Published: January 2009
More than 1 million cases of skin cancer were diagnosed in the United States in 2007. About 80% of these new skin cancer cases will be basal cell carcinoma (BCC), 16% will be squamous cell carcinoma, and 4% will be melanoma. On a preventive health note, it has been estimated that regular application of sunscreen with a sun protection factor (SPF) of 15 or greater for the first 18 years of life would reduce the lifetime incidence of nonmelanoma skin cancers by 78%. Although nonmelanoma skin cancers (basal and squamous cell carcinomas) are the most common types of malignancies in humans, melanoma ranks as the sixth most common cancer in men and the seventh most common in women. Although the number of nonmelanoma skin cancers is staggering, both basal cell and squamous cell carcinomas have a better than 95% cure rate if detected and treated early.
BCC is the most common cutaneous malignancy in humans. This tumor is believed to arise from the pluripotential primordial cells in the basal layer of the epidermis and less often from the outer root sheath of the hair follicle or sebaceous gland or other cutaneous appendages.1 Although BCCs grow slowly and rarely metastasize, they can cause extensive tissue destruction through direct extension, leading to significant patient morbidity if untreated.
It is estimated that more than 800,000 cases of BCC will occur in the United States this year. The annual incidence in Americans is 146 cases per 100,000 people.2 Although the incidence of BCC increases with advancing age, it is becoming more common in younger adults. An Australian study showed that the incidence of BCC is higher in men, but the incidence in women has been steadily increasing.3 Factors such as excessive, chronic sun exposure, indoor tanning, fair complexion, prior exposure to ionizing radiation, exposure to chemical cocarcinogens such as arsenic, and genetic determinants are significant risks factors.
The most common causative factor in the induction of BCC is ultraviolet (UV) light, specifically ultraviolet B (UVB, 290-320 nm). It has been shown that UVB induces characteristic DNA mutations in the skin called pyrimidine dimers. The p53 tumor suppressor gene is responsible for arresting the cell cycle so that any induced mutations can be repaired by the cell. In BCC, the same UV light–induced pyrimidine dimer mutations have also been found in the p53 tumor suppressor gene. This mutated p53 gene is nonfunctional and leads to dysregulation of the cell cycle, with resultant unlimited cell proliferation (cancer).
Although the exact mechanism of BCC propagation is unknown, it is believed that basal cell carcinomas arise when mutations that control cell growth via the hedgehog pathway activate immature pluripotential cells in the epidermis. This most often occurs through inactivation of the tumor suppressor gene PTC (patched), located on chromosome 9. Other mutations in SMO (smoothened) and Hh (hedgehog) have also been seen. RAS and p53 mutations may also play a role in oncogenesis. Additionally, the distinctive biologic behavior of BCC, characterized by local invasiveness but rare metastatic spread, may be related to alterations in certain basement membrane components.4
The natural progression of untreated BCC is slow growth with progressive invasion and destruction of adjacent tissues. Metastasis is very rare in BCC, with a relative rate of 0.0028% to 0.1%. When metastasis has occurred, the site of the primary lesion has most often been on the head and neck. The sites of BCC metastasis in order of frequency are the regional lymph nodes, lung, bone, skin, liver, and pleura. The average interval for metastasis is 9 years. Metastatic BCC has a poor prognosis, with a median survival of 8 months. BCC metastasis has usually been observed in men with large neglected ulcerated tumors.
BCCs are most often found on the head and neck; the nose is the most common site. The typical lesion is a small pearly (waxy) nodule with a central depression and rolled border containing dilated blood vessels. It might have a history of ulceration, crusting, or bleeding. BCC has five clinicopathologic subtypes: nodular-ulcerative, superficial, pigmented, morpheaform (sclerosing), and basosquamous.
The nodular-ulcerative variant (Fig. 1) is the most common type of BCC. It manifests as a small, pearly dome-shaped papule with surface telangiectasias and a typical rolled border. Over time, central ulceration with bleeding or crusting is often seen. Differential diagnosis of this lesion includes sebaceous hyperplasia, squamous cell carcinoma, verruca vulgaris virus, molluscum contagiosum, intradermal nevus, appendageal tumors, amelanotic melanoma, and stasis ulcers (when located on the shins).
Superficial BCCs (Fig. 2) are the least aggressive form. They often manifest as several scaly, dry, round-to-oval erythematous plaques with a threadlike raised border on the trunk and extremities. If untreated, superficial BCCs can enlarge to 10 to 15 cm in diameter without ulceration. Differential diagnosis of superficial BCC includes eczema, psoriasis, and Bowen's disease.
