Actinic keratosis (also called "solar keratosis" and "senile keratosis"; abbreviated as "AK") is a precancerous patch of thick, scaly, or crusty skin.:719 These growths are more common in fair-skinned people and those who are frequently in the sun. They usually form when skin gets badly damaged by ultraviolet (UV) radiation from the sun or indoor tanning beds. AKs are considered potentially pre-cancerous; left untreated, they may turn into a type of cancer called squamous cell carcinoma. Untreated lesions have up to a 20% risk of progression to squamous cell carcinoma, so treatment by a dermatologist is recommended.
Development of these growths occur when skin is constantly exposed to the sun over time. They usually appear as thick, scaly, or crusty areas that often feel dry or rough. In fact, AKs are often felt before they are seen, and the texture is often compared to sandpaper. They may be dark, light, tan, pink, red, a combination of all these, or have the same color as the surrounding skin. An actinickeratosis growth commonly ranges between 2 and 6 millimeters in size but can grow to be a few centimeters in diameter. They often appear on sun-exposed areas, such as the face, ears, neck, scalp, chest, backs of hands, forearms, or lips. Because they are related to sun-damage on the skin, most people who have an AK have more than one.
Diagnosis is made clinically on physical exam, but can be confirmed by biopsy. There are various options for treatment, but 5-Fluorouracil seems to be the most effective. By following up with a dermatologist, AKs can be treated before they turn into skin cancer. If skin cancer does develop, it can be caught early, when treatment can be curative.
Actinic keratoses ("AKs") most commonly present as a white, scaly plaque of variable thickness with surrounding redness; they are most notable for having a sandpaper-like texture when felt with a gloved hand. Skin nearby the lesion often shows evidence of solar damage characterized by notable pigmentary alterations, being yellow or pale in color with areas of hyperpigmentation; deep wrinkles, coarse texture, purpura and ecchymoses, dry skin, and scattered telangiectasias are also characteristic. Photoaging leads to an accumulation of oncogenic changes, resulting in a proliferation of mutated keratinocytes that can manifest as AKs or other neoplastic growths. With years of sun damage, it is possible to develop multiple AKs in a single area on the skin. The lesions are usually asymptomatic, but can be tender, itch, bleed, or produce a stinging or burning sensation. AKs are typically graded in accordance with their clinical presentation: Grade I (easily visible, slightly palpable), Grade II (easily visible, palpable), and Grade III (frankly visible and hyperkeratotic).
Actinic keratoses can have various clinical presentations, often characterized as follows:
Classic (or Common): Classic AKs present as white, scaly macules, papules or plaques of various thickness, often with surrounding erythema. They are usually 2-6mm in diameter but can sometimes reach several centimeters in diameter.
Hypertrophic (or Hyperkeratotic): Hypertrophic AKs (HAKs) appear as a thicker scale or rough papule or plaque, often adherent to an erythematous base. Classic AKs can progress to become HAKs, and HAKs themselves can be difficult to distinguish from malignant lesions.
Atrophic: Atrophic AKs lack an overlying scale, and therefore appear as a nonpalpable change in color (or macule). They are often smooth and red, and are less than 10mm in diameter.
AK with cutaneous horn: A cutaneous horn is a keratinic projection with its height at least one-half of its diameter, often conical in shape. They can be seen in the setting of actinic keratosis as a progression of an HAK, but are also present in other skin conditions. 38-40% of cutaneous horns represent AKs.
Pigmented AK: Pigmented AKs are rare variants that often present as macules or plaques that are tan to brown in color. They can be difficult to distinguish from a solar lengtigo or lentigo maligna.
Actinic cheilitis: When an AK forms on the lip, it is called actinic cheilitis. This usually presents as a rough, scaly patch on the lip, often accompanied by the sensation of dry mouth and symptomatic splitting of the lips.
Bowenoid AK: Usually presents as a solitary, erythematous, scaly patch or plaque with well-defined borders. Bowenoid AKs are differentiated from Bowen's disease by degree of epithelial involvement as seen on histology.
The presence of ulceration, nodularity, or bleeding should raise concern for malignancy. Specifically, clinical findings suggesting an increased risk of progression to squamous cell carcinoma can be recognized as: IDRBEU. I (Induration /Inflammation), D (Diameter > 1 cm), R (Rapid Enlargement), B (Bleeding), E (Erythema) and U (Ulceration). AKs are usually diagnosed clinically, but because they are difficult to clinically differentiate from squamous cell carcinoma, any concerning features warrant biopsy for diagnostic confirmation.
Actinic keratosis, atrophic form
Actinic keratoses have three possible clinical outcomes: they may regress, remain stable, or advance to become invasive disease. Occasionally they come and go, appearing on the skin, remaining for months, and then disappearing. Often they will reappear in a few weeks or months, particularly after unprotected sun exposure. Left untreated, there is a chance that the lesion will advance to become invasive. While it is difficult to predict whether an AK will advance to become squamous cell carcinoma, it has been noted that squamous cell carcinomas originate in lesions formerly diagnosed as AKs with frequencies reported between 65 to 97%.
