Section 11. Pre Cancer/Early Cancer

A 57-year-old woman presented with red and scaling skin on both arms (Figure 166-1) with a request for a prescription for 5-fluorouracil (5-FU). The patient had blue eyes and white hair and was found to have 2 basal cell carcinomas (BCCs) on her face and shoulder. The patient stated that 5-FU had helped her arms in the past, but that the scaly lesions had returned. She avoids sun exposure now, but acknowledges receiving too much sun exposure while growing up. Another course of 5-FU was prescribed for her arms to prevent new skin cancers from forming.

Actinic keratoses (AKs) are precursors on the continuum of carcinogenesis toward squamous cell carcinomas (SCCs). However, each AK has a low risk of progression to malignancy and a high probability of spontaneous regression.1 Bowen disease (BD) is SCC in situ confined to the epidermis.

AK is also known as solar keratosis. AK on the lips is known as actinic cheilitis (Figure 166-2). BD is also known as SCC in situ of the skin. SCC in situ involving the penis is known as erythroplasia of Queyrat (Figure 166-3).

• AKs and BD are seen frequently in light-skinned individuals who have had significant sun exposure.
• The prevalence of AK is estimated at 11% to 25% in adults older than age 40 years in the northern hemisphere, and increases with age.1 AKs are so common that they account for more than 10% of visits to dermatologists.
• The prevalence of BD is unknown.1

AKs and BD are both caused by cumulative UV exposure, most commonly from sunlight.

UV rays induce mutation of the tumor-suppressor gene P53. Subsequent proliferation of mutated atypical epidermal keratinocytes give rise to the clinical lesion of AK.2 Multiple clinical and subclinical lesions may exist in an area of sun-damaged skin, a concept known as “field cancerization.”

AKs have the potential to become SCCs. The rate of malignant transformation has been variably estimated, but is probably no greater than 6% per AK over a 10-year period.3

In a large prospective cohort study, the risk of progression of AK to primary SCC (invasive or in situ) was 0.60% at 1 year and 2.57% at 4 years. Approximately 65% of all primary SCCs and 36% of all primary BCCs diagnosed in the study arose in lesions that previously were diagnosed clinically as AKs. Many AKs did resolve spontaneously, 55% AKs that were followed clinically were not present at 1 year and the 70% were not present at the 5-year follow-up.4

On a spectrum of malignant transformation, BD is SCC in situ before the SCC becomes invasive.

• Total lifetime dose of UV radiation (natural sunlight, UV from tanning beds and radiation).1
• Fair skin.1
• Site-specific risk factors include tobacco for actinic cheilitis and human papilloma virus for genital and anal lesions.1
• Exposure to immunosuppressive drugs, especially organ transplant recipients.
• Personal or family history of skin cancers.

Clinical Features

AKs are rough scaly spots seen on sun-exposed areas (Figure 166-1, 166-2, 166-3, 166-4, 166-5, and 166-6). They may be found by touch, as well as close visual inspection of the patient's skin. BD appears similar to an AK, but tends to be larger in size and thicker with a well-demarcated border (Figure 166-7 and 166-8).

Typical Distribution

Both lesions are seen in areas with greatest sun exposure such as the face, forearms, dorsum of hands, lower legs of women, and the balding scalp (Figure 166-5) and tops of the ears in men.

Laboratory Studies

AKs that appear premalignant may be diagnosed by observation only and treated with destructive methods (e.g., excision, electrosurgery, or cryosurgery) without biopsy. BD requires a biopsy for diagnosis. BD or SCC should be biopsied prior to treatment. A shave biopsy should produce enough tissue for histopathology.

