|Classification and external resources|
Actinic keratosis on the lip
|Patient UK||Actinic keratosis|
Actinic keratosis (also called "solar keratosis" and "senile keratosis") is a premalignant condition of thick, scaly, or crusty patches of skin.:719 It is more common in fair-skinned people and it is associated with those who are frequently exposed to the sun, as it is usually accompanied by solar damage. They are considered as potentially pre-cancerous, since some of them progress to squamous cell carcinoma, so treatment is recommended. Untreated lesions have up to 20% risk of progression to squamous cell carcinoma.
Progressive development of these lesions occurs when skin is exposed to the sun constantly and thick, scaly, or crusty areas appear. The scaly or crusty portion is dry and rough. The lesions start out as flat scaly areas and later grow into a tough, wart-like area.
An actinic keratosis site commonly ranges between 2 and 6 millimetres in size, and may be dark or light, tan, pink, red, a combination of all these, or have the same pigment as the surrounding skin. The lesion may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, backs of hands, forearms, or lips.
Actinic keratoses may be divided into the following types:
- Hyperkeratotic actinic keratosis
- Pigmented actinic keratosis
- Lichenoid actinic keratosis
- Atrophic actinic keratosis
Physicians can usually identify actinic keratosis by doing a thorough examination; in principle actinic keratosis is a clinical diagnosis. A biopsy may be necessary when the keratosis is large or thick, to make sure that the lesion is a keratosis and not a skin cancer. Seborrheic keratoses are other lesions that appear in groups as the actinic keratosis do, but are not caused by sun exposure, and are not related to skin cancers. Seborrheic keratoses may be mistaken for an actinic keratosis.
Specialized forms of actinic keratoses include cutaneous horns, in which the skin protrudes in a thick, hornlike manner, and actinic cheilitis, a scaling and roughness of the lower lip and blurring of the border of the lip and adjacent skin.
Actinic keratosis usually shows focal parakeratosis with associated loss of the granular layer of, and thickening of the epidermis. The normal ordered maturation of the keratinocytes is disordered to varying degrees, there may be widening of the intracellular spaces, and they may also have some cytologic atypia, such as abnormally large nuclei. The underlying dermis often shows severe actinic elastosis and a mild chronic inflammatory infiltrate.
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
- Wearing sun protective clothing such as hats, long-sleeved shirts, long skirts, or trousers
- 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."
Various other treatments may also be used including:
- Ingenol mebutate gel for treatment of the trunk and extremities or the face and scalp, respectively. Duration of therapy is 2 days for the 0.05% gel and 3 days for the 0.015% gel
- Diclofenac sodium gel, a nonsteroidal anti-inflammatory drug, Recommended duration of therapy is 60 to 90 days
- Cryosurgery, e.g. with liquid nitrogen, by "freezing off" the actinic keratosis
- Photodynamic therapy: this new therapy involves injecting a chemical into the bloodstream, which makes the lesions more sensitive to any form of light.
- Laser, notably CO
2 and Er:YAG lasers, a laser resurfacing technique is often used with diffuse actinic keratosis
- Electrocautery: burning off actinic keratosis with electricity
- Imiquimod, an immune enhancing agent for topical treatment
- Different forms of surgery
Regular follow-up after the treatment is advised. 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 latter 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.
- Rapini, Ronald P.; c, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. pp. Chapter 108. ISBN 1-4160-2999-0.
- Prajapati V, Barankin B (May 2008). "Dermacase. Actinic keratosis". Can Fam Physician 54 (5): 691, 699. PMC 2377206. PMID 18474700.
- Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ISBN 0-07-138076-0.
- Quaedvlieg PJ, Tirsi E, Thissen MR, Krekels GA (2006). "Actinic keratosis: how to differentiate the good from the bad ones?". Eur J Dermatol 16 (4): 335–9. PMID 16935787.
- "actinic keratosis" at Dorland's Medical Dictionary
- Weedon, David (2010). Weedon's Skin Pathology, 3rd Edition. Elsevier. ISBN 978-0-7020-3485-5.
- Gupta, AK; Paquet, M (August 2013). "Network meta-analysis of the outcome 'participant complete clearance' in nonimmunosuppressed participants of eight interventions for actinic keratosis: a follow-up on a Cochrane review.". The British journal of dermatology 169 (2): 250–9. doi:10.1111/bjd.12343. PMID 23550994.
- Picato Gel label
- Ericson MB, Wennberg AM, Larkö O (February 2008). "Review of photodynamic therapy in actinic keratosis and basal cell carcinoma". Ther Clin Risk Manag 4 (1): 1–9. PMC 2503644. PMID 18728698.
- Pariser D, Loss R, Jarratt M, et al. (October 2008). "Topical methyl-aminolevulinate photodynamic therapy using red light-emitting diode light for treatment of multiple actinic keratoses: A randomized, double-blind, placebo-controlled study". J. Am. Acad. Dermatol. 59 (4): 569–76. doi:10.1016/j.jaad.2008.05.031. PMID 18707799.
- 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. PMID 16557235.
- 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 dermatology 169 (3): 502–18. doi:10.1111/bjd.12420. PMID 23647091.
- Amini, S; Viera, MH; Valins, W; Berman, B (Jun 2010). "Nonsurgical innovations in the treatment of nonmelanoma skin cancer.". The Journal of clinical and aesthetic dermatology 3 (6): 20–34. PMC 2921754. PMID 20725548.