A lesion biospy is performed if the diagnosis remains uncertain after a clinical physical exam. The most common tissue sampling techniques include shave or punch biopsy. When only a portion of the lesion can be removed due to its size or location, the biopsy should sample tissue from the thickest area of the lesion, as SCCs are most likely to be detected in that area. If a shave biopsy is performed, it should extend through to the level of the dermis in order to provide sufficient tissue for diagnosis; ideally, it would extend to the mid-reticular dermis. Punch biopsy usually extends to the subcutaneous fat when the entire length of the punch blade is utilized.
Specific findings depend on the clinical variant and particular lesion characteristics. The seven major histopathologic variants are all characterized by atypical keratinocytic proliferation beginning in the basal layer and confined to the epidermis; they include:
Hypertrophic: Notable for marked hyperkeratosis, often with evident parakeratosis. Keratinocytes in the stratum malphigii may show a loss of polarity, pleomorphism, and anaplasia. Some irregular downward proliferation into the uppermost dermis may be observed, but does not represent frank invasion.
Atrophic: With slight hyperkeratosis and overall atrophic changes to the epidermis; the basal layer shows cells with large, hyperchromatic nuclei in close proximity to each other. These cells have been observed to proliferate into the dermis as buds and duct-like structures.
Lichenoid: Demonstrate a band-like lymphocytic infiltrate in the papillary dermis, directly beneath the dermal-epidermal junction.
Achantholytic: Intercelleular clefts or lacunae in the lowermost epidermal layer that result from anaplastic changes; these produce dyskeratotic cells with disrupted intercellular bridges.
Bowenoid: This term is controversial and usually refers to full-thickness atypia, microscopically indistinguishable from Bowen's Disease. However most dermatologists and pathologists will use it in reference to tissue samples that are notable for small foci of atypia that involve the full thickness of the epidermis, in the the background of a lesion that is otherwise consistent with an AK.
Pigmented: Show pigmentation in the basal layer of the epidermis, similar to a solar lentigo.
Dermoscopy is a noninvasive technique utilizing a handheld magnifying device coupled with a transilluminating lift. It is often used in the evaluation of cutaneous lesions, but lacks the definitive diagnostic ability of biopsy-based tissue diagnosis. Histopathologic exam remains the gold standard
Polarized contact dermoscopy of AKs occasionally reveals a "rosette sign," described as four white points arranged in a clover pattern, often localized to within a follicular opening. It is hypothesized that the "rosette sign" corresponds histologically to the changes of orthokeratosis and parakeratosis known as the "flag sign."
Non-pigmented AKs: linear or wavy vascular patterning, or a "strawberry pattern," described as unfocused vessels between hair follicles, with white-haloed follicular openings.
Pigmented AKs: gray to brown dots or globules surrounding follicular openings, and annular-granular rhomboidal structures; often difficult to differentiate from lentigo maligna.
Preventive measures recommended for actinic keratosis are similar to those for skin cancer:
Not staying in the sun for long periods of time without protection (e.g., sunscreen, clothing, hats)
Frequently applying powerful sunscreens with SPF ratings greater than 30 and that also block both UVA and UVB light
Avoiding sun exposure during noon hours is very helpful because ultraviolet light is the most powerful at that time
According to an article in the Journal of Investigative Dermatology (2005) 125, 93–97; doi:10.1111/j.0022-202X.2005.23733.x, entitled, "Human Papillomavirus-DNA Loads in Actinic Keratoses Exceed those in Non-Melanoma Skin Cancers", actinic keratosis may contain a significant amount of infectious human papillomavirus. Verbatim: "HPV presents in significantly higher viral loads in actinic keratosis (AK), which are the precursor lesions of squamous cell carcinoma (SCC), than in SCC. Viral loads of 1 HPV-DNA copy per less than 50 cells were measured in 40% of AK. The higher viral loads in AK are likely to reflect enhanced HPV-DNA replication. This may be because of intense keratinocyte proliferation and differentiation in AK favoring amplification of commensalic HPV. Active HPV replication and presumably enhanced gene expression may in turn stimulate keratinocyte proliferation and contribute to carcinogenesis in these early stages of NMSC development. HPV-E6 proteins were recently shown to inhibit UV-induced apoptosis by abrogation of BAK in response to UV damage (Jackson and Storey, 2000) and to bind a protein required for repair of single-strand DNA breaks (Iftner et al, 2002). Thereby, accumulation of UV-induced mutations and oncogenic transformation might be facilitated in cases of active HPV infection."
Cryosurgery instrument used to treat actinic keratoses
Interim result of phototherapy for actinic keratosis with Methyl aminolevulinate one week after exposure. Patient has light skin, blue eyes.
Regular follow-up is advisable after the treatment. The regular checks are to make sure no new lesions have developed and that old ones haven't become thicker.
The risk of an actinic keratosis turning into squamous cell carcinoma is between 0% and 0.5% per year. The higher risk is in those who have previously had skin cancer. They go away in 15-60% of cases over a year. In cases that resolve, they come back in 15-50% of people.
Actinic keratosis is very common, affecting half of the global population. It is seen more often in fair-skinned individuals, and prevalence may vary with geographical location and age. People who take immunosuppressive drugs, such as organ transplant patients, are 250 times more likely to develop actinic keratoses that may lead to skin cancer.