• Nummular eczema—a type of eczema in which the scaly patches are coin-shaped. The patches are often seen in patients who have already had some eczema or atopic conditions. The patches usually respond well to topical corticosteroids and are not related to sun damage (see Chapter 145, Atopic Dermatitis).
• Seborrheic keratoses—occur in aging adults but do not have any malignant potential. Typical seborrheic keratoses are brown in color and have a stuck on appearance. Seborrheic keratoses may look greasy or verrucous and have surface cracks. Their borders tend to be more well demarcated than AKs and their color is usually more brown than pink (see Chapter 158, Seborrheic Keratosis).
• Superficial BCCs—can look like an AK or BD. Look for the pearly and thready border that may distinguish a superficial BCC from an AK or BD. Histopathology is the proven method to diagnose (see Chapter 170, Basal Cell Carcinoma).
• When in doubt, perform a shave biopsy to differentiate between an AK, BD, SCC, and superficial BCC.

Actinic Keratoses

• No therapy or the application of an emollient is a reasonable option for mild AKs.5 SOR A
• Sun screen applied twice daily for 7 months may protect against development of AKs.2 SOR A
• AKs are most often treated by cryosurgery using liquid nitrogen (Figure 166-9). It is simple, rapid, and inexpensive, and may be used as first-line treatment.1 SOR C One metaanalysis showed a 2-month cure rate of 97.0% with 2.1% recurrences in 1 year.6
• Treating AKs with liquid nitrogen using a 1-mm halo freeze demonstrated complete response of 39% for freeze times of less than 5 seconds, 69% for freeze times greater than 5 seconds, and 83% for freeze times greater than 20 seconds.7 There is considerably more hypopigmentation caused by 20 seconds of freeze time. Determine the length of the freeze time based on the size and thickness of the lesion, using sufficient time for clearance while attempting to avoid hypopigmentation and scarring. SOR B
• Treat multiple AKs of the face, scalp, forearms, and hands topically with 5-FU, imiquimod, or diclofenac.1,5 SOR A Table 166-1.
• Topical 5-FU is an efficient therapeutic method and may be used for treatment of isolated, as well as large, areas of AK. It may be applied by the patient, and is inexpensive compared with other topical modalities.1 SOR A
• 5-FU cream used twice daily for 3 to 6 weeks is effective for up to 12 months in clearance of the majority of AKs (Figure 166-10).5 SOR A Because of side-effects of soreness, less-aggressive regimens are often used, which may be effective, but have not been fully evaluated.5
• Diclofenac gel applied twice daily for 10 to 12 weeks has moderate efficacy with low morbidity in mild AKs.2 SOR B There are few follow-up data to indicate the duration of benefit.2 In one study, diclofenac 3% gel was as effective as 5-FU cream for AK of the face and scalp and diclofenac produced fewer signs of inflammation.8
• Imiquimod 5% cream has been demonstrated to be effective over a 16-week course of treatment, but studies have only measured 8 weeks of follow up.5 SOR B By weight, it is 19 times the cost of 5-FU. They have similar side effects.5
• One metaanalysis comparing imiquimod to 5-FU showed average complete clearance of AKs for each drug was 5-FU, 52 ± 18% and imiquimod, 70 ±d 12%.9
• Imiquimod applied topically for 12 to 16 weeks produced complete clearance of AKs in 50% of patients compared to 5% with vehicle (number needed to treat [NNT] = 2.2). Adverse events included erythema (27%), scabbing or crusting (21%), flaking (9%), and erosions (6%) (number needed to harm [NNH] = 3.2 to 5.9).10
• Because of its immunostimulatory properties, imiquimod cream must be used with caution in transplant patients on immunosuppression therapy.1 SOR C
• Topical tretinoin has some efficacy on the face, with partial clearance of AKs, but may need to be used for up to a year at a time to optimize benefit.5 SOR B
• Cryosurgery was effective for up to 75% of lesions in trials comparing it with photodynamic therapy. It may be particularly superior for thicker lesions, but may leave scars.5 SOR A
• Photodynamic therapy (PDT) was effective in up to 91% of AKs in trials comparing it with cryotherapy, with consistently good cosmetic results. It may be particularly good for superficial and confluent AKs, but is likely to be more expensive than most other therapies. It is of particular value where AKs are numerous or when located at sites of poor healing, such as the lower leg.5 SOR B
• Other less accessible and expensive methods include lasers, dermabrasion, and chemical peels.
• Investigational treatment—ingenol mebutate. A short 2 to 3 days of treatment with daily topical ingenol mebutate from the sap of Euphorbia peplus plant, showed promising efficacy with a favorable safety profile in several randomized controlled trials (RCTs). One multicenter RCT showed 34.1% to 42.2% complete clearance of AKs with ingenol mebutate gel 0.05% for trunk and extremities, and 0.015% for face.11 Another RCT with 0.05% gel showed a complete clearance of 71% of treated lesions.12 Ingenol mebutate appears to have a dual mechanism of action by rapid lesion necrosis and subsequent immune mediated cellular cytotoxicity, providing efficacy with short treatment period. 13

