CASE #1: Superficial basal cell 

An antifungal cream/steroid combination prescribed earlier by the patient’s primary-care clinician provided no beneficial effect. The man’s skin was quite fair. An abundance of sun damage was noted, primarily on the patient’s face and arms. He had a history of a number of sun-caused skin cancers, including basal cell carcinomas (BCCs).

Shave biopsy confirmed the expected diagnosis of superficial BCC. The most common treatment for superficial BCC is electrodessication and curettage, but this is not practical for such a large lesion. This procedure would result in a large raw area that would be painful and slow to heal. Pyogenic granuloma formation is a frequent complication associated with this treatment as well. Moreover, a large scar would certainly result, and the chance of recurrence with curettement of such a large lesion is all too high.1 Surgical excision of this lesion, with margins, would result in a scar roughly 3.5 times longer than the maximum dimension of the cancer; in this case, almost 1 ft long.2

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Radiation therapy has long been used to good effect in individuals with BCCs. In actual practice, however, this treatment is usually reserved for recurrent or other aggressive tumors not amenable to surgical resolution.3 For many patients, radiation treatment is also impractical because it requires multiple visits over the course of several weeks (i.e., five sessions a week for four weeks).

Two of the most common topical medicines indicated in the treatment of superficial BCC are 5-fluorouracil (Carac, Efudex, Fluoroplex) cream or solution and imiquimod (Aldara) cream.4 The former is a pyrimidine analog that blocks DNA replication5 while the latter boosts the immune response to the cancer. Neither medication has been studied in cancers as big as this patient’s.

Superficial BCC bears no resemblance to any of the other types of BCC. In fact, superficial BCC is often misdiagnosed as fungal infection, psoriasis or eczema.6 The most obvious clue to its identity is the fact that superficial BCC will almost always occur on sun-exposed skin of fair, sun-damaged individuals, typically on the back and shoulders and often in multiples.

Unlike psoriasis or eczema, superficial BCCs are fixed to the same location and grow slowly but steadily over several years’ time. The annular, sharply defined palpable border — sometimes called “field fire” for its resemblance to the advancing border of a grass fire — is essentially pathognomonic.

While UV exposure is the most common cause of BCC, other triggers include arsenic exposure (mostly through groundwater contamination), coal, tar, ionizing radiation exposure, local trauma, vaccination and even tattooing.7-9 Geographic location, heredity and skin type are often involved as well.6

BCCs primarily appear on older patients (average age 67.5 years) because it typically takes 20 to 50 years from UV exposure to tumor genesis. However, BCCs are beginning to be seen on younger and younger patients — even in teenagers. Men are more than twice as likely as women to develop BCC. Patients aged 55 to 70 years are 100 times more likely to be diagnosed with BCC than an individual aged 20 years. Immunosuppression (as seen in HIV and transplant patients, for example) also increases risk.6

As for distribution, 70% of BCCs occur somewhere on the head (usually the face);10 25% on the trunk;11 and most of the rest on the hands, arms and legs. BCCs have been reported in non-sun-exposed areas, including axillae, and on genitials.12,13 At most, only about 0.1% metastasize,6 first to local nodes, then to the lungs, and finally to bones.

The predominant theory is that most BCCs develop from pluripotential cells in the basal layer of the epidermis or from certain parts of the follicular structure. In susceptible individuals, the hedgehog gene encodes an extracellular protein that binds to a cell membrane receptor complex, triggering a cascade of cellular events leading to cellular proliferation. Overexposure to UV radiation suppresses immunologic responsiveness to cutaneous tumors.

As mentioned, superficial BCCs do not resemble such far more common types as nodular or noduloulcerative tumors. These BCCs are familiar to most providers as a pearly papule or nodule. Other types of BCCs include sclerosing (scarlike) and pigmented types, which can be quite dark, especially in dark-skinned patients.

Some BCCs are more aggressive than others, as indicated by their clinical behavior and such histologic features as perineural involvement. Location — especially on the perinasilar and canthal areas of the face — can be associated with aggressive behavior and increased rates of recurrence. The superficial BCC in this case was so indolent as to be on the opposite end of the spectrum, requiring many years of neglect before becoming invasive.

Given the dearth of suitable treatment choices, the decision was made to begin the application of imiquimod 5% cream five days a week. The treatment is still in progress at this time. Such therapy will certainly cause irritation and weeping during the expected two-month treatment period but has a good chance of eradicating this lesion by promoting the production of cytokine precursors.