^Moy, RL (2000 Jan). "Clinical presentation of actinic keratoses and squamous cell carcinoma.". Journal of the American Academy of Dermatology42 (1 Pt 2): 8–10. PMID10607350.Check date values in: |date= (help)
^ abcdRosen, T; Lebwohl, MG (2013 Jan). "Prevalence and awareness of actinic keratosis: barriers and opportunities.". Journal of the American Academy of Dermatology68 (1 Suppl 1): S2–9. PMID23228302.Check date values in: |date= (help)
^Stockfleth, E; Kerl, H; Guideline Subcommittee of the European Dermatology, Forum (2006 Nov-Dec). "Guidelines for the management of actinic keratoses.". European journal of dermatology : EJD16 (6): 599–606. PMID17229598.Check date values in: |date= (help)
^Jadotte, YT; Schwartz, RA (2012 Feb). "Solar cheilosis: an ominous precursor: part I. Diagnostic insights.". Journal of the American Academy of Dermatology66 (2): 173–84; quiz 185–6. PMID22243721.Check date values in: |date= (help)
^Taylor, CR; Stern, RS; Leyden, JJ; Gilchrest, BA (1990 Jan). "Photoaging/photodamage and photoprotection.". Journal of the American Academy of Dermatology22 (1): 1–15. PMID2405022.Check date values in: |date= (help)
^ abcDuncan, KO; Geisse, JK (2008). Epithelial precancerous lesions. In: Fitzpatrick's Dermatology in General Medicine. McGraw-Hill. p. 1007.
^Butani, AK; Arbesfeld, DM; Schwartz, RA (2005 Apr). "Premalignant and early squamous cell carcinoma.". Clinics in plastic surgery32 (2): 223–35. PMID15814119.Check date values in: |date= (help)
^Yu, RCH (1991). "A histopathological study of 643 cutaneous horns". Br J Dermatol (24): 449.
^Zalaudek, I; Ferrara, G; Leinweber, B; Mercogliano, A; D'Ambrosio, A; Argenziano, G (2005 Dec). "Pitfalls in the clinical and dermoscopic diagnosis of pigmented actinic keratosis.". Journal of the American Academy of Dermatology53 (6): 1071–4. PMID16310072.Check date values in: |date= (help)
^Bagazgoitia, L; Cuevas, J; Juarranz, A (2010 Feb). "Expression of p53 and p16 in actinic keratosis, bowenoid actinic keratosis and Bowen's disease.". Journal of the European Academy of Dermatology and Venereology : JEADV24 (2): 228–30. PMID19515076.Check date values in: |date= (help)
^Quaedvlieg, PJ; Tirsi, E; Thissen, MR; Krekels, GA (2006 Jul-Aug). "Actinic keratosis: how to differentiate the good from the bad ones?". European journal of dermatology : EJD16 (4): 335–9. PMID16935787.Check date values in: |date= (help)
^ abcdefRossi, R; Mori, M; Lotti, T (2007 Sep). "Actinic keratosis.". International journal of dermatology46 (9): 895–904. PMID17822489.Check date values in: |date= (help)
^Ackerman, AB (2014-10-31). "Respect at last for solar keratosis". Dermatopathology (3): 101–103.
^ abcdefSchaffer, edited by Jean L. Bolognia, Joseph L. Jorizzo, Julie V. (2012). Dermatology (3rd ed. ed.). [Philadelphia]: Elsevier Saunders. ISBN9780723435716.
^ abCuellar, F (June 2009) . "New Dermoscopic Pattern in Actinic Keratosis and Related Conditions.". Arch Dermatol (145 ed.) 6: 732. doi:10.1001/archdermatol.2009.86.
^Peris, K; Micantonio, T; Piccolo, D; Fargnoli, MC (November 2007). "Dermoscopic features of actinic keratosis.". Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG5 (11): 970–6. PMID17908179.
^Akay, BN; Kocyigit, P; Heper, AO; Erdem, C (December 2010). "Dermatoscopy of flat pigmented facial lesions: diagnostic challenge between pigmented actinic keratosis and lentigo maligna.". The British journal of dermatology163 (6): 1212–7. PMID21083845.
^Gupta, AK; Paquet, M (August 2013). "Network meta-analysis of the outcome 'participant complete clearance' in non-immunosuppressed participants of eight interventions for actinic keratosis: a follow-up on a Cochrane review.". The British Journal of Dermatology169 (2): 250–9. doi:10.1111/bjd.12343. PMID23550994.
^Hadley G, Derry S, Moore RA (June 2006). "Imiquimod for actinic keratosis: systematic review and meta-analysis". J. Invest. Dermatol.126 (6): 1251–5. doi:10.1038/sj.jid.5700264. PMID16557235.
^Werner, RN; Sammain, A; Erdmann, R; Hartmann, V; Stockfleth, E; Nast, A (Sep 2013). "The natural history of actinic keratosis: a systematic review.". The British journal of dermatology169 (3): 502–18. doi:10.1111/bjd.12420. PMID23647091.