Bowen Disease

• Table 166-2 compares and summarizes the main treatment options.
• The risk of progression to invasive cancer is approximately 3%. This risk is greater in genital BD, and particularly in perianal BD. A high risk of recurrence, including late recurrence, is a particular feature of perianal BD and prolonged follow up is recommended for this variant.14 SOR A
• There is reasonable evidence to support use of 5-FU.14 SOR B It is more practical than surgery for large lesions, especially at potentially poor healing sites, and has been used for “control” rather than cure in some patients with multiple lesions.8
• Topical imiquimod may be used off-label for BD for larger lesions or difficult/poor healing sites.14 SOR B However, it is costly and the optimum regimen has yet to be determined.14
• One prospective study suggests a superiority of curettage and electrodesiccation over cryotherapy in treating BD, especially for lesions on the lower leg (Figure 166-11).10 Curettage was associated with a significantly shorter healing time, less pain, fewer complications, and a lower recurrence rate when compared with cryotherapy.15

• Protection from UV exposure by limiting outdoor activities, and using sunscreens and protective gears (hat, umbrella, long sleeve garments, etc).
• Avoid artificial tanning beds and tobacco.

Prognosis of treated AK and BD is excellent.

Patients need skin examinations every 6 to 12 months to identify new precancers and cancers. SOR C More frequent examinations may be needed for those who have continued exposure to offending agents (eg. organ transplant recipients on immunosuppressant therapy), and those with history of recurrent skin malignancies.

Patients must understand that they acquired these conditions through cumulative sun damage, and they need to avoid further sun damage to minimize the likelihood of additional precancers and cancers. The sun damage is often from childhood and early adulthood, so the lesions are likely to form even with future sun protection. Self skin examination is recommended.

All topical treatments for AKs and BD will make the lesions look worse before they get better (Figure 166-10). The 5-FU treatments are often given with topical corticosteroid preparations to use after the treatment is over so as to minimize the symptoms of the inflammation.

Patient Resource

• Skin Cancer Foundation has an excellent website with photos and patient information—http://www.skincancer.org/ak/index.php.

Provider Resource and Guidelines

• Cox NH, Eedy DJ, Morton CA. Guidelines for management of Bowen's disease: 2006 update. Br J Dermatol 2007;156(1):11-21.

A 71-year-old woman presented with a rapidly growing lesion on her face over the past 4 months (Figure 167-1). The lesion had features of a basal cell carcinoma with a pearly border and telangiectasias (Figure 167-2). Also the central crater with keratin gave it the appearance of a keratoacanthoma (KA). A shave biopsy was performed and the pathology showed squamous cell carcinoma (SCC)-KA type. A full elliptical excision with 4-mm margins was then performed.

The KA is a unique epidermal tumor characterized by rapid, abundant growth and a spontaneous resolution, with the classic presentation in middle-aged, light-skinned individuals in hair-bearing, sun-exposed areas. In the late 1940s, Freudenthal of Wroclaw coined the term keratoacanthoma, owing to the considerable acanthosis observed in the tumor. Controversies have arisen since the 1950s about the real nature of the tumor; some KAs may metastasize, and there is debate over the relationship to SCC.1,2 Many dermatopathologists now classify this tumor as a subtype of SCC.

