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PHOTOSENSITIVITY

A number of substances known as photosensitizers may induce an abnormal

reaction in skin exposed to sunlight or its equivalent. Contact of the skin withthese substances may be external, or internal by enteral or parenteral

administration, or by host synthesis of photosensitizers in response to an

administered drug. The result may be either a markedly increased sunburn

response without prior allergic sensitization (phototoxicity) or actual allergic

sensitization triggered by sunlight, produced either internally (photoallergic

dermatitis, photodrug reaction) or by external contact (photocontact dermatitis).

Drugs associated with photosensitivity (photosensitizers), according to Baer and

Harber, are usually resonating compounds with a ram-molecular weight of less

than 500. Absorption of radiant energy (sunlight) by the photosensitizer

produces an excited state, which then reacts to dissipate itself throughfluorescence, phosphorescence, charge transfer, heat, or free radical formation.

Each photosensitizing substance absorbs only a specific wavelength of light.

Depending upon the cellular localization of the photosensitizer, primary damage

may occur in the nucleus, cytoplasmic organelles, or cell membrane. A

representative list of photosensitizers in man is shown in Table 3-2.

Action Spectrum. The specific wavelengths of light required to evoke a

photosensitive drug reaction are known as the action spectrum. This action

spectrum is approximately the same as the absorption spectrum of the

photosensitizing substance.

The action spectrum for photoallergy is mostly in the long ultraviolet (UVA) (320

to 423 nm) region and may extend into the visible light region.

Apparatus. Various types of apparatus are avail-able to produce these specific

wavelength radiation ranges. The fluorescent sunlamp tube (Westinghouse) has

a range 'between 285 and 350 nm. The fluorescent black light tube

(Westinghouse tube, GE, Sylvania) has 'a 320 to 450 rim range. Other light

sources that may also be of use in eliciting photosensitivity reactions include the

high-pressure mercury-vapor lamp (hot-quartz), carbon arc, and an intense Wood

light (Black-Ray 13-100 A).

Types of Photosensitivity. In order that a photosensitivity reaction may occur,

several factors must be present. The photosensitizing substance must be in or on

the skin and exposed to specific wavelengths of light characteristic of the

absorption spectrum of the photosensitizer. The prime factors determining the

magnitude of a cutaneous photosensitivity response are the concentration of the

photosensitizer and the intensity of the light absorbed.

Adverse photosensitivity may occur through diverse mechanisms. Three major

pathways are phototoxic, photoallergic, and enzyme-induced photosensitization.



Phototoxic Reaction. A phototoxic reaction is a non immunologic reaction that

develops within two to six hours after the skin has been exposed to a

photosensitizing substance and light of the proper wavelength and intensity.

There is a sunburn-type of reaction, with erythema occurring only on the sun-

exposed parts. This type of reaction can be elicited in many persons who have

no previous history of sensitivity to that particular substance: individual

susceptibility varies widely. To elicit a phototoxic reaction a considerably greater

amount of the photosensitizing substance is necessary than in the case of the

photoallergic reaction. The erythema begins (like any sunburn) within a few

hours, but worsens for 48 to 96 hours before beginning to subside. In severe

cases, nails may be involved (photo-onycholysis).

Photoallergic Reaction. After exposure of the photosensitizing substance on the

skin to a suitable light source, a clinical response is elicited in 24 to 48 hours.

There is a papulovesicular, eczematous, or exudative dermatitis that occurs

chiefly on the light-exposed areas; in addition, the eruption may extend ontoother parts of the body. This type of reaction occurs only in the previously

sensitized person.

The reaction may be produced with only small amounts of the photosensitizing

substance. However, there is evidence to suggest that a sufficiently high

concentration of the particular substance will also show phototoxic attributes.

Enzyme-Induced Photosensitivity. Some drugs taken internally may act upon the

metabolism systemically to induce changes in enzyme activity. In response to

these enzymes the host manufactures the photosensitizer, such as tetrapyrroles,

which figure prominently in the porphyrias. The drugs producing exacerbations inacute porphyria increase the delta aminolevulinic acid synthetase in hepatic cells

and increase tetrapyrrole (porphyrin) synthesis.