Pigmented BCCs (Fig. 3) are seen more often in darker-skinned persons such as Latin Americans and Asians. This subtype has all the characteristics of the nodular-ulcerative variety plus brown or black pigmentation from melanin. A history of arsenic ingestion has been seen with pigmented and superficial BCCs.
An indurated yellow to white plaque with an indistinct border and an atrophic surface characterizes morpheaform or sclerosing BCC (Fig. 4). Ulceration and crusting are usually absent. This variety has an aggressive growth pattern, and invasion of muscle, nerve, and bone may be seen. Morpheaform BCC is particularly insidious because of its benign scarlike appearance. Differential diagnosis of morpheaform BCC includes scarring and localized superficial scleroderma (morphea).
The basosquamous or metatypical variant of BCC is diagnosed on a histologic basis. This tumor possesses features of both BCC and SCC. It is mentioned because it is associated with a higher rate of metastasis.
Two syndromes that have multiple BCCs as a feature include nevoid basal cell carcinoma syndrome (Gorlin's syndrome) and Basex's syndrome. Gorlin's syndrome is characterized by BCCs; odontogenic jaw cysts; pitted depression of the hands and feet; osseous anomalies of the ribs, spine, and skull; and characteristic facies (frontal bossing, hypoplastic maxilla, a broad nasal root, and true ocular hypertelorism). 5 This genetic disorder occurs in an autosomal dominant pattern. There is a mutation of the PTC tumor suppressor gene located on chromosome 9. 5 Basex's syndrome is another autosomally dominant inherited disorder. It is characterized by multiple BCCs of the face, follicular atrophoderma of the extremities, localized or generalized hypohidrosis, and hypotrichosis.
Clinical diagnosis of BCC is confirmed by performing a biopsy of the suspected lesion for histopathologic interpretation. For the majority of BCC subtypes, a shave biopsy suffices. However, when the lesion is believed to be a morpheaform BCC, a deep shave, punch biopsy, or incisional biopsy is recommended to obtain a sufficient tissue sample for correct interpretation.
BCC may be effectively treated by a variety of therapeutic modalities. Among the clinical subtypes of BCC, small nodular or superficial BCCs respond to most treatment options; large nodular ulcerative or morpheaform lesions can require more aggressive therapy. No single treatment method is ideal for all lesions. The treating physician should carefully evaluate each BCC on an individual basis and choose the modality that is most appropriate for the lesion's size, site, and histologic type, as well as the patient's age and functional status.1
According to the American Academy of Dermatology (AAD) Guidelines of Care, electrodesiccation and curettage (ED&C) is best suited for primary lesions, but it may be useful in some recurrent lesions. It is less effective in the cure of recurrent lesions that are in scar tissue.1 Superficial and nodular BCCs respond especially well to ED&C. It is less effective in the cure of recurrent lesions or in the morpheaform subtype because of indistinct margins. Select low-risk lesions (small, well-defined primary lesions with nonaggressive histology usually in noncritical sites) can achieve 5-year cure rates of up to 97% when treated with ED&C.6
Primary nonmorpheaform basal cell carcinomas are more friable than surrounding normal skin and are initially debulked with a curette. The stroma and surrounding dermis are then electrodesiccated. This process is usually repeated two more times. The resulting wound heals with a hypopigmented scar over 2 to 6 weeks. The main disadvantage of this treatment is the absence of histologic margin control. Treatment of facial lesions with this modality is not advocated because of the risk of deep invasion in embryonal fusion planes, the difficulty of adequate curettage in the sebaceous skin of the nose, and poor cosmetic appearance.
According to the AAD Guidelines of Care, cryosurgery is useful in treating primary lesions and some recurrent lesions. It is especially useful in certain areas of the body and in patients with multiple lesions.1 Superficial and small nodular BCCs respond well to liquid nitrogen cryosurgery. Liquid nitrogen (temperature −196°C) produces tissue destruction by reducing the temperature of the skin cancer to tumoricidal levels. It is not indicated for tumors deeper than 3 mm or those with indistinct margins. The main disadvantages include a hypopigmented scar, prolonged healing, pain during the procedure, and risk of recurrence.
