Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Sun-related skin diseases Steven Earl Prawer MD To cite this article: Steven Earl Prawer MD (1991) Sun-related skin diseases, Postgraduate Medicine, 89:8, 51-66, DOI: 10.1080/00325481.1991.11700953 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11700953
Published online: 17 May 2016.
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Second of three articles on skin disorders
Sun-related skin diseases Preview Persons who avoid the sun often reach old age with relatively smooth, unblemished skin, whereas those who are repeatedly exposed to ultraviolet light risk sunburn, premature aging of the skin, and cancer. Dr Prawer explains the deleterious effects of sunlight on the skin and recommends that methods of photoprotection be explained to all patients.
Steven Earl Prawer, MD •:• Ultraviolet (UV) radiation affects human skin continuously from binh to death. In addition to acute adverse effects such as sunburn, chronic exposure may cause premature aging of the skin, actinic keratoses, and basal and squamous cell carcinoma. To compound the problem, the "perfect tan'' can now be maintained all year by visiting commercial tanning salons. (Adolescent girls and young women are the most frequent patrons.) The equipment in tanning booths can emit five times more ultraviolet A (UVA) radiation per unit of time than solar radiation measured at the equator. 1 This may result in damaging biologic effects on the skin. Even an ultraviolet B (UVB) emission of 1% from the
equipment used at tanning salons can significantly increase the potential for skin cancer. 1
Acute effects of sun exposure The acute adverse effects of sun exposure on the skin include phototrauma (sunburn), photosensitivity, and tanning. PHO'IOTRAUMA-This is the initial actinic or solar insult to the skin. Redness is produced by vasodilation and increased blood flow in the dermis. Biochemically, it is a manifestation of (1) damage to membranes and to DNA, (2) transient disturbances in protein synthesis, and (3) elaboration of many cytokines and inflanunatory mediators. 2 Pain and itching are produced by the effect of chemical mediators on the nerve endings.
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All three wavelengths ofUV radiation (see box on page 54) 14 cause phototrauma. The epidermis absorbs ultraviolet C (UVC) and UVB radiation, but UVA radiation penetrates into the dermis, 5 where the potential for damage is greater. Sunburn is delayed in its onset, usually becoming evident 2 to 6 hours after exposure and reaching maximum intensity after 15 to 24 hours. 2 It is less severe in persons over age 60 than in those under age 30. However, redness persists longer in older persons. 5 PHOTOSENSITIVriY-This refers to an abnormal response of the skin to sun exposure. 2 It includes phototoxic and phoroallergic reactions and polymorphous light eruption. PHOTOTOXIC REACTION-This
reaction presents as an exaggerated sunburn (ie, fur more severe than expected from the length of exposure) after ingestion of or contact with a phorosensitizer.6 Because this reaction is not mediated immunologically, it may occur in anyone. 6 Phorosensitizers are usually polycyclic compounds capable of absorbing UVA radiation; therefore, most phototoxic reactions are caused by UVA exposure.6 The drugs most commonly implicated in phototoxic reactions are thiazides (figure 1), sulfonylureas, sulfonarnides, tetracyclines, phenothiazines, psoralens, nalidixic acid, and coal tar. 2 Exposure to sunlight after skin contact with plants containing psoralens or continued
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A polymorphous light eruption with itchy papules and plaques may occur after the first intense exposure to the sun in the spring.
Figure 2. Polymorphous light eruption with extensive red plaques. Patients often call this "sun poisoning" or "sun allergy."
Figure 1. Phototoxic drug reaction after
Figures 1 and 2 courtesy of Frederick S. Fish, MO.
ingestion of thiazides and exposure to sun. Note intense erythema in sun-exposed areas.
furocoumarins (eg, limes, parsley, celery, bishop's-weed, figs) can cause topical photosensitivity. 2·6 PHOTOALLERGIC REACTION-
This abnormal response of chemically exposed skin to sunlight occurs when the immune system is involved.6 The reaction appears more as a rash than as a sunburn. &sentially, all phototoxins are also photoallergens.6 POLYMORPHOUS LIGHT ERUPTION-This is the most common
abnormal response of skin to sunlight and may affect up to 10% of the population.6The response is often triggered by the first intense exposure to the sun in the spring or during a southern midwinter vacation. Patients usually call it "sun
52
poisoning" or "sun allergy."6Within hours after the patient sunbathes, itchy papules and plaques occur over some, but not all, exposed areas (figure 2). They gradually subside 1 to 2 weeks later if the patient avoids further exposure to the sun. There is no systemic involvement.6 TANNING-This form of sun exposure can be divided into two types:
1. Immediate pigmented darkening. Exposure to UVA radiation results in photo-oxidation of preformed melanin. Darkening lasts only a few minutes after short exposure to UVA radiation bur can remain for 36 hours after longer, highintensity exposure. 4 This darkening does not protect the skin from UVB erythema. 1 2. Delayed pigmented darkening.
This occurs 48 to 72 hours after exposure to either UVA or UVB radiation, peaks in 7 to 10 days, and may persist for weeks to months. It results from an increase both in the production of new melanin (melanogenesis) and in the size of melanocytes. 4 Afrer exposure to sunlight, the skin acclimatizes; that is, it is less sensitive to sunburn on subsequent exposure. Acclimatization results from both pigmentation and gradual thickening of the stratum corneum (uppermost layer of the epidermis). It is lost after 1 to 2 months of nonexposure.2 UVA radiation from tanning booths provides less protection against future sunburn than natural sunlight. Artifical sunlight stimulates melanogenesis without appreciable thickening of the stratum corneum.2
Long-term ef&cts of sun exposure Prolonged exposure of the skin to sunlight may lead to both photoaging and photocarcinogenesis. PHOOOAGING-Premature aging of the skin, or photoaging, has unique clinical and histologic features and should be differentiated from true chronologie or intrinsic aging. Because UVB radiation is responsible for erythema, DNA darnage, and skin cancer, it has also been implicated as a cause of connective tissue damage that results in photoaging.7 However, when the total dose ofUVA radiation is at least 1,000 times higher than that of UVB radiation, it can be both
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Moderate photoaging is manifested by deep wrinkles, sallowness, vascular lesions, laxity, and atrophic or thickened, leathery skin.
Figure 3. Large solar lentigo on cheek. Lesion presents as irregular pigmented macule.
erythemogenic and carcinogenic. If multiple exposures to UVA radiation from sunlight, fluorescent lamps, and tanning in salons are added together, the result may be 100 to 1,000 times that ofUVB radiation. 8 Also, as noted previously, the longer wavelength ofUVA penetrates more deeply into the dermis. 7 Clinically, photoaging can be classified as mild, moderate, or severe (figures 3 through 7). Mild damage is characterized by dryness, roughness, pigmentary abnormalities (eg, irregular hyperpigmentation, solar lentigines, guttate hypopigmentation), and fine lines or wrinkles. Moderate damage is manifested by deep wrinkles (eg, cutis rhomboidalis nuchae, or deep folds and wrinkles on the back of the neck), sallowness, vascular lesions (telangiectaSes, ecchymoses, purpura, venous lakes), laxity (loss of elasticity), and thickened, leathery skin or, conversely, atrophic skin. Severe damage ultimately results in both actinic
Figure 4. Diffuse solar lentigines on Vshaped area of upper chest and neck. Note sparing of adjacent area not exposed to sun.
Figure 5. Cutis rhomboidalis nuchae. Solar damage appears as deep rhomboidal wrinkles on nape of neck.
Figure 6. Extensive photodamage of face. Note deep wrinkles, irregular pigmentation, loss of elasticity, and coarse, leathery skin.