This type of photosensitivity may be induced by estrogens, Sedormid ([2-

isopropyl-4 pentenoyl] urea), barbiturates, and griseofulvin. Similar abnormalities

have been noted in thousands of people who developed porphyria from the

ingestion of cereals sprayed with hexachlorobenzene. In addition, alcohol

(chlorinated phenols) may alter enzyme activity. This photosensitivity is an

expression of a phototoxic reaction to a porphyrin produced by the host as a

result of an ingested drug or chemical.



PHOTOTOXICITY

Phototoxic dermatitis usually occurs with the first exposure to the

photosensitizing substance, when it is in a high cutaneous cellular concentration

and is followed by exposure to sunlight. Prior sensitization is not required.

As already noted, the dermatitis occurs upon the sun-exposed areas within a few

hours after exposure. Clinically the most common finding is the sunburned

appearance of the skin, followed later by hyper pigmentation. Sometimes bullae

develop.

The action spectrum is usually in the 285 to 450 nm range. The phototoxic

substances causing this type of dermatitis usually absorb radiation in the

ultraviolet or visible light range and have a gram-molecular weight of 500 or less.

Phototoxic Tar Dermatitis. Coal tar, creosote, crude coal tar, or pitch, in

conjunction with sunlight exposure, may induce a sunburn reaction with episodesof severe burning sensation. This is followed by hyper pigmentation, which may

persist for years, especially in those whose occupations involve constant

exposure to sunlight.

Coal tar or its derivatives may be found in cosmetics, drugs, dyes, insecticides,

and disinfectants. In the Goeckerman therapy of psoriasis, the phototoxic effect

is utilized to advantage by making the skin more susceptible to ultraviolet light.

Phytophotodermatitis. The phototoxicity-inducing furocoumarins in many plants

may bring about phytophotodermatitis when these plants come in contact with

moist skin which is then exposed to sunlight. Several hours after exposure to theplant at burning erythema occurs, followed by edema and the development of

small vesicles. The following day the small blisters coalesce into large bullae.

This is followed by involution and then by an intense residual hyper pigmentation

that may persist for weeks or months.

The hyper pigmentation is the post inflammatory type. It is epidermal as well as

dermal, i.e., increased melanin within keratinocytes and also in dermal

histiocytes, and is only very slowly reversible with time.

Phytophotodermatitis is believed to be caused mostly by plants containing

furocoumarin (psoralen, 8-methoxypsoralen and 5-methoxypsoralen), which are



primarily in the families of the Umbelliferae, Rutaceae (rue), Compositae,

Papilionaceae, and Moraceae.

Plants known to cause phytophotodermatitis include the fig, cowslip, garden and

wild parsnip, fennel, dill, parsley, wild carrot, garden carrot, masterwort, atrillal,

angelica, common rice, gas plant, lime bergamot, lime, Persian lime, buttercup,mustard, blind weed, agrimony, yarrow, goose foot, bavachi, and St. John's wort.

In Hawaii the anise scented mokihana berry (Pelea anisata) was known to natives

for its phototoxic properties (the "mokihana burn"). Like the lime, it is a member

of the rue family.

Occupational disability from exposure to the pink rot fungus (Sclerotizzia

sclerotiorunz) present on celery roots, which occurs in celery farmers in upper

Michigan and Florida, has been reported by Birmingham. However, disease-

resistant celery of high quality contains furanocoumarins and was the probable

source of phytophotodermatitis in an epidemic studied by Berkley et al in 1984.

Phytophotodermatitis must be differentiated from vesicles and bullae due to

poison ivy dermatitis. The vesicles and bullae of poison ivy are not necessarily

limited to the sun-exposed areas. Itching is the most prominent symptom in

poison ivy dermatitis, whereas there is burning in phytophotodermatitis.

