A 68-year-old man presents with symptoms of urine retention. He is incidentally found to have these lesions on his bilateral upper extremities. What is this, and which treatment is recommended? Continued on p. 18.
Actinic keratosis (AK), also known as solar keratosis, is a premalignant skin lesion that occurs only on sun-exposed areas of the skin. Actinic means caused by sunlight, and keratosis means thickened scaly growth. It is the most common skin lesion with malignant potential, and it can regress, persist, or progress. Ultraviolet-induced genetic mutations, including mutations in tumor suppression gene proteins, are a noted etiology of lesions. (J Am Acad Dermatol 2000;42[1 Pt 2]:18.) Beta-papillomavirus also has been implicated in the development of AK, but the exact impact and mechanism have yet to be fully elucidated. (Arch Dermatol 2007;143:862.)
Lesions are typically dry rough scaly and crusty (hyperkeratotic) on an erythematous base, and can be flat or progress to impressive hornlike projections. Lesions can vary from light to dark, and be tan, pink, or red. They vary in size from 1 mm to more than an inch in diameter, and most commonly occur on the face, ears, scalp, neck, and upper extremities where direct sun exposure is most concentrated, but can occur on leg, back and chest areas in those with direct sun exposure. Typically patients with AK have more than one lesion (average of six to eight; J Am Acad Dermatol 2000;42[1 Pt 2]:4), and it is not uncommon for single lesions in the same area to become confluent. The diagnosis is typically made clinically, but may require biopsy and histopathologic review to exclude squamous cell carcinoma.
Risk factors for the development of AK include those with fair skin, high sun exposure (occupational and recreational sun exposure and those living at higher elevations), and those on immunosuppressive medications (250 times increased risk). The prevalence of AK is highest in Australia (40% to 60% in people over age 40), the country with the highest skin cancer rates in the world, where the reported incidence is 11 percent to 26 percent. (Br J Dermatol 1994;131:455.) AK essentially does not exist in black skin. (J Am Acad Dermatol 2006;55(5):741.)
The differential diagnosis of AK is fairly limited and includes seborrheic keratoses, melanoma, squamous cell carcinoma, warts, discoid lupus, porokera-tosis (keratinization disorder), and Bowen disease (intraepidermal squamous cell carcinoma in situ). Fortunately, most AKs do not progress to squamous cell carcinoma, with one recent study reporting that the risk of malignant transformation to be less thavn one percent over one year and less than three percent over four years. (Cancer 2009;115:2523.) Interestingly, up to 50 percent of cases will resolve on their own if patients stay out of the sun for a year.
Unfortunately, it is difficult to tell which AK lesions will progress to invasive squamous cell (J Am Acad Dermatol 2000;42[1 Pt 2]:4), but lesions that are quick growing or changing are at increased risk for malignant transformation as are ones that are large (> 1 cm), inflamed, ulcerated, or spontaneously bleeding. (Eur J Dermatol 2006;16:335.) An estimated 10 percent to 15 percent of these “active” AK lesions progress to squamous cell cancer of the skin, and less than 10 percent will metastasize. But those that do metastasize have a poor five-year survival prognosis. (J Am Acad Dermatol 1992;26:976.) Of those with squamous cell carcinoma of the skin, 60 percent arise from an AK lesion. (Am J Clin Dermatol 2000;1:167.)
Because AK is considered a carcinoma in situ and a premalignant lesion, treatment is warranted in most cases. The most common initial treatment of AK is cryotherapy with liquid nitrogen. Other treatments include surgical removal (curettage) or topical pharmacotherapy (e.g., 5-fluorouracil, diclofenac, imiquimod). There may also be a role for dermabrasion and laser phototherapy, but more research is needed before this becomes a mainstay of treatment. (Dermatol Surg 1996;22:17; J Am Acad Dermatol 2001;45:96; J Photochem Photobiol B 2009;96:159.)
Patients with AK by definition have sustained sun damage, and are at risk for other forms of skin cancer, including melanoma and basal cell carcinoma. Sun exposure is considered cumulative and not quantified as episodic, with more than half of a person's average total life sun exposure occurring before age 20. (American Osteopathic College of Dermatology; http://bit.ly/AOCD-AK.) As much as 80 percent of ultraviolet rays can permeate though the clouds, so patients should still be counseled to wear sunscreen or protective clothing on cloudy days.
This patient was referred for outpatient treatment of his AK lesions.
Comments about this article? Write to EMN at firstname.lastname@example.org.
Click and Connect! Access the links in this article by reading it on www.EM-News.com.
In the December issue, Quick Consult incorrectly said prolonged QTc intervals should be treated with sodium bicarbonate. Although rare, antihistamine toxicity can cause QRS prolongation via sodium channel blockade, which can be treated with intravenous sodium bicarbonate. Diphenhydramine is also known to prolong the rate adjusted QTc, leading to Torsades de pointes. Prophylactic intraveous magnesium sulfate could be considered in these cases. It is rarely needed, however. EMN apologizes for the error.