• Keratocarcinoma.1
• Molluscum sebaceum.
• Molluscum pseudocarcinomatosum.
• Cutaneous sebaceous neoplasm.
• Self-healing squamous epithelioma.
• Intracutaneous cornifying epithelioma.
• Idiopathic cutaneous pseudoepitheliomatous hyperplasia.
• Verrugoma.

• KA develops as a solitary nodule in sun-exposed areas.
• Seen more commonly later in life with a predilection for males.1
• Develops rapidly within 6 to 8 weeks.
• May spontaneously regress after 3 to 6 months or may continue to grow and rarely metastasize.3

• KAs share features such as infiltration and cytologic atypia with SCCs.
• KAs have been reported to metastasize.
• KA is considered to be a variant of SCC, called SCC-KA type.
• Histologic criteria are not sensitive enough to discriminate reliably between KA and SCC.4

• Ages 40s to 60s.
• Occurs on sun-exposed areas of skin.
• Light complexion.
• Male gender.

Clinical Features

Solitary nodule in sun exposed areas. Often have a central keratin plug that resembles a volcano (Figures 167-1, 167-2, 167-3, 167-4, and 167-5). KAs may grow rapidly (Figure 167-6). Rare cases of multiple eruptive KAs have been reported.1

Typical Distribution

Face, arms, hands, and trunk (Figures 167-3 and 167-5). KAs can be found anywhere on the head and neck, including the ears (Figures 167-6 and 167-7).

Laboratory Studies

Biopsy is the only reliable method to make the diagnosis. KAs are well-differentiated squamoproliferative skin lesions.

• Actinic keratoses are precancerous lesions found on sun-exposed areas that may progress to SCC. Because these lesions are generally flat they are rarely confused with KAs (see Chapter 166, Actinic Keratosis and Bowen Disease).
• Cutaneous horn is a raised, keratinaceous lesion that can arise in actinic keratoses and in all types of nonmelanoma skin cancers. It generally does not have pearly raised skin around the keratin horn and therefore does not have the crater appearance of a KA (see Chapter 169, Cutaneous Horn).
• SCCs of the skin have many forms and KA is considered to be one type of SCC (see Chapter 171, Squamous Cell Carcinoma).

• A shave biopsy may be used for diagnosis but is not an adequate final treatment. Options for definitive treatment should be discussed with patient.
• Although some KAs may regress spontaneously, there is no way to distinguish between these and the ones that are variants of SCC, which may go on to metastasize. Therefore, the standard of care is to remove or destroy the remaining tumor. SOR C
• Elliptically excise a KA with margins of 3 to 5 mm as you would a SCC.4 SOR C
• Smaller, less-aggressive KAs diagnosed with shave biopsy may be destroyed with curettage and desiccation or cryotherapy with 3- to 5-mm margins. SOR C
• Mohs surgery may be indicated for large or recurrent KAs or KAs located in anatomic areas with cosmetic or functional considerations.4 SOR C
• Multiple eruptive KAs have been treated with oral retinoids, methotrexate, and cyclophosphamide.1 SOR C

When compared to other skin cancers, prognosis is good. Excision is typically curative.5

Patients should perform their own skin exams and have yearly clinical skin examinations to examine for recurrence and the development of new skin cancers.

KA is similar to other nonmelanoma skin cancers in that it occurs on sun-exposed areas and patients that have one are at increased risk of developing new skin cancers. Therefore, sun avoidance and sun protection should be emphasized.

Patient Resources

• Skinsight. Keratoacanthoma—http://www.skinsight.com/adult/keratoacanthoma.htm.

Provider Resources

• Medscape. Keratoacanthoma—http://emedicine.medscape.com/article/1100471.

A 65-year-old woman noted that a brown spot on her face was growing larger and darker (Figure 168-1). A broad shave biopsy showed lentigo maligna (LM) (melanoma in situ). The patient was referred for Mohs surgery for definitive treatment.

LM begins as a tan-brown macule melanoma usually in sun-damaged areas of the skin in older individuals. It is a subtype of melanoma in situ.