Figure 7. Actinic cheilitis. Photodamage of lower lip is seen as irregular, white, scaly patches.
keratoses and skin cancers.2·7·9 Photoaging can be striking, especially when the skin of outdoor workers, such as f.umers and sailors, is compared with that of indoor workers. 7 Even in darkly pigmented individuals, such as South American blacks, photodamage can develop when exposure to sunlight is prolonged and intense. 8 Age, however, may have no bearing on the amount of photodamage seen. Sun worshippers in their 30s and 40s may have rough, leathery,
mottled skin as well as actinic keratoses and carcinomas.9 In contrast, persons who avoid the sun most of their lives can reach their 80s and 90s with smooth, unblemished skin that has sustained only deepening of the surface ll).arkings and some loss of elasticity.4·9 This intrinsic aging contrasts strikingly with photoaging, especially histologically. The most dramatic feature of severely photodamaged skin is massive accumulation of thickened, degenerated elastic fibers in the dermis. continued
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Most sunburn and redness of human skin is caused by UVB radiation.
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Ultraviolet radiation and depletion of the ozone layer The spectrum of sunlight at sea level includes wavelengths that range from 290 to 3,000 nm. 2 VIsible light ranges from 400 to 800 nm. 3 Ultraviolet (UV) light, which falls at the shorter end of the spectrum and is responsible for chronic adverse effects on the skin, is divided (according to wavelength) into ultraviolet C (UVC), ultraviolet B (UVB), and ultraviolet A (UVA) radiation. UVC (shon-wave) radiation ranges from 200 to 290 nm and is completely absorbed by the earth's owne layer. 4 However, artificial sources (eg, lamps for sterilization or disinfecting) may emit UVC radiation, which is mildly germicidal. UVB (middle-wave) radiation ranges from 290 to 320 nm. A significant amount is absorbed by the owne layer,4 and window glass attenuates it. This type of radiation causes most sunburn and redness of human skin. UVA (long-wave) radiation ranges from 320 to 400 nm, and very little is absorbed by the owne layer.4 It is 1,000 times less likely than UVB radiation to produce skin redness. 1 However, because 100 to
Mature collagen decreases, whereas ground substance, which is composed of proteoglycans, greatly increases. Capillaries become dilated and tortuous, producing clinically visible telangiectases. 7 The epidermis is generally thickened but eventually may become atrophic and display cellular arypia. 9 Cigarette smoking has been associated with premature skin aging, which is most noticeable in sunexposed areas. 2 Taking sun exposure into consideration, investigators have
1,000 times more UVA than UVB radiation reaches the earth's surface, it has been estimated that 15% of the erythema sustained by persons exposed to full sun at midday may be produced by UVA radiationY Persons living closer to the equator are exposed to more UV radiation than those living elsewhere. This is also true fur persons living at higher altitudes. For every 1,000 ft above sea level, there is a compounded 4% increase in exposure to UV radiation. 1 Chlorofluorocarbons found in aerosols and refrigerants are depleting the stratosphere of its owne layer. Land- and satellite-based measurements have confirmed the presence of a seasonal hole in the owne layer over the Antarctic. 1 The US Environmental Protection Agency has predicted that the owne layer will be depleted by 40% by the year 2075 if chlorofluorocarbons are not controlled. For every 1% decrease in owne, there would be a compounded 2% increase in the more damaging UVB radiation reaching the earth4 and a predicted additional 1% to 3% increase in nonmelanoma skin cancer cases each year. 1
found that persons who smoke 10 or more cigarettes a day for at least 10 years are more likely than nonsmokers to have leathery, atrophic, and deeply wrinkled skin. These changes may be the result of reduced cutaneous oxygenation. 2 PHOTOCARCINOGENESIS-Ex:-
tensive evidence supports the role of exposure to direct sunlight in the development of common precancerous and cancerous skin lesions. A large number of these lesions are caused by UVB radiation.
ACTINIC (SOLAR) KERATOSES-
These precancerous lesions consist of clones of anaplastic keratinocytes within the epidermis.4 Actinic keratoses eventually develop in about 75% of the white population. 10 One study 11 found that 50% of whites over age 40 are affected. 11 Investigators showed that the presence of actinic keratoses is a far more sensitive indicator oflong-term accumulation of sunlight than the development of true invasive skin cancer. 11 The prevalence of actinic ker-
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The dramatic increase in the incidence of both basal cell and squamous cell carcinoma may be due in part to greater exposure to both natural and artificial UV light.
Figure 9. Cutaneous horn appearing as elongated hyperkeratotic papilloma. Pathologic examination of base showed hypertrophic actinic keratosis.
Figure 10. Pigmented actinic keratosis. Lesion above eye is large, irregular, thickened, brown plaque.
Figure 11. Multiple actinic keratoses treated with fiuorouracil. Note dramatic red crusted response.
Figure 12. Squamous cell carcinoma on helix of ear. Crusted nodule is well demarcated and elevated.
Atrophic actinic keratoses are red, scaly, nonindurated lesions with indistinct borders. Hypertrophic actinic
sions (figure 11) are best treated with topical fluorouracil (Efudex:, Fluoroplex).
keratoses are thicker-scaled lesions, which may become cutaneous horns (figure 9). Bowenoidactinic keratoses are red plaques with sharply distinct borders. Pigmented actinic keratoses are smooth, brown plaques that may become larger than 1 em in diameter (figure 10). 10 These lesions may be treated with liquid nitrogen cryosurgery or, alternatively, by electrodesiccation with or without curettage. Multiple le-
The incidence of these lesions, which comprise both squamous and basal cell carcinoma, has increased dramatically. A 1978 estimate4 predicted that 500,000 new cases would be diagnosed each year, which may be due in part to increasing exposure to both natural and artificial UV light. These cancers commonly occur on the head, neck, arms, and hands.4 Risk factors are essentially the same
Figure 8. Multiple actinic keratoses of forehead manifested as somewhat ill-defined areas of scaling, erythema, and crusting. Note background of pigmented solar lentigines. Courtesy of Frederick S. Fish, MD.
atoses increases with age, irrespective of the amount of sun exposure. 4 Celtic (Scottish, Irish, Welsh) males who have blonde or red hair, fair skin, blue or green eyes, freckles, and the tendency to sunburn easily are particularly prone to the development oflarge numbers of actinic keratoses (figure 8). Immunosuppressed individuals who have had renal transplantation have a higher incidence of actinic keratoses and nonrnelanoma skin cancers. 12 This may be due to a defect in immune surveillance and tumor rejection capability. 10 There are four clinical types of actinic keratoses: atrophic, hypertrophic, bowenoid, and pigmented.
NONMELANOMA SKIN 0\NCERS--
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Physical sunscreen preparations block all UVA and UVB radiation but are messy and may be uncomfortable in hot, humid weather.
