the causative agent, use sunscreen and amelirarea symptomatic.
Topical corticosteroids and cold compresses may relieve the condition. systemic corticosteroids should be
reserved for severe cases. If solar screens are not the cause photosensitivity they should be used. SPF may
not be a reliable indicator of protection against drug photosensitivity. This refers to protection from sunburn
caused by UV-B. Most photosensitivity reactions are caused by UV-B rays. Therefore, solar screens which absorb
UV-A are the ones that should be used. Sunscreens that contain avobenzone, titanium dioxide, zinc oxide is more
effective in blocking UV-A.

Prognostic
Chronic Effects photosensitive cutaneous lesions were evaluated only for psoralen. Note the premature skin
aging and skin cancer . incidence of squamous cell carcinoma is higher than that of basal cell carcinoma. And
the risk of melanoma increases with time. Effects of chronic exposure to other compounds incriminated are
unknown. persistent reactivity to light is a form of chronic actinic dermatitis occurs in patients with
photoallergic contact dermatitis. The disease may involve sun-exposed areas and extends to the areas covered.
Some patients are closing in dark rooms due to severe photosensitivity. Treatment involves avoiding contact
with agents that exacerbate the condition and photoallergic. Use topical corticosteroids, systemic and
hidroxicloroquina. Patients who show signs of improvement require immunosuppressive agents: azathioprine,
cyclosporine. At most patients the prognosis is excellent once incriminated agent is removed. complete resolution
of photosensitivity still require several weeks - months for some compounds.

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Drug-induced photosensitivity

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