Hutchinson melanotic freckle.

• The incidence of LM is directly related to sun exposure. In the United States, the incidence is greatest in Hawaii, intermediate in the central and southern states, and lowest in the northern states.1
• Generally, patients with LM are older than age 40 years, with a peak incidence between the ages of 65 and 80 years.2
• Persons with LM melanoma (LMM) tend to be older, fair-skinned persons with markers of actinic skin damage and prior skin cancers, and the incidence is increasing.3
• The lesions occur more commonly on the driver's side of the head and neck in men in Australia.4

• LM is a subtype of melanoma in situ, a preinvasive lesion confined to the epidermis (Figures 168-1, 168-2, and 168-3).
• It is caused by cumulative sun exposure and, therefore, seen later in life.
• LMM occurs when the lesion extends into the dermis (Figure 168-4).
• LM can be present for long periods (5 to 15 years) before invasion occurs, although rapid progression within months has been described.5
• The risk for progression to LMM appears to be proportional to the size of the lesion of LM.5

• UV radiation exposure: risk increases with increased hours of exposure to sunlight, with the amount of actinic damage, and with a history of nonmelanoma skin cancer.
• Increased number of melanocytic nevi, including large or giant congenital nevi.
• Fair skin.
• History of severe sunburns.
• Porphyria cutanea tarda.
• Tyrosine-positive oculocutaneous albinism.
• Xeroderma pigmentosum.
• Occupational risk with sun exposure.

Clinical Features

• Large pigmented patch with multiple colors, including brown, black, pink, and white (signifying regression) (Figures 168-1, 168-2, and 168-3).
• May have ill-defined borders and microscopic extension that can determine the clinical borders and complete removal of the lesion difficult.
• One retrospective study revealed the four most important features of LM: asymmetric pigmented follicular openings, dark rhomboidal structures, slate-gray globules, and slate-gray dots with a sensitivity of 89% and a specificity of 96% (see Appendix C, Dermoscopy).6

Typical Distribution

• Face, head, and neck. There is a predilection for the nose and cheek (Figures 168-1 and 168-2).

Biopsy

• Complete excisional biopsy is rarely practical because these lesions are frequently large and are on the face (Figure 168-1). There is debate in the literature between doing broad shave biopsy, multiple punch biopsy, and incisional biopsy.7 The goal is to avoid sampling error and misdiagnosing a LM or LMM as a benign lesion.
• A lesion suspicious for LM or LMM can be biopsied using a broad scoop shave biopsy approach with a Derma blade or sharp razor blade (Figure 168-4).7 The goal is to sample the dermal-epidermal junction and still produce a good cosmetic result (especially if the lesion turns out to be benign).
• One option is multiple smaller biopsy samples of each morphologically distinct region of the lesion.7
• If an area suspicious for invasion is noted, or if there is an area of induration suspicious for associated desmoplastic melanoma, a deeper incisional biopsy of this area should be performed.7
• If sampling is incomplete, the presence of a solar lentigo, pigmented actinic keratosis, or reticulated seborrheic keratosis (SK) could mislead the pathologist and clinician to the wrong conclusion that the incisional specimen is representative of the whole, and that no LM is present.7
• In a study of LM, contiguous pigmented lesions were present in 48% of the specimens obtained by broad shave biopsy or Mohs surgery. The most common lesion was a benign solar lentigo (30%), followed by pigmented actinic keratosis (24%).7 This should be kept in mind when interpreting biopsy results to avoid false negatives.