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Characteristics of sunscreens There are two major types of sunscreen: physical and chemical. Physical sunscreens are thick, opaque substances that block all ultraviolet A (UVA) and ultraviolet B (UVB) radiation. They contain titanium dioxide, zinc oxide, or talc. Unfortunatdy, they are messy and may be uncomfortable in hot, humid weather. 18•19 Chemical sunscreens are lotions, gels, oils, or creams that contain one or more UV-absorbing chemicals19 : • Benzophenones (oxybenzone, dioxybenzone) absorb UVB radiation and up to 60% ofUVA radiation. 18 When they are combined with p-aminobenzoic acid (PABA) esters, a "broad-spectrum'' sunscreen results. Allergic reactions to benzophenones have been reported. 18 • PABA absorbs only UVB radiation. Because PABA stains clothing and causes stinging in the skin, PABA esters (glyceryl PABA, padirnate 0 and A) were furmulated. 18 Allergic reaction to these compounds also may occur. • Cinnarnates {cinoxate, ethylhexyl p-methoxycinnamate) absorb UVB radiation but only small amounts ofUVA radiation. They are often recommended fur patients allergic to PABA • Salicylates (octyl salicylate, homosalate) are also safe for PABA-sensitive patients but absorb only UVB radiation. 18 • Avobenzone (Parsol 1789) is a superior blocker ofUVA radiation and currently is combined with padimate 0 (Photoplex Broad Spectrum Sunscreen). 18
as those for actinic keratosis: age, sex, occupation (indoors or outdoors), tanning ability, propensity to sunburn, and location of residence in relation to the equator. 11 SQUAMOUS CELL
CARCINO~
This accounts for about 20% of all skin cancers, with 100,000 new cases occurring each year in the United States. Squamous cell carcinoma is more common than basal cell carcinoma in blacks, although its overall incidence in this group is low. 4
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One studi 3 showed that, in 60% of cases, squamous cell carcinoma arose from a lesion diagnosed clinically as an actinic keratosis. In 40% of cases, it devdoped on skin that had been clinically normal12 months previously. The risk of transformation of an actinic keratosis to squamous cell carcinoma within a year was less than 1 in 1,000. Squamous cell carcinoma occurs as a painless, scaly, crusted, or verrucous indurated red plaque on sun-
exposed areas, especially the lower lip, helix of the ear (figure 12), and bald scalp. Lesions may also arise in scars caused by thermal burns and in cases of chronic stasis dermatitis or chronic radiation dermatitis. They have a tendency to bleed and grow fairly rapidly, attaining a size of 1 em in diameter or more. Those that occur in scar tissue or mucous membrane or in black or immunosuppressed patients tend to metastasize. 14 Surgical excision and histologic examination of margins are recommended because of the potential for metastasis. Mohs' technique is indicated for recurrent or large lesions, those arising in the posterior auricular sulcus, and those in irradiated or scarred skin. 15 BASAL CELL CARCINOU4-This is the most common skin cancer in the white population. It accounts for about 75% of all malignant lesions of the skin, or approximatdy 400,000 new cases each year in the United States. About one third occur on areas of limited sun exposure. This type of cancer is rare in blacks.4 Ifleft untreated for 10 to 20 years, 1% to 3% oflesions around the eyes, nose, or ears become aggressive and invade bone, nerves, and cartilage, which can result in death. Metastasis is rare. 4 Several different types have been described. Noduk:tr basal cell carcinoma is the most common. It occurs as a pearly, waxy, tdangiectatic nodule that is 0.5 to 1 em in diameter (figure 13). As it enlarges, it outgrows its blood supply, resulting in central ul-
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A pigmented basal cell carcinoma may be misdiagnosed as a mole or a melanoma.
Figure 13. Nodular basal cell carcinoma. Lesion is pearly, waxy, telangiectatic nodule with central ulceration.
ceration, and takes on a rodent ulcer appearance (figure 14).'4 Occasionally, when brown or black pigmentation is present in this lesion (pigmented basal cell carcinoma, figure 15), it can be misdiagnosed as a mole or even a melanoma.
Figure 14. Extensive basal cell carcinoma with ulcerations on neck, cheek, and forehead.
Figure 15. Pigmented basal cell carcinoma. Irregularly pigmented nodule clinically resembles melanoma.
Figure 16. Superficial multicentric basal cell carcinoma. Lesion on patient's back is a 5X6-cm, red, indurated, scaly plaque with an elevated, threadlike border.
Figure 17. Morpheaform basal cell carcinoma manifested as hypopigmented, indurated, thickened, sclerotic plaque on cheek.
lowed by histologic examination. The highest cure rate, approaching 99%, is obtained with Mohs' micrographically controlled surgery. This technique is recommended for lesions occurring in the "H wne," or embryonic fusion planes of the Face, such as the nasolabial fold, nose, periorbital region, and periauricular
area. Mohs' technique is also indicated for aggressive morpheaform or sclerotic types of basal cell carcinoma, tumors larger than 2 em in diameter, lesions in immunosuppressed patients, and recurrent lesions. Radiation therapy offers an excellent alternative for frail, elderly individuals who have multiple medi-
A superficial multicentric type grows as multiple buds of basal cells extending centrifugally under the epidermis (figure 16).1t can reach several centimeters in diameter and commonly occurs on the trunk as a scaly, red plaque with an elevated, threadlike border. 14 A morpheafonn (sclerotic, fibrosing) type occurs as an indurated, thickened, ill-defined invasive plaque. It is typically seen on the Face (figure 17). 14 Small basal cell carcinomas on the cheeks and superficial multicentric lesions on the trunk can be satisfactorily treated by curettage and fulguration. Large lesions and those on the scalp, forehead, ear rim, chin, neck, and other body sites can be managed with elliptic excision, fol-
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Men are affected more frequently than women by cutaneous malignant melanoma, and the prognosis is often poorer.
Figure 18. Superficial spreading malignant melanoma. Note various tones of dark and light brown, red, and pink. Surface is irregular and borders are notched.
Figure 19. Nodular melanoma. Welldemarcated black nodule with normal surrounding skin is rapidly growing and invasive.
Figure 20. Acral-lentiginous melanoma.
Figure 21. Lentigo maligna melanoma.
Lesion is deeply blue-black, invasive, irregular plaque with ulceration.
Large, invasive, black nodule, usually appearing on cheek of elderly persons. Lesion in this case has ulcerated.
cal problems and are unable to tolerate surgery. 15
whites in the United States is expeaed to be 1 in 90. 16 Controversy exists as to whether cutaneous malignant melanoma is related to sunlight exposure. Evidence in support ofUVB exposure as a cause includes (1) higher incidence in areas closer to the equator, (2) occurrence primarily in lightly pigmented persons, and (3) rare occunence in heavily pigmented persons. Risk is increased if a person has
CUTANEOUS MAUGNANT MELA-
NOMA-About 5% of all skin cancers are malignant melanoma. 4 In the United States, the incidence has risen by 100% in the past decade, faster than any other cancer except lung cancer. The projected US incidence for 1990 was 27,600 cases with 6,300 deaths. By the year 2000, the lifetime risk of melanoma for
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a past history of severe blistering sunburn or sun sensitivity16 or several years of exposure to UV lamps and sunbeds. 17 Evidence against UVB exposure as a cause includes (1) lower rates in outdoor workers, (2) higher rates in white collar groups who work indoors, and (3) uncommon occurrence on the head, neck, and hands. 16 Men are affected more frequently than women and ofi:en have a poorer prognosis. The disease is seen more typically on the trunk and extremities in men and on the lower extremities in women. Survival rates tend to be lower when the disease occurs in the midline of the body and the so-called BANS-HF areas: upper back, lateral upper arms, posterior neck and scalp, hands, and feet. 14 Several types of cutaneous malignant melanoma have been described. The most common, superficial spreading malignant melanoma (figure 18), accounts for 70% of cases. It appears as an irregular, pigmented plaque with various hues of red, white, and blue. 14 Noduktr melanoma (figure 19) is seen in 15% of patients who have melanoma. It is a highly invasive, violaceous, brown-black nodule with fairly normal surrounding skin. It tends to ulcerate as it outgrows its blood supply. 14 Acral-lentiginous melanoma presents as an irregularly shaped, deeply pigmented macule on the hands, feet (figure 20), and phalanges and also under the nails. It is associated
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When sunscreens are applied correctly, they can greatly decrease the deleterious effects of UV radiation.