According to the AAD guidelines, excision is useful in both primary and recurrent tumors. The main goal of any excisional surgery is to remove the tumor entirely. Postoperatively, the surgical margins of the specimen are examined histologically for assessment of adequate tumor removal. The wound defect can be closed primarily with side-to-side closures, flaps, or grafts, or it may be allowed to heal by secondary intention. 1 For small (<20 mm) primary, well-defined BCCs, 3-mm peripheral surgical margins will clear the tumor in 85% of cases, and a 4 to 5 mm margin increases the peripheral clearance rate to approximately 95%. 6 Larger and morpheaform lesions require wider and potentially deeper surgical margins for complete histologic resection. The main disadvantage of surgical excision is incomplete margin control, 6 because the routine vertical sectioning technique (breadloafing and quartering methods of margin checking) only assess 1% of the margin.
According to the AAD guidelines, Mohs micrographic surgery (MMS) is particularly efficacious in dealing with recurrent tumors in certain anatomic locations, with tumors that have been present for a long time and have become relatively large, and with certain subtypes including large, nodular, and morpheaform BCCs. 1 MMS consists of the removal of the tumor by scalpel in sequential hori zontal layers. Each tissue specimen is mapped, frozen, stained, and microscopically examined. This procedure is especially suited for recurrent lesions and for primary tumors displaying one or more of the risk factors listed in Box 1.7
|Box 1: Tumor Features Appropriate for Mohs Micrographic Surgery|
|Basal Cell Carcinoma|
|III-defined clinical borders|
|Anatomic sites with a high risk of local recurrence in areas of important tissue conservation:
|History of incomplete removal|
|History of prior irradiation therapy|
|History of recurrence|
|Specific histologic patterns including:
|Deep tissue or bone involvement|
|Perineural or perivascular involvement|
|Rapidly growing or aggressive BCCs|
|Tumors in immunocompromised patients|
|Squamous Cell Carcinoma|
|Size >1 cm|
|Growth into deeper tissues
|Occurrence in a previously inflammatory or degenerative process or scar|
|Perineural invasion (may be indicated by pain or paresthesia)|
The procedure is predicated on histologically inspecting the entire perimeter and undersurface of the excised specimen to ensure a tumor-free margin. MMS has an extremely high cure rate: 99% for primary BCCs and more than 96% for recurrent lesions. Defects after MMS can be closed immediately, or a delayed repair may be performed in select cases. Repair can be achieved with primary linearclosure, adjacent tissue transfer (flap), skin grafting, or healing by second intention.1
The AAD guidelines state that radiation is useful for definitive treatment of primary tumors and some recurrent cancers and for palliation of inoperable tumors.2 This modality is useful for treating elderly patients who are not suitable candidates for surgical procedures. Superficial x-rays are administered in multiple, divided doses over several weeks. In general, 10 treatments are needed. Radiation therapy is contraindicated for morpheaform BCC or recurrent BCC tumors regardless of pathologic subtype.
According to the AAD guidelines, laser surgery is a recognized and evolving therapy that may be used to vaporize superficial and multiple basal cell carcinomas. The laser can also be used in lieu of a scalpel for excisional surgery to provide for improved hemostasis. 1 Other modalities such as retinoids, imiquimod, 5-fluorouracil, immunotherapy (IL-1, IL-2, interferon alfa-2b, and interferon gamma), and photodynamic therapy have been used with varying success. Chemotherapy used in the treatment of metastatic disease may have a role in treating patients with multiple lesions or as adjunctive therapy in patients being treated with radiation. 1
Five-year recurrence rates after treatment of primary BCC are 1% for MMMS, 7.5% for cryotherapy, 7.7% for ED&C, 8.7% for radiation therapy, and 10.1% for surgical excision.8 The main goal in the treatment of BCC should be complete removal of the malignancy with the highest cure rate and least cosmetic disfigurement or functional impairment.
Monthly self examination and long-term follow-up in patients who have had a BCC are essential because of the possibility of recurrence and because these patients have a much higher propensity to develop new cutaneous malignancies.1 Studies show that patients who have had one BCC are at significantly higher risk (50%) of developing new primary lesions, which can go undetected by patients.6 Early detection and appropriate re-treatment of either recurrent BCCs or new primary BCCs can increase the chances of a permanent cure and ultimately can minimize morbidity. Prevention and education are also integral parts of the total care of a patient with BCC.6 Daily sunscreen application, sun-protective clothing, and sun avoidance during peak hours are essential.