• Solar lentigo—These hyperpigmented patches are very common on the faces and the dorsum of the hands of persons with significant sun exposure and the incidence increases with age. A possible solar lentigo is more suspicious for LM or LMM when it is larger, more asymmetric, has irregular borders and has more variation in colors. Pigmented lesions with these characteristics should be biopsied to determine the correct diagnosis. Many fair-skinned individuals have a number of solar lentigines making this a challenge. The use of dermoscopy and judicious biopsies is necessary to avoid missing LM and LMM (Figures 168-5 and 168-6).
• SKs are ubiquitous benign growths that occur more frequently with age. An early SK can be flat and easily resemble a solar lentigo or LM. The SKs on the back are less likely to be confused for LM, but a large flat SK on the face can easily be mistaken for a LM. More importantly, avoid missing a LM because it is assumed to be a flat early SK. When in doubt, biopsy the lesion with a quick and easy shave biopsy. Do not freeze a possible SK unless you are sure that it is truly benign (see Chapter 158, Seborrheic Keratosis).
• LMM is the feared outcome of missing an LM and not treating it properly. Any suspicious lesion requires biopsy. Don't be afraid to do a quick and easy shave biopsy rather than a full-thickness excision. If it turns out to be a LM or LMM, you can refer for definitive treatment and your biopsy technique does not change the prognosis. Early diagnosis does. LMM accounts for 4% to 15% of cutaneous melanoma (Figure 168-4) (see Chapter 172, Melanoma).

• Therapy is directed toward preventing progression to invasive LMM.

Nonsurgical

• Nonsurgical therapy for primary cutaneous melanomas should only be considered when surgical excision is not possible.
• Alternatives to surgery include topical imiquimod, cryosurgery, and observation. Efficacy of nonsurgical therapies for LM has not been fully established.8 SOR C

Medications

• Topical imiquimod 5% cream has been described in multiple studies to be effective in treating LM, especially in patients who are not surgical candidates. It is an immune response modifier that is indicated for the treatment of actinic keratosis and superficial basal cell carcinomas. Studies are limited by highly variable treatment regimens and lack of long-term follow-up.8-10 SOR B

Surgical

• For melanoma in situ, wide excision with 0.5- to 1.0-cm margins is recommended. For LM histologic subtype may require larger than 0.5-cm margins to achieve histologically negative margins, because of characteristically broad subclinical extension.8,10 SOR A
• Standard therapy is margin controlled surgical excision with Mohs surgery or rush permanent sections.10,11 SOR B
• The perimeter technique is a method of margin-controlled excision of LM with rush permanent sections. The main advantage is that all margins are examined with permanent sections. The main drawback is that multiple operative sessions are required to complete the procedure.12
• Recommended margins for standard excision of melanoma in situ are 0.5 cm. This margin is often inadequate for LM because of the subclinical extension that can occur.10 The average margin required to clear LM in 90% to 95% of cases in one study was greater than 0.5 cm.11 Consequently, margin-controlled excision of LM is recommended.11 SOR B
• Cryosurgery may be used in patients who are not good surgical candidates. In a study of 18 such patients with LM, the lesions resolved clinically in all cases, with no recurrence or metastasis detected during a mean follow-up of 75.5 months.13 SOR C These patients were treated with two freeze-thaw cycles of liquid nitrogen under local anesthesia in a single sitting.

• Because LMM is related to a lifetime of exposure to UV radiation, patients should limit sun exposure, especially between 10 am and 4 pm. When in the sun, make sure to wear sunscreen with a high sun-protection factor (SPF) that blocks both UVA and UVB. It's also a good idea to protect skin by wearing a broad-brim hat and clothing that covers your arms and legs.

• There is a 5% estimated lifetime risk of developing LMM in patients diagnosed with LM at age 45 years.5

• The National Comprehensive Cancer Network recommends that patients have regular clinical skin examinations at least yearly by their family physician or a dermatologist.14
• Regional lymph nodes should also be examined.

• Patients diagnosed with LM need to minimize sun exposure and do regular self-skin examinations.

Patient Resources

• Medline Plus. Melanoma—http://www.nlm.nih.gov/medlineplus/melanoma.html.

Provider Resources

• The Skin Cancer Foundation. Melanoma—1-800-SKIN-490 or http://www.skincancer.org.
• National Cancer Institute. Melanoma—http://www.cancer.gov/cancertopics/types/melanoma.
• Dermoscopy. A website on dermoscopy to learn how to improve early diagnosis of melanoma—http://www.dermoscopy.org/.