with accelerated metastasis. 14 Lentigo maligna melanoma, the least common type, is a palpable black nodule that may ulcerate (figure 21).1t usually occurs on the cheek of an elderly person and has a more favorable prognosis than other melanomas of similar thickness. 14 The mainstays of management of these melanomas are early diagnosis and excision. The classic excision of 5-cm margins is no longer recommended and does not affect survival. Current recommendations for margins are 0.5 to 1 em for in situ lesions, 1.5 em fur lesions less than 0.85 mm in depth, and 3 em for lesions deeper than 0.85 mm. 15 Prognosis is determined by level of invasion. The classification of Clark and colleagues has been replaced by Breslow's measure of invasion in millimeters of thickness. The thicker the lesion, the worse the prognosis. Patients with lesions thicker than 3.64 mm have a 42% five-year survival rate. 15
Photoprotection All patients, including the elderly, and parents of young children should be counseled on the dangers of all sources ofUV radiation. They should also be advised regarding methods of photoprotection. When applied correctly, sunscreens (see box on page 60) 18·19 can greatly decrease the deleterious effects ofUV radiation. The thickness and evenness of application are very important. An adult body can be covered completely with less than
The &cas of sun exposure • Maximum exposure to ultraviolet (UV) radiation occurs between 11 AM and 3 PM. • A thin cloud cover reduces UV radiation by only 20% to 40%. • Reflected UV radiation is as damaging as direct UV radiation. Snow reflects 85% and water up to 100% ofUV radiation. White sand reflects 25%, so an umbrella on a beach does not block exposure. • As much as 60% to 80% ofUV radiation is transmitted through the first 12 in. of water in a pool. • Dry, tightly knit clothing blocks almost all UVA and UVB radiation. Wet clothing allows 50% transmission. • Wmdow glass blocks all UVB radiation and at least 50% ofUVA radiation. Adaptedfivm Odom4 and Nicol 19
1 oz of sunscreen. This can be accomplished as followi0 : • Face and neck: 1/2 tsp • Arms and shoulders: 1/2 tsp to each side • Torso: 1/2 tsp to front and back • Legs and tops of feet: 1 tsp to each side Sunscreens should be applied 1 to 2 hours before exposure to allow adequate penetration into the stratum comeum. 18 The sun protection faaor (SPF) is also important. (The following example is a simplified explanation of SPF: If a person's skin normally bums in 15 minutes without a sunscreen, use of an SPF 10 preparation will allow exposure for 10 times longer [150 minutes] before the same degree of erythema is sustained.19) A sunscreen with an SPF
of 15 or more is recommended for persons with fair skin who often bum and for those who have photosensitivity syndromes or have had radiation therapy or skin cancer. SPF 15 offers 93% protection from UV radiation. SPF 34 only increases this protection to 97%.20 How long the sunscreen stays on the skin is as important as its aaive ingredients. "Sweat resistant" means that the produa is protective for up to 30 minutes in persons who perspire heavily and continuously. "Water resistant" means it is protective for up to 40 minutes of continuous water exposure. "Waterproof" products are proteaive for up to 80 minutes of continuous water exposure.19 The Food and Drug Administration (FDA) currently does not rec-
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Avoidance of sun or physical protection is recommended instead of sunscreens in children younger than 6 months old.
mote skin cancer by suppressing the immune system and has asked the FDA to ban sales of these products. The FDA is reviewing the petition.
Summary
Steven Earl Prawer, MD Dr Prawer is clinical associate professor, department of dermatology, University of Minnesota Medical School-Minneapolis. He also teaches in the department of dermatology, St Paul-Ramsey Medical Center, where he is head of the occupational dermatology division. He has a special interest in workrelated skin diseases.
ommend sunscreens for use in children who are younger than 6 months of age. Avoidance of the sun or physical protection is advised instead. It is estimated that regular use of SPF 15 sunscreens during the first 18 years oflife could reduce a person's lifetime risk of nonmelanoma skin cancer by 78%. 19 Minimizing exposure (see box on page 65) is also helpful. A consumer group has recently charged that sunscreen preparations containing urocanic acid may pro-
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logic examination. Although metastasis is rare with basal cell carcinoma, neglected lesions around the eyes, nose, or ears can invade bone, nerves, and cartilage and may cause death. Avoidance of sun, physical protection, and regular use of sunscreens are recommended. IIICIWI
Severe photoaging of the skin, which may be caused by exposure to both natural and artificial ultraviolet light, ultimately results in actinic keratoses and cancer. Can-
-®
cers are common on the head, neck, anns, and hands. Because of the potential fur metastasis, squamous cell carcinomas generally require surgical excision and histo-
Address for correspondence: Steven Earl Prawer, MD, Associated Skin Care Specialists, PA, 7205 University Ave NE, Fridley, MN 55432-3133.
References I. Sunlight, ultraviolet radiation, and the skin. Narl lnst Health Consensus Dev Conf Consensus Statement 1989;7(8):1-10 2. Taylor CR, Stem RS, 4'den JL, et al. Photoaging/photodamage and photoprotection. JAm Acad Dermatol 1990;22(1 ): 1-15 3. Young AR. Cumulative effects of ultraviolet radiation on the skin: cancer and photoaging. Semin Dermatol 1990;9(1):25-31 4. Odom RB. Focus on photodamage: a medical problem. Parsippany, NJ: Skin Phototrauma Foundation, 1990:1-29 5. Soter NA. Acute effects of ultraviolet radiation on the skin. Semin Dermatoll990;9(1):11-5 6. Gilchrest 8A. Actinic injury. Annu Rev Med 1990;41: 199-210 7. Kligman LH. Photoaging. Manifestations, prevention, and treatment. Clin Geriatr Med 1989;5(1):235-51 8. Sams WM Jr. Sun-induced aging: clinical and laboratory observations in humans. Clin Geriatr Med 1989;5(1):223-33 9. Lober CW; Fenske NA. Photoaging and the skin: differentiation and clinical response. Geriatrics 1990;45(4):36-40, 42 I 0. Basler RS, Eberspacher DL Actinic keratoses. Nebr MedJ 1989;74(7):174-7 II. Marks R, Rennie G, Selwood T. The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses. Arch Dermatol
1988; 124(7): 1039-42 12. Marks R. Solar keratoses. Br J Dermatol 1990;122(Suppl35):49-54 13. Marks R, Rennie G, Selwood TS. Malignant transformation of solar keratoses to squamous cell carcinoma. Lancet 1988;1(8589):795-7 14. Proper SA, Fenske NA. Common skin tumors in the geriatric population. Geriatr Med Today 1985;4(9):17-34 15. Arnold HL, Odom RB,James WD. Squamous cell carcinoma, basal cell carcinoma, malignant melanoma. In: Odom RB, James WD, eds. Andrews' diseases of the skin: clinical dermatology. Philadelphia: WB Saunders, 1990:763-865 16. Koh HK, Kligler BE, Lew RA. Sunlight and cutaneous malignant melanoma: evidence tor and against causation. Photochem Photobiol 1990; 51 (6):765-79 17. Swerdlow AJ, English JS, MacKie RM, et al. Fluorescent lights, ultraviolet lamps, and risk of cutaneous melanoma. BMJ 1988;297(6649):647-50 [erratum, BMJ 1988;297(6657):1172] 18. Rumsfidd J. Sunscreens: what you and your patients should know. Dermatol Nurs 1990;2(3): 134-47 19. Nicol NH. Actinic keratosis: preventable and treatable like other precancerous and cancerous skin lesions. Plast Surg Nurs 1989;9(2):49-55 20. Jacob R. Sunscreens: prevention by the ounce. Tex DentJ 1990;107(6):7-11
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HELIOPATHIC LESIONS • VOL 89/NO 8/JUNE 1991/POSTGRADUATE MEDICINE
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Sun-related skin diseases Steven Earl Prawer MD To cite this article: Steven Earl Prawer MD (1991) Sun-related skin diseases, Postgraduate Medicine, 89:8, 51-66, DOI: 10.1080/00325481.1991.11700953 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11700953
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Second of three articles on skin disorders
Sun-related skin diseases Preview Persons who avoid the sun often reach old age with relatively smooth, unblemished skin, whereas those who are repeatedly exposed to ultraviolet light risk sunburn, premature aging of the skin, and cancer. Dr Prawer explains the deleterious effects of sunlight on the skin and recommends that methods of photoprotection be explained to all patients.