Treatment of a severe, acute reaction is wet compresses (1:5000) for 20 to 30

minutes daily and topical applications of Sarna lotion, Acid Mantle Creme, bland

or corticosteroid cream, lotion, or ointment. Calamine lotion is a popular

layman's remedy.

Berloque (Berlock, Perfume) Dermatitis. In 1916 Freund described a peculiar

artificial discoloration of the skin that appeared with the use of eau de Cologne

during sunbathing. Clinically this pigmentary disturbance is characterized by

lavaliere (hanging drop)-shaped pigmented patches. The word for pendant in

French is berloque, and in German it is Berlocke. Other patches may be

quadrilateral or occur in streaks of erythema or pigmentation.

This dermatitis is seen most frequently on the sides of the neck and in the retro

auricular areas of women. In addition, the shoulders, breasts, face, and other

areas may be involved. When men have this type of dermatitis, it is usually on

the bearded area and is caused by bergamot oil or related substances inaftershave lotion.

The chief cause, oil of bergamot, contains a furocoumarin (5-methoxypsoralen),

a potent photosensitizer. However, such compounds hive been re-moved from

most perfumes and lotions, and berlock dermatitis is rarely seen anymore.

Treatment consists of stopping the use of furocoumarin preparations. Benoquin,

though a fairly effective bleach, is a potential sensitizer and should seldom be

used unless total depigmentation (in nearly universal vitiligo) is being attempted.

Effective, safe bleach which may be used is a modification of Kligman's formula:

5 per cent hydroquinone, 0.1 per cent retinoic acid, and 0.1 per cent

dexamethasone in hydrophilic ointment rubbed in daily.



Azelaic acid cream may also be effective.

Dermatitis Bullosa Siriata Pratensis (Grass or Meadow Dermatitis). This is a

phytophotodermatitis with an eruption consisting of streaks and bizarre

configurations with vesicles and bullae that heal with residual hyper

pigmentation.

Sunbathing in the fields with exposure to furocoumarin-containing plants is the

cause of this unusual dermatitis. Treatment is that recommended for any

phytophotoderrnatitis.

Photosensitivity in Tattoo. Yellow cadmium sulfide, a known photosensitizer, has

been incorporated into red mercuric sulfide pigment to produce a brighter red

color. Bjornberg has reported extensively on the photosensitivity in tattoos due

to the yellow pigment of cadmium sulfide. Goldstein has reported swollen

erythematous verrucose lesions in the red parts of tattoos, containing cadmium

sulfide, after exposure to sunlight. The other colors do not produce this disorder.

Either the tattooed person must avoid sunlight exposure or the red part of the

tattoo must be removed.

Dyes Acridine Eosin

Calcium cyclamate

Oral

Antitnicrobials Demeclocycline (Declomycin) Tetracycline (rarely) Sulfonamides

Nalidixic acid (NegGram) Griseofulvin (infrequently) Furocoumarins (psoralens)

Methoxsalen (Oxsoralen) Trimethylpsoralen (Trisoralen)

Oral ("Photodrug")

Diuretics - Chlorothiazides (Diuril, Hydrodiuril) Quinethazine (Hydromox)

Hypoglycemics Chlorpropamide (Diabinese) Tolbutamide (Orinase)

Phenothiazines Chlorpromazine (Thorazine) Promazine (Sparine)

Percttlorperazine (Compazine) Promethazine (Phenergan) Trifluoperazine

(Stelazine)

Coal Tar Derivatives Acridine Anthracene Phenanthrene Pyridine Crude coal tar

Furocoumarins (psoralens) Methoxsalen (S-MOP) in lime, rue, orange, celery, dill,

anise, or mokihana berry. Bergapten (3-methoxypsoralen) in oil of bergamot

Topical ("Photocontact")

Antimicrobials Bithionol Sulfathiazole Halogenated salicylanilides and

carbanilides Hexachlorophene (usually only secondary sensitizer)

Antihistamines Diphenhydramine? (Benadryl)

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