A 74-year-old man asks about a lesion on the back of his right ear (Figure 169-1). It has been present for approximately 5 years. Although the lesion does not bother him, his wife is concerned because it has been slowly growing. Shave biopsy revealed that the horn was from a basal cell carcinoma. The patient was referred for Mohs surgery to excise the remainder of the cancer.

Cutaneous horn (cornu cutaneum) is a morphologic (not pathologic) designation for a hyperkeratotic protuberant mass rising above the skin, resembling the horn of an animal.

• Relatively rare lesion, most often occurring on sun-exposed areas of the skin in elderly men; a recent Brazilian case series, however, found a higher prevalence in women.1

• Results from unusual cohesiveness of keratinized material from the superficial layers of the skin or deeply embedded in the cutis. Etiology is unknown but may be related to skin damage from sun exposure or trauma; infectious causes have also been reported including molluscum contagiosum and leishmaniasis.2
• Consists of marked retention of stratum corneum.
• May be benign, premalignant, or malignant (Figures 169-1, 169-2, and 169-3) at the base; in 2 large series, 58.6% and 38.9% had malignant or premalignant base pathology.1,3
• A history of other malignant or premalignant lesions, tenderness at the base, large size, older age, and location on the penis increase the risk of underlying malignancy.2-4
• Associated with many types of skin lesions (at the base) that can retain keratin and produce horns including actinic keratosis, warts (Figures 169-4 and 169-5), seborrheic keratosis (Figures 169-6 and 169-7), keratoacanthoma (Figure 169-3), sebaceous gland, and basal or squamous cell carcinoma (Figures 169-1, 169-2, and 169-3). In the more recent case series, actinic keratosis was found in 83.8% of the premalignant cases and squamous cell carcinoma was found in 93.75% of the malignant cases.1
• Rare cases have been described in association with metastatic renal cell carcinoma, lymphoma, dermatofibroma, pyogenic granuloma (Figure 169-8), and, recently, Kaposi sarcoma.5

• Advanced age (>70 years).
• Sun/radiation exposure.

Clinical Features

• Horn-like protuberance.
• Lesions are usually firm; have been described as flat, keratotic, nodular, pedunculated, and ulcerated.3
• Size may vary from a few millimeters to several centimeters; gigantic cutaneous horns (17 to 25 cm length and up to 2.5 cm width) have been reported, and in one series of 4 cases, all were benign.6
• Because of their height, cutaneous horns may be traumatized causing bleeding or pain.

Typical Distribution

• May occur on any area of the body; approximately 30% are found on the face (Figures 169-2, 169-6, and 169-7) and scalp and another 30% on the upper limbs.1

Biopsy

• The horn itself consists of concentric layers of cornified epithelial cells (hyperkeratosis). The base may display features of the associated pathologic etiology.

• Common warts are well-demarcated, rough, hard papules with an irregular papillary surface. Although they may form cylindrical projections, these often fuse to form a surface mosaic pattern; paring the surface exposes punctate hemorrhagic capillaries (see Chapter 131, Common Warts).

• Shave excision, ensuring that the base of the epithelium is obtained for histologic examination, and send to pathology; if benign, may freeze remainder of the lesion.
• Excisional biopsy may also be performed, with wider margins (tumor-free margin of at least 3 mm) if suspected malignancy.

• Routine follow-up is not needed provided complete removal is accomplished for malignant and premalignant lesions; in one case series of 48 eyelid cutaneous horns, there was no recurrence over a mean of 21 months.7
• Patients with any skin cancer should be seen yearly for skin exams because one cancer puts them at higher risk for all skin cancers. SOR C

Patient and Provider Resources

• http://emedicine.medscape.com/article/1056568-overview.
• http://www.accessmedicine.com/search/searchAMResultImg.aspx?searchStr=acquired+brachial+cutaneous+dyschromatosis&rootTerm=cutaneous+horn&searchType=1&rootID=45192.