Steven Earl Prawer, MD •:• Ultraviolet (UV) radiation affects human skin continuously from binh to death. In addition to acute adverse effects such as sunburn, chronic exposure may cause premature aging of the skin, actinic keratoses, and basal and squamous cell carcinoma. To compound the problem, the "perfect tan'' can now be maintained all year by visiting commercial tanning salons. (Adolescent girls and young women are the most frequent patrons.) The equipment in tanning booths can emit five times more ultraviolet A (UVA) radiation per unit of time than solar radiation measured at the equator. 1 This may result in damaging biologic effects on the skin. Even an ultraviolet B (UVB) emission of 1% from the
equipment used at tanning salons can significantly increase the potential for skin cancer. 1
Acute effects of sun exposure The acute adverse effects of sun exposure on the skin include phototrauma (sunburn), photosensitivity, and tanning. PHO'IOTRAUMA-This is the initial actinic or solar insult to the skin. Redness is produced by vasodilation and increased blood flow in the dermis. Biochemically, it is a manifestation of (1) damage to membranes and to DNA, (2) transient disturbances in protein synthesis, and (3) elaboration of many cytokines and inflanunatory mediators. 2 Pain and itching are produced by the effect of chemical mediators on the nerve endings.
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All three wavelengths ofUV radiation (see box on page 54) 14 cause phototrauma. The epidermis absorbs ultraviolet C (UVC) and UVB radiation, but UVA radiation penetrates into the dermis, 5 where the potential for damage is greater. Sunburn is delayed in its onset, usually becoming evident 2 to 6 hours after exposure and reaching maximum intensity after 15 to 24 hours. 2 It is less severe in persons over age 60 than in those under age 30. However, redness persists longer in older persons. 5 PHOTOSENSITIVriY-This refers to an abnormal response of the skin to sun exposure. 2 It includes phototoxic and phoroallergic reactions and polymorphous light eruption. PHOTOTOXIC REACTION-This
reaction presents as an exaggerated sunburn (ie, fur more severe than expected from the length of exposure) after ingestion of or contact with a phorosensitizer.6 Because this reaction is not mediated immunologically, it may occur in anyone. 6 Phorosensitizers are usually polycyclic compounds capable of absorbing UVA radiation; therefore, most phototoxic reactions are caused by UVA exposure.6 The drugs most commonly implicated in phototoxic reactions are thiazides (figure 1), sulfonylureas, sulfonarnides, tetracyclines, phenothiazines, psoralens, nalidixic acid, and coal tar. 2 Exposure to sunlight after skin contact with plants containing psoralens or continued
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A polymorphous light eruption with itchy papules and plaques may occur after the first intense exposure to the sun in the spring.
Figure 2. Polymorphous light eruption with extensive red plaques. Patients often call this "sun poisoning" or "sun allergy."
Figure 1. Phototoxic drug reaction after
Figures 1 and 2 courtesy of Frederick S. Fish, MO.
ingestion of thiazides and exposure to sun. Note intense erythema in sun-exposed areas.
furocoumarins (eg, limes, parsley, celery, bishop's-weed, figs) can cause topical photosensitivity. 2·6 PHOTOALLERGIC REACTION-
This abnormal response of chemically exposed skin to sunlight occurs when the immune system is involved.6 The reaction appears more as a rash than as a sunburn. &sentially, all phototoxins are also photoallergens.6 POLYMORPHOUS LIGHT ERUPTION-This is the most common
abnormal response of skin to sunlight and may affect up to 10% of the population.6The response is often triggered by the first intense exposure to the sun in the spring or during a southern midwinter vacation. Patients usually call it "sun
52
poisoning" or "sun allergy."6Within hours after the patient sunbathes, itchy papules and plaques occur over some, but not all, exposed areas (figure 2). They gradually subside 1 to 2 weeks later if the patient avoids further exposure to the sun. There is no systemic involvement.6 TANNING-This form of sun exposure can be divided into two types:
1. Immediate pigmented darkening. Exposure to UVA radiation results in photo-oxidation of preformed melanin. Darkening lasts only a few minutes after short exposure to UVA radiation bur can remain for 36 hours after longer, highintensity exposure. 4 This darkening does not protect the skin from UVB erythema. 1 2. Delayed pigmented darkening.
This occurs 48 to 72 hours after exposure to either UVA or UVB radiation, peaks in 7 to 10 days, and may persist for weeks to months. It results from an increase both in the production of new melanin (melanogenesis) and in the size of melanocytes. 4 Afrer exposure to sunlight, the skin acclimatizes; that is, it is less sensitive to sunburn on subsequent exposure. Acclimatization results from both pigmentation and gradual thickening of the stratum corneum (uppermost layer of the epidermis). It is lost after 1 to 2 months of nonexposure.2 UVA radiation from tanning booths provides less protection against future sunburn than natural sunlight. Artifical sunlight stimulates melanogenesis without appreciable thickening of the stratum corneum.2
Long-term ef&cts of sun exposure Prolonged exposure of the skin to sunlight may lead to both photoaging and photocarcinogenesis. PHOOOAGING-Premature aging of the skin, or photoaging, has unique clinical and histologic features and should be differentiated from true chronologie or intrinsic aging. Because UVB radiation is responsible for erythema, DNA darnage, and skin cancer, it has also been implicated as a cause of connective tissue damage that results in photoaging.7 However, when the total dose ofUVA radiation is at least 1,000 times higher than that of UVB radiation, it can be both
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Moderate photoaging is manifested by deep wrinkles, sallowness, vascular lesions, laxity, and atrophic or thickened, leathery skin.
Figure 3. Large solar lentigo on cheek. Lesion presents as irregular pigmented macule.
erythemogenic and carcinogenic. If multiple exposures to UVA radiation from sunlight, fluorescent lamps, and tanning in salons are added together, the result may be 100 to 1,000 times that ofUVB radiation. 8 Also, as noted previously, the longer wavelength ofUVA penetrates more deeply into the dermis. 7 Clinically, photoaging can be classified as mild, moderate, or severe (figures 3 through 7). Mild damage is characterized by dryness, roughness, pigmentary abnormalities (eg, irregular hyperpigmentation, solar lentigines, guttate hypopigmentation), and fine lines or wrinkles. Moderate damage is manifested by deep wrinkles (eg, cutis rhomboidalis nuchae, or deep folds and wrinkles on the back of the neck), sallowness, vascular lesions (telangiectaSes, ecchymoses, purpura, venous lakes), laxity (loss of elasticity), and thickened, leathery skin or, conversely, atrophic skin. Severe damage ultimately results in both actinic
Figure 4. Diffuse solar lentigines on Vshaped area of upper chest and neck. Note sparing of adjacent area not exposed to sun.
Figure 5. Cutis rhomboidalis nuchae. Solar damage appears as deep rhomboidal wrinkles on nape of neck.
Figure 6. Extensive photodamage of face. Note deep wrinkles, irregular pigmentation, loss of elasticity, and coarse, leathery skin.