Squamous cell carcinoma (SCC) is a malignant tumor arising from the keratinocytes in the epidermis or its dermal appendages. 9 SCC is the second most common cutaneous malignancy after BCC. Unlike BCC, cutaneous SCC is associated with a greater risk of metastasis. 10 Like BCC, exposure to UV radiation is the most common cause of SCC in fair-complected persons. 10
It is estimated that more than 160,000 cases of cutaneous SCC will occur in 2007. The age-adjusted incidence of SCC among whites is 100 to 150 per 100,000 persons per year. The age-specific incidence among persons older than 75 years is approximately 10 times that rate. The most recent data report that the lifetime risk of SCC is 9% to 14% among men and 4% to 9% among women. 5 The incidence of SCC doubles with each 8 to 10 degrees decline in latitude (proximity to the equator). Since the 1970s, the age-adjusted incidence of SCC has increased by 50% to 200%. 11
Although UVB (wavelength 290-320 nm) is mainly responsible, UVA is also important. Any exposure to UV radiation produces mutations in the DNA by forming thymidine dimers in the p53 tumor-suppressor gene. Mutations in p53 result in a nonfunctional protein that cannot repair a mutated keratinocyte. This leads to uncontrolled growth and proliferation of these aberrant cells (malignancy). 10 Other factors that have been associated with the development of SCC are listed in Box 2.
|Box 2: Risk Factors for Squamous Cell Carcinoma|
|Photochemotherapy (PUVA) for skin disorders such as psoriasis|
|Thermal injury to the skin|
|Exposure to chemical carcinogens|
|Polycyclic aromatic hydrocarbons|
|Chronic radiation dermatitis|
|Human papillomavirus (HPV) infections, especially from HPV types 16, 18, 30, and 33|
|Previously injured or chronically diseased skin|
|Scars of various causes|
|Bowen's disease (SCC in situ)|
|Erythroplasia of Queyrat (SCC in situ of the penis)|
SCC, squamous cell carcinoma.
Invasive SCC can recur and metastasize. The 5-year recurrence of primary cutaneous lesions is 8%, and the 5-year metastasis rate is 5%. 10 Risk factors for metastasis include size >2 cm, site (lip, ear), immunosuppression, history of prior treatment, and aggressive histologic features (depth >4 mm, poorly differentiated appearance, and perineural invasion). 10 Additional variables that put SCC in the high-risk category include cause (scar, chronic ulcer, sinus tract, radiation dermatitis) and rapid growth pattern. 11
Actinic keratoses are premalignant skin lesions that result from chronic sun exposure and are found chiefly on the face, ears, dorsal hands, and forearms. They are usually multiple, discrete, flat or raised, verrucous or keratotic, pigmented, erythematous or skin-colored. The surface is usually scaly (Fig. 5).
Actinic keratoses are potential precursors to SCC. The annual transformation rate into SCC is 0.24% for each actinic keratosis. 11 However, approximately 5% to 20% of actinic keratoses develop into invasive SCC over 10 to 25 years. 11 The transformation may be heralded by the development of erosion, induration, inflammation, or enlargement.
Options for treatment include cryosurgery, ED&C, topical fluorouracil, photodynamic therapy, dermabrasion, chemical peel, and laser resurfacing. It has been calculated that there is a 10.2% chance of at least one actinic keratosis on a given patient transforming into an SCC within a 10-year period. However, this rate might actually be much higher, especially in immunocompromised patients such as organ transplant recipients.
Well-demarcated erythematous, scaly, slowly enlarging plaques that can occur on any part of the body characterize Bowen's disease or SCC in situ (Fig. 6). When it occurs on the glans penis, it is referred to as erythroplasia of Queyrat. The development of ulceration or induration can portend transformation into invasive SCC, which occurs in up to 5% of cases. Bowen's disease affects mostly older white men. Chronic sun damage and arsenicism have been implicated in Bowen's disease. Treatment options include excision, ED&C, photodynamic therapy, imiquimod, cryosurgery, 5-fluorouracil, and MMS.
This rapidly growing tumor is believed to be a low-grade SCC. Keratoacanthomas usually start out as a 1-mm flesh-colored macule or papule and grow to as large as a 2.5-cm nodule with a keratin-filled crater in only 3 to 8 weeks (Fig. 7). In most cases, solitary keratoacanthomas involute over 2 to 6 months, often healing with scarring. Keratoacanthomas are generally found on sun-exposed areas such as the central face, dorsal hands, arms, and legs, although they can occur anywhere on the body including the mucosa. Although keratoacanthomas might ultimately involute, the duration of regression is unpredictable.
