Actinic Keratoses
Actinic keratoses synonymous with solar keratosis are areas of skin which have become keratotic due to lifetime skin sun light exposure, cumulative exposure is the risk. They can be discrete lesions or areas of confluent erythema and scaling on predominantly sun-exposed skin. They tend to affect middle aged to older adults.
AKs are generally premalignant lesions with low malignancy potential. However AKs have the potential to develop into malignant lesions such as SCCs. AK’s also have the potential to spontaneously regress. AKs are graded on a three point scale. Grade 1 just visible and palpable – gritty to feel and difficult to see. Grade 2 usually red and scaly, easy to feel and see. Grade 3 are thicker and hyperkeratotic, because of this they are therefore more difficult to differentiate from SCCs. AKs are often asymptomatic, however on occasions can be sore and itchy. Field change is a term used to describe skin extensively covered with multiple AKs.
Aetiology
AKS occur due to chronic exposure to ultraviolet radiation. AKs tend to affect fair coloured skin and predominantly involve the head and dorsa of the hands. Risk factors for developing AKs, include exposure to sunlight as shown in molecular evidence where UVB-specific p53 mutations have been demonstrated. Those receiving chronic immunosuppression, particularly organ transplant, also patients on long term inflammatory bowel and rheumatological disease are more likely to develop AKs. There is also considered to be a link to arsenic exposure and sun bed use. (16)
Incidence and prevalence
There are many studies looking into the incidence of AK, proving difficult to truly quantify. This is thought to be partly to do with stages 1-2 being able to regress spontaneously over time. It is therefore likely to be underestimated. Figures range between 25% and 70% for resolution of AKs over a period of 1–4 years. It is likely that the incidence of AKs is underestimated. It is difficult to measure the burden of AKs reliably in the population. In summary, combined data suggest the possibility of regression and a low risk of malignant progression for any given AK. The presence of AK predicts an excess risk for subsequently developing an alternative NMSC or melanoma compared with a matched population.
There is a body of professional opinion that believes AKs are part of a spectrum that includes SCC in situ, and that prevention of SCC is therefore the reason for therapy. However with spontaneous regression not all AKs therefore need treatment. There is inadequate evidence to justify treatment of all AKs to try to prevent malignant change.
BAD advise the most appropriate management of AKs should be a combination of patient preferences, the severity, extent, duration and presence of symptoms alongside the patient’s general health and well-being.