Figure 7. Actinic cheilitis. Photodamage of lower lip is seen as irregular, white, scaly patches.
keratoses and skin cancers.2·7·9 Photoaging can be striking, especially when the skin of outdoor workers, such as f.umers and sailors, is compared with that of indoor workers. 7 Even in darkly pigmented individuals, such as South American blacks, photodamage can develop when exposure to sunlight is prolonged and intense. 8 Age, however, may have no bearing on the amount of photodamage seen. Sun worshippers in their 30s and 40s may have rough, leathery,
mottled skin as well as actinic keratoses and carcinomas.9 In contrast, persons who avoid the sun most of their lives can reach their 80s and 90s with smooth, unblemished skin that has sustained only deepening of the surface ll).arkings and some loss of elasticity.4·9 This intrinsic aging contrasts strikingly with photoaging, especially histologically. The most dramatic feature of severely photodamaged skin is massive accumulation of thickened, degenerated elastic fibers in the dermis. continued
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Most sunburn and redness of human skin is caused by UVB radiation.
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Ultraviolet radiation and depletion of the ozone layer The spectrum of sunlight at sea level includes wavelengths that range from 290 to 3,000 nm. 2 VIsible light ranges from 400 to 800 nm. 3 Ultraviolet (UV) light, which falls at the shorter end of the spectrum and is responsible for chronic adverse effects on the skin, is divided (according to wavelength) into ultraviolet C (UVC), ultraviolet B (UVB), and ultraviolet A (UVA) radiation. UVC (shon-wave) radiation ranges from 200 to 290 nm and is completely absorbed by the earth's owne layer. 4 However, artificial sources (eg, lamps for sterilization or disinfecting) may emit UVC radiation, which is mildly germicidal. UVB (middle-wave) radiation ranges from 290 to 320 nm. A significant amount is absorbed by the owne layer,4 and window glass attenuates it. This type of radiation causes most sunburn and redness of human skin. UVA (long-wave) radiation ranges from 320 to 400 nm, and very little is absorbed by the owne layer.4 It is 1,000 times less likely than UVB radiation to produce skin redness. 1 However, because 100 to
Mature collagen decreases, whereas ground substance, which is composed of proteoglycans, greatly increases. Capillaries become dilated and tortuous, producing clinically visible telangiectases. 7 The epidermis is generally thickened but eventually may become atrophic and display cellular arypia. 9 Cigarette smoking has been associated with premature skin aging, which is most noticeable in sunexposed areas. 2 Taking sun exposure into consideration, investigators have
1,000 times more UVA than UVB radiation reaches the earth's surface, it has been estimated that 15% of the erythema sustained by persons exposed to full sun at midday may be produced by UVA radiationY Persons living closer to the equator are exposed to more UV radiation than those living elsewhere. This is also true fur persons living at higher altitudes. For every 1,000 ft above sea level, there is a compounded 4% increase in exposure to UV radiation. 1 Chlorofluorocarbons found in aerosols and refrigerants are depleting the stratosphere of its owne layer. Land- and satellite-based measurements have confirmed the presence of a seasonal hole in the owne layer over the Antarctic. 1 The US Environmental Protection Agency has predicted that the owne layer will be depleted by 40% by the year 2075 if chlorofluorocarbons are not controlled. For every 1% decrease in owne, there would be a compounded 2% increase in the more damaging UVB radiation reaching the earth4 and a predicted additional 1% to 3% increase in nonmelanoma skin cancer cases each year. 1
found that persons who smoke 10 or more cigarettes a day for at least 10 years are more likely than nonsmokers to have leathery, atrophic, and deeply wrinkled skin. These changes may be the result of reduced cutaneous oxygenation. 2 PHOTOCARCINOGENESIS-Ex:-
tensive evidence supports the role of exposure to direct sunlight in the development of common precancerous and cancerous skin lesions. A large number of these lesions are caused by UVB radiation.
ACTINIC (SOLAR) KERATOSES-
These precancerous lesions consist of clones of anaplastic keratinocytes within the epidermis.4 Actinic keratoses eventually develop in about 75% of the white population. 10 One study 11 found that 50% of whites over age 40 are affected. 11 Investigators showed that the presence of actinic keratoses is a far more sensitive indicator oflong-term accumulation of sunlight than the development of true invasive skin cancer. 11 The prevalence of actinic ker-
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The dramatic increase in the incidence of both basal cell and squamous cell carcinoma may be due in part to greater exposure to both natural and artificial UV light.
Figure 9. Cutaneous horn appearing as elongated hyperkeratotic papilloma. Pathologic examination of base showed hypertrophic actinic keratosis.
Figure 10. Pigmented actinic keratosis. Lesion above eye is large, irregular, thickened, brown plaque.
Figure 11. Multiple actinic keratoses treated with fiuorouracil. Note dramatic red crusted response.
Figure 12. Squamous cell carcinoma on helix of ear. Crusted nodule is well demarcated and elevated.
Atrophic actinic keratoses are red, scaly, nonindurated lesions with indistinct borders. Hypertrophic actinic
sions (figure 11) are best treated with topical fluorouracil (Efudex:, Fluoroplex).
keratoses are thicker-scaled lesions, which may become cutaneous horns (figure 9). Bowenoidactinic keratoses are red plaques with sharply distinct borders. Pigmented actinic keratoses are smooth, brown plaques that may become larger than 1 em in diameter (figure 10). 10 These lesions may be treated with liquid nitrogen cryosurgery or, alternatively, by electrodesiccation with or without curettage. Multiple le-
The incidence of these lesions, which comprise both squamous and basal cell carcinoma, has increased dramatically. A 1978 estimate4 predicted that 500,000 new cases would be diagnosed each year, which may be due in part to increasing exposure to both natural and artificial UV light. These cancers commonly occur on the head, neck, arms, and hands.4 Risk factors are essentially the same
Figure 8. Multiple actinic keratoses of forehead manifested as somewhat ill-defined areas of scaling, erythema, and crusting. Note background of pigmented solar lentigines. Courtesy of Frederick S. Fish, MD.
atoses increases with age, irrespective of the amount of sun exposure. 4 Celtic (Scottish, Irish, Welsh) males who have blonde or red hair, fair skin, blue or green eyes, freckles, and the tendency to sunburn easily are particularly prone to the development oflarge numbers of actinic keratoses (figure 8). Immunosuppressed individuals who have had renal transplantation have a higher incidence of actinic keratoses and nonrnelanoma skin cancers. 12 This may be due to a defect in immune surveillance and tumor rejection capability. 10 There are four clinical types of actinic keratoses: atrophic, hypertrophic, bowenoid, and pigmented.
NONMELANOMA SKIN 0\NCERS--
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Physical sunscreen preparations block all UVA and UVB radiation but are messy and may be uncomfortable in hot, humid weather.