Keratoacanthomas can also mimic invasive SCC with regard to rapid growth pattern and clinical characteristics. 10 Therefore, a method of removal that ensures adequate depth for histopathologic review is important. Options for therapy include observation, surgical excision, ED&C, topical or intralesional 5-fluorouracil, cryosurgery, radiation, and MMS.
SCC can occur on the skin or mucous membranes. It generally occurs in middle-aged and elderly adults, and more lesions occur in men. The most common sites affected are the scalp, dorsal hands, ears, lower lip, neck, forearms, and legs. Clinically SCC manifests as an enlarging indurated erythematous papule, nodule, or plaque with scale (Fig. 8). Ulceration and crusting occur later, followed by possible invasion of underlying structures and development of regional lymphadenopathy. On the lower lip, SCC arises on the chronically sun-damaged skin of the vermilion border. Patients usually note the presence of a firm nodule growing either inward or outward with ulceration. Squamous cell carcinomas of the lip metastasize approximately 10% to 15% of the time.
Verrucous carcinoma is a variant of well-differentiated invasive SCC. They manifest as indolent cauliflower-shaped nodules that resemble warts (Fig. 9). They are locally aggressive but are less likely to metastasize. 10 Verrucous carcinoma can occur on the soles, glans penis, scrotum, vulva, scalp, face, back, nail beds, or larynx. The most effective treatment is excision, and MMS is required in some cases. 10
As with BCC, a total body examination of the skin is the only screening test available for cutaneous SCC. A physical examination of a patient with SCC should always include a thorough examination of the areas of lymphatic drainage. 9 The clinical presence of lymphadenopathy necessitates exclusion of metastatic disease. Suspicious cutaneous lesions for SCC should be promptly biopsied. Because even the most astute physicians can make incorrect clinical diagnoses, most biopsies of all suspected nonmelanoma skin cancers should be adequate to allow proper diagnosis and treatment. This sample can be obtained as a shave or punch biopsy. The tissue is then sent for histopathologic review.
Fortunately, most SCCs are small, low-risk tumors. 11 A variety of surgical and nonsurgical therapeutic modalities provide effective treatment of SCC.
According to the AAD guidelines, ED&C may be suitable for small primary lesions on sun-exposed skin. In select patients, curettage used alone or in conjunction with cryosurgery or ionizing radiation is an acceptable treatment method. ED&C is less effective in curing recurrent lesions that have associated scar tissue. Tumors that extend into the subcutaneous tissues histologically or are found to have clinically invaded the subcutaneous fat at the time of treatment are less likely to result in cure when treated with this method. 9
ED&C is a process used to sequentially scrape the tumor away followed by destruction of an extra margin of normal skin by electrodesiccation performed up to three times to maximize the possibility of complete removal. Five-year cure rates with small primary SCCs treated with ED&C may be as high as 96%. 10 The main drawbacks with ED&C are that there is no tissue available for histologic evaluation to ensure tumor-free resection. ED&C can also have a poor cosmetic outcome. ED&C is not advisable for treating tumors on the face because the tumor can extend along the hair follicles beyond the reach of the curette.
This modality uses liquid nitrogen to destroy the tumor by lowering the temperature to tumoricidal levels. According to the AAD guidelines, it is especially useful in patients with bleeding disorders. It is also a good alternative in patients for whom other forms of surgery are contraindicated or who refuse other forms of surgery. 9 During treatment, it is important to include a rim of 3 to 4 mm of normal tissue beyond clinically visible margins of the tumor.
According to AAD guidelines, this surgical procedure is useful for primary and recurrent tumors. The advantages are that tissue can be assessed microscopically, the wound heals rapidly, and the cosmetic result is good. 9 The wound is closed primarily with side-to-side closure, flaps, or grafts or is allowed to heal by second intention. 9 Chance of clearance is 95% in SCCs that are well differentiated; are smaller than 2 cm; do not occur on the scalp, ears, eyelids, lips, or nose; do not involve the subcutaneous fat; and are removed with a margin of 4 mm around the clinical border of the lesion. For tumors that have a high risk of recurrence and are larger than 2 cm, a 6-mm margin is recommended. 10
According to AAD guidelines, MMS is particularly efficacious in dealing with some recurrent and some primary tumors that display risk factors associated with aggressive biologic behavior (Box 1). 9 The Mohs procedure offers the highest cure rates for patients with high-risk, primary, or recurrent SCC.