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Characteristics of sunscreens There are two major types of sunscreen: physical and chemical. Physical sunscreens are thick, opaque substances that block all ultraviolet A (UVA) and ultraviolet B (UVB) radiation. They contain titanium dioxide, zinc oxide, or talc. Unfortunatdy, they are messy and may be uncomfortable in hot, humid weather. 18•19 Chemical sunscreens are lotions, gels, oils, or creams that contain one or more UV-absorbing chemicals19 : • Benzophenones (oxybenzone, dioxybenzone) absorb UVB radiation and up to 60% ofUVA radiation. 18 When they are combined with p-aminobenzoic acid (PABA) esters, a "broad-spectrum'' sunscreen results. Allergic reactions to benzophenones have been reported. 18 • PABA absorbs only UVB radiation. Because PABA stains clothing and causes stinging in the skin, PABA esters (glyceryl PABA, padirnate 0 and A) were furmulated. 18 Allergic reaction to these compounds also may occur. • Cinnarnates {cinoxate, ethylhexyl p-methoxycinnamate) absorb UVB radiation but only small amounts ofUVA radiation. They are often recommended fur patients allergic to PABA • Salicylates (octyl salicylate, homosalate) are also safe for PABA-sensitive patients but absorb only UVB radiation. 18 • Avobenzone (Parsol 1789) is a superior blocker ofUVA radiation and currently is combined with padimate 0 (Photoplex Broad Spectrum Sunscreen). 18
as those for actinic keratosis: age, sex, occupation (indoors or outdoors), tanning ability, propensity to sunburn, and location of residence in relation to the equator. 11 SQUAMOUS CELL
CARCINO~
This accounts for about 20% of all skin cancers, with 100,000 new cases occurring each year in the United States. Squamous cell carcinoma is more common than basal cell carcinoma in blacks, although its overall incidence in this group is low. 4
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One studi 3 showed that, in 60% of cases, squamous cell carcinoma arose from a lesion diagnosed clinically as an actinic keratosis. In 40% of cases, it devdoped on skin that had been clinically normal12 months previously. The risk of transformation of an actinic keratosis to squamous cell carcinoma within a year was less than 1 in 1,000. Squamous cell carcinoma occurs as a painless, scaly, crusted, or verrucous indurated red plaque on sun-
exposed areas, especially the lower lip, helix of the ear (figure 12), and bald scalp. Lesions may also arise in scars caused by thermal burns and in cases of chronic stasis dermatitis or chronic radiation dermatitis. They have a tendency to bleed and grow fairly rapidly, attaining a size of 1 em in diameter or more. Those that occur in scar tissue or mucous membrane or in black or immunosuppressed patients tend to metastasize. 14 Surgical excision and histologic examination of margins are recommended because of the potential for metastasis. Mohs' technique is indicated for recurrent or large lesions, those arising in the posterior auricular sulcus, and those in irradiated or scarred skin. 15 BASAL CELL CARCINOU4-This is the most common skin cancer in the white population. It accounts for about 75% of all malignant lesions of the skin, or approximatdy 400,000 new cases each year in the United States. About one third occur on areas of limited sun exposure. This type of cancer is rare in blacks.4 Ifleft untreated for 10 to 20 years, 1% to 3% oflesions around the eyes, nose, or ears become aggressive and invade bone, nerves, and cartilage, which can result in death. Metastasis is rare. 4 Several different types have been described. Noduk:tr basal cell carcinoma is the most common. It occurs as a pearly, waxy, tdangiectatic nodule that is 0.5 to 1 em in diameter (figure 13). As it enlarges, it outgrows its blood supply, resulting in central ul-
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A pigmented basal cell carcinoma may be misdiagnosed as a mole or a melanoma.
Figure 13. Nodular basal cell carcinoma. Lesion is pearly, waxy, telangiectatic nodule with central ulceration.
ceration, and takes on a rodent ulcer appearance (figure 14).'4 Occasionally, when brown or black pigmentation is present in this lesion (pigmented basal cell carcinoma, figure 15), it can be misdiagnosed as a mole or even a melanoma.
Figure 14. Extensive basal cell carcinoma with ulcerations on neck, cheek, and forehead.
Figure 15. Pigmented basal cell carcinoma. Irregularly pigmented nodule clinically resembles melanoma.
Figure 16. Superficial multicentric basal cell carcinoma. Lesion on patient's back is a 5X6-cm, red, indurated, scaly plaque with an elevated, threadlike border.
Figure 17. Morpheaform basal cell carcinoma manifested as hypopigmented, indurated, thickened, sclerotic plaque on cheek.
lowed by histologic examination. The highest cure rate, approaching 99%, is obtained with Mohs' micrographically controlled surgery. This technique is recommended for lesions occurring in the "H wne," or embryonic fusion planes of the Face, such as the nasolabial fold, nose, periorbital region, and periauricular
area. Mohs' technique is also indicated for aggressive morpheaform or sclerotic types of basal cell carcinoma, tumors larger than 2 em in diameter, lesions in immunosuppressed patients, and recurrent lesions. Radiation therapy offers an excellent alternative for frail, elderly individuals who have multiple medi-
A superficial multicentric type grows as multiple buds of basal cells extending centrifugally under the epidermis (figure 16).1t can reach several centimeters in diameter and commonly occurs on the trunk as a scaly, red plaque with an elevated, threadlike border. 14 A morpheafonn (sclerotic, fibrosing) type occurs as an indurated, thickened, ill-defined invasive plaque. It is typically seen on the Face (figure 17). 14 Small basal cell carcinomas on the cheeks and superficial multicentric lesions on the trunk can be satisfactorily treated by curettage and fulguration. Large lesions and those on the scalp, forehead, ear rim, chin, neck, and other body sites can be managed with elliptic excision, fol-
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Men are affected more frequently than women by cutaneous malignant melanoma, and the prognosis is often poorer.
Figure 18. Superficial spreading malignant melanoma. Note various tones of dark and light brown, red, and pink. Surface is irregular and borders are notched.
Figure 19. Nodular melanoma. Welldemarcated black nodule with normal surrounding skin is rapidly growing and invasive.
Figure 20. Acral-lentiginous melanoma.
Figure 21. Lentigo maligna melanoma.
Lesion is deeply blue-black, invasive, irregular plaque with ulceration.
Large, invasive, black nodule, usually appearing on cheek of elderly persons. Lesion in this case has ulcerated.
cal problems and are unable to tolerate surgery. 15
whites in the United States is expeaed to be 1 in 90. 16 Controversy exists as to whether cutaneous malignant melanoma is related to sunlight exposure. Evidence in support ofUVB exposure as a cause includes (1) higher incidence in areas closer to the equator, (2) occurrence primarily in lightly pigmented persons, and (3) rare occunence in heavily pigmented persons. Risk is increased if a person has
CUTANEOUS MAUGNANT MELA-
NOMA-About 5% of all skin cancers are malignant melanoma. 4 In the United States, the incidence has risen by 100% in the past decade, faster than any other cancer except lung cancer. The projected US incidence for 1990 was 27,600 cases with 6,300 deaths. By the year 2000, the lifetime risk of melanoma for
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a past history of severe blistering sunburn or sun sensitivity16 or several years of exposure to UV lamps and sunbeds. 17 Evidence against UVB exposure as a cause includes (1) lower rates in outdoor workers, (2) higher rates in white collar groups who work indoors, and (3) uncommon occurrence on the head, neck, and hands. 16 Men are affected more frequently than women and ofi:en have a poorer prognosis. The disease is seen more typically on the trunk and extremities in men and on the lower extremities in women. Survival rates tend to be lower when the disease occurs in the midline of the body and the so-called BANS-HF areas: upper back, lateral upper arms, posterior neck and scalp, hands, and feet. 14 Several types of cutaneous malignant melanoma have been described. The most common, superficial spreading malignant melanoma (figure 18), accounts for 70% of cases. It appears as an irregular, pigmented plaque with various hues of red, white, and blue. 14 Noduktr melanoma (figure 19) is seen in 15% of patients who have melanoma. It is a highly invasive, violaceous, brown-black nodule with fairly normal surrounding skin. It tends to ulcerate as it outgrows its blood supply. 14 Acral-lentiginous melanoma presents as an irregularly shaped, deeply pigmented macule on the hands, feet (figure 20), and phalanges and also under the nails. It is associated
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When sunscreens are applied correctly, they can greatly decrease the deleterious effects of UV radiation.
with accelerated metastasis. 14 Lentigo maligna melanoma, the least common type, is a palpable black nodule that may ulcerate (figure 21).1t usually occurs on the cheek of an elderly person and has a more favorable prognosis than other melanomas of similar thickness. 14 The mainstays of management of these melanomas are early diagnosis and excision. The classic excision of 5-cm margins is no longer recommended and does not affect survival. Current recommendations for margins are 0.5 to 1 em for in situ lesions, 1.5 em fur lesions less than 0.85 mm in depth, and 3 em for lesions deeper than 0.85 mm. 15 Prognosis is determined by level of invasion. The classification of Clark and colleagues has been replaced by Breslow's measure of invasion in millimeters of thickness. The thicker the lesion, the worse the prognosis. Patients with lesions thicker than 3.64 mm have a 42% five-year survival rate. 15
Photoprotection All patients, including the elderly, and parents of young children should be counseled on the dangers of all sources ofUV radiation. They should also be advised regarding methods of photoprotection. When applied correctly, sunscreens (see box on page 60) 18·19 can greatly decrease the deleterious effects ofUV radiation. The thickness and evenness of application are very important. An adult body can be covered completely with less than
The &cas of sun exposure • Maximum exposure to ultraviolet (UV) radiation occurs between 11 AM and 3 PM. • A thin cloud cover reduces UV radiation by only 20% to 40%. • Reflected UV radiation is as damaging as direct UV radiation. Snow reflects 85% and water up to 100% ofUV radiation. White sand reflects 25%, so an umbrella on a beach does not block exposure. • As much as 60% to 80% ofUV radiation is transmitted through the first 12 in. of water in a pool. • Dry, tightly knit clothing blocks almost all UVA and UVB radiation. Wet clothing allows 50% transmission. • Wmdow glass blocks all UVB radiation and at least 50% ofUVA radiation. Adaptedfivm Odom4 and Nicol 19
1 oz of sunscreen. This can be accomplished as followi0 : • Face and neck: 1/2 tsp • Arms and shoulders: 1/2 tsp to each side • Torso: 1/2 tsp to front and back • Legs and tops of feet: 1 tsp to each side Sunscreens should be applied 1 to 2 hours before exposure to allow adequate penetration into the stratum comeum. 18 The sun protection faaor (SPF) is also important. (The following example is a simplified explanation of SPF: If a person's skin normally bums in 15 minutes without a sunscreen, use of an SPF 10 preparation will allow exposure for 10 times longer [150 minutes] before the same degree of erythema is sustained.19) A sunscreen with an SPF
of 15 or more is recommended for persons with fair skin who often bum and for those who have photosensitivity syndromes or have had radiation therapy or skin cancer. SPF 15 offers 93% protection from UV radiation. SPF 34 only increases this protection to 97%.20 How long the sunscreen stays on the skin is as important as its aaive ingredients. "Sweat resistant" means that the produa is protective for up to 30 minutes in persons who perspire heavily and continuously. "Water resistant" means it is protective for up to 40 minutes of continuous water exposure. "Waterproof" products are proteaive for up to 80 minutes of continuous water exposure.19 The Food and Drug Administration (FDA) currently does not rec-
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Avoidance of sun or physical protection is recommended instead of sunscreens in children younger than 6 months old.
mote skin cancer by suppressing the immune system and has asked the FDA to ban sales of these products. The FDA is reviewing the petition.
Summary
Steven Earl Prawer, MD Dr Prawer is clinical associate professor, department of dermatology, University of Minnesota Medical School-Minneapolis. He also teaches in the department of dermatology, St Paul-Ramsey Medical Center, where he is head of the occupational dermatology division. He has a special interest in workrelated skin diseases.
ommend sunscreens for use in children who are younger than 6 months of age. Avoidance of the sun or physical protection is advised instead. It is estimated that regular use of SPF 15 sunscreens during the first 18 years oflife could reduce a person's lifetime risk of nonmelanoma skin cancer by 78%. 19 Minimizing exposure (see box on page 65) is also helpful. A consumer group has recently charged that sunscreen preparations containing urocanic acid may pro-
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logic examination. Although metastasis is rare with basal cell carcinoma, neglected lesions around the eyes, nose, or ears can invade bone, nerves, and cartilage and may cause death. Avoidance of sun, physical protection, and regular use of sunscreens are recommended. IIICIWI
Severe photoaging of the skin, which may be caused by exposure to both natural and artificial ultraviolet light, ultimately results in actinic keratoses and cancer. Can-
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cers are common on the head, neck, anns, and hands. Because of the potential fur metastasis, squamous cell carcinomas generally require surgical excision and histo-
Address for correspondence: Steven Earl Prawer, MD, Associated Skin Care Specialists, PA, 7205 University Ave NE, Fridley, MN 55432-3133.
References I. Sunlight, ultraviolet radiation, and the skin. Narl lnst Health Consensus Dev Conf Consensus Statement 1989;7(8):1-10 2. Taylor CR, Stem RS, 4'den JL, et al. Photoaging/photodamage and photoprotection. JAm Acad Dermatol 1990;22(1 ): 1-15 3. Young AR. Cumulative effects of ultraviolet radiation on the skin: cancer and photoaging. Semin Dermatol 1990;9(1):25-31 4. Odom RB. Focus on photodamage: a medical problem. Parsippany, NJ: Skin Phototrauma Foundation, 1990:1-29 5. Soter NA. Acute effects of ultraviolet radiation on the skin. Semin Dermatoll990;9(1):11-5 6. Gilchrest 8A. Actinic injury. Annu Rev Med 1990;41: 199-210 7. Kligman LH. Photoaging. Manifestations, prevention, and treatment. Clin Geriatr Med 1989;5(1):235-51 8. Sams WM Jr. Sun-induced aging: clinical and laboratory observations in humans. Clin Geriatr Med 1989;5(1):223-33 9. Lober CW; Fenske NA. Photoaging and the skin: differentiation and clinical response. Geriatrics 1990;45(4):36-40, 42 I 0. Basler RS, Eberspacher DL Actinic keratoses. Nebr MedJ 1989;74(7):174-7 II. Marks R, Rennie G, Selwood T. The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses. Arch Dermatol
1988; 124(7): 1039-42 12. Marks R. Solar keratoses. Br J Dermatol 1990;122(Suppl35):49-54 13. Marks R, Rennie G, Selwood TS. Malignant transformation of solar keratoses to squamous cell carcinoma. Lancet 1988;1(8589):795-7 14. Proper SA, Fenske NA. Common skin tumors in the geriatric population. Geriatr Med Today 1985;4(9):17-34 15. Arnold HL, Odom RB,James WD. Squamous cell carcinoma, basal cell carcinoma, malignant melanoma. In: Odom RB, James WD, eds. Andrews' diseases of the skin: clinical dermatology. Philadelphia: WB Saunders, 1990:763-865 16. Koh HK, Kligler BE, Lew RA. Sunlight and cutaneous malignant melanoma: evidence tor and against causation. Photochem Photobiol 1990; 51 (6):765-79 17. Swerdlow AJ, English JS, MacKie RM, et al. Fluorescent lights, ultraviolet lamps, and risk of cutaneous melanoma. BMJ 1988;297(6649):647-50 [erratum, BMJ 1988;297(6657):1172] 18. Rumsfidd J. Sunscreens: what you and your patients should know. Dermatol Nurs 1990;2(3): 134-47 19. Nicol NH. Actinic keratosis: preventable and treatable like other precancerous and cancerous skin lesions. Plast Surg Nurs 1989;9(2):49-55 20. Jacob R. Sunscreens: prevention by the ounce. Tex DentJ 1990;107(6):7-11
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HELIOPATHIC LESIONS • VOL 89/NO 8/JUNE 1991/POSTGRADUATE MEDICINE