MMS uses horizontal frozen sectioning of the tumor to provide a view of 100% of the peripheral and deep margins of the specimen to ensure tumor-free planes. 10 The 5-year rates of local control for primary SCC at any site, except for the lips and ears, for MMS is 96.9% compared with 92.1% with other forms of treatment. 10 In patients with recurrent SCC, MMS is associated with 5-year cure rates of 90% to 93.3%, compared with a rate of 76.7% for recurrent tumors treated with standard excision. 10 SCCs that have lymph node involvement are additionally treated with radiation and lymph node dissection. This therapy combination offers the 5-year cure rate of 30% to 40%. 10 Cases involving distant metastases may be treated with systemic chemotherapy or other biologic response modifiers. 10
According to AAD guidelines, the CO2 laser may be used to excise or destroy SCC. The laser excises tissue in a bloodless fashion because the laser seals small blood vessels during the treatment, while also allowing margin control by histopathologic evaluation. 9
According to AAD guidelines, this modality is useful for definitive treatment of primary tumors in select patients and some recurrent cancers. It is also used for palliation of inoperable tumors. Radiation is not used for treatment of verrucous carcinoma because some evidence suggests that the metastatic potential may be enhanced. 9
Photodynamic therapy employs a photoactive compound applied to the SCC lesion followed by photoirradiation. Intralesional interferon and other agents might also prove useful in the future. Oral and topical retinoids are being evaluated for therapeutic and chemoprophylaxis management. 9
Most patients with primary cutaneous SCC have a very good prognosis. 10 Conversely, those with metastatic disease have a poor long-term prognosis. Patients with regional lymphadenopathy have a less than 20% 10-year survival rate, and patients with distant metastases have a less than 10% 10-year survival rate. 10
When metastasis does occur, it mainly involves the regional lymph nodes. 10 Distant sites, including the lungs, liver, brain, skin, and bone, are less often affected. 10 Patients with SCC are at risk for developing other malignancies such as cancers of the respiratory organs, buccal cavity, pharynx, small intestines (in men), non-Hodgkin's lymphoma, and leukemia.
The natural course of invasive SCCs in the skin is variable. The incidence of metastases from cutaneous SCC ranges from 1% to 20% in most surveys. In reference to metastatic disease, the metastatic rates result from SCCs arising in scars (37.9%), the lip (13.7%), and the external ear (8.8%). Five-year cure rates after treatment for primary SCC were 96.9% with MMS compared with 92.1% with all other forms of treatment.
As with all skin cancer treatment, therapy should be carefully tailored to the specific lesion and influenced by the medical status of the patient. Because there is a 30% risk of having a second primary SCC within 5 years after therapy for the first malignancy, skin cancer patients should have a total body examination once or twice yearly. 10 Patients with squamous cell carcinoma should also follow sun-safety tips (Box 3).
|Box 3: American Academy of Dermatology Sun Safety Tips|
|Because overt exposure to ultraviolet light contributes to the formation of skin cancer, dermatologists recommend the following precautions:|
|Avoid peak sunlight hours—10 a.m. until 4 p.m.—when the sun's rays are the strongest.|
|Apply a broad-spectrum sunscreen, one that protects against UVA and UVB rays with a SPF 15 or higher.|
|Sunscreens with the following ingredients provide broad-spectrum protection:
|For people with sensitive skin, chemical-free sunblocks containing titanium dioxide or zinc oxide, which also afford broad-spectrum coverage, can be used.|
|Reapply sunscreen every 2 hours, especially after swimming or heavy perspiration.|
|Wear protective clothing including a wide-brimmed hat, sunglasses, long-sleeved shirt, and long pants.|
|Apply lip balm that contains sunscreen with SPF 15 or higher.
|Protect children by minimizing sun exposure and regularly applying sunscreen. This is crucial, because excessive sun exposure in the first 18 years of life increases a person's chances of developing melanoma. Eighty percent of lifetime sun exposure occurs before age 18 years.|
|Avoid reflective surfaces such as water, snow, and sand that can reflect up to 85% of the sun's damaging rays.|
|Avoid tanning beds.|
SPF, sun protection factor; UVA, ultraviolet A; UVB, ultraviolet B.; Adapted from AAD patient resource materials.
In the United Stated more than 100,000 people have solid organ transplants. Due to their heavy immunosuppressive regimens, theyare at risk for developing both internal and cutaneous malignancies. Skin cancer is the most common type of cancer after transplantation. The ratio of BCC to SCC is reversed in this population. These patients should be screened before transplantation to assess their risk of developing skin cancer, and they must be educated regarding safe sun protection measures and skin self examination. Aggressive screening and early treatment of skin cancers are imperative. 12