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Guidelines for the management of actinic keratoses

GUIDELINESDOI for the management of actinic keratosesD. de Berker, McGregor* and Hughes on behalf of the British Association of DermatologistsTherapy Guidelines and Audit SubcommitteeBristol Dermatology Centre, Bristol Royal Infirmary, Bristol BS2 8HW, *Department of Dermatology, St Bartholomew s and the London NHS Trust, London E1 1BB, Portsmouth Dermatology Centre, St Mary s Hospital, Milton Road, Portsmouth PO3 6AD, de : for publication21 May 2006 Key wordsactinic keratosis, Guidelines , treatmentConflicts of interestD. de B., none; has received anhonorarium from 3M as an invited member of anadvisory board for the treatment of actinickeratoses; , of the British Association ofDermatologists Therapy Guidelines and AuditSubcommittee are: Ormerod (Chairman), Eedy, D. Mitchell, F. Humphreys, J. Peters,R. Bull, H. Bell, M. Kouimtzi and S. Guidelines stemmed from a consensus meeting held by the British Photo-biology Group (BPG) in 1999.

the membrane zone but no invasion is seen. Histological vari-ants of AK have been described, including hypertrophic, bow-enoid, lichenoid, acantholytic and pigmented.

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Transcription of Guidelines for the management of actinic keratoses

1 GUIDELINESDOI for the management of actinic keratosesD. de Berker, McGregor* and Hughes on behalf of the British Association of DermatologistsTherapy Guidelines and Audit SubcommitteeBristol Dermatology Centre, Bristol Royal Infirmary, Bristol BS2 8HW, *Department of Dermatology, St Bartholomew s and the London NHS Trust, London E1 1BB, Portsmouth Dermatology Centre, St Mary s Hospital, Milton Road, Portsmouth PO3 6AD, de : for publication21 May 2006 Key wordsactinic keratosis, Guidelines , treatmentConflicts of interestD. de B., none; has received anhonorarium from 3M as an invited member of anadvisory board for the treatment of actinickeratoses; , of the British Association ofDermatologists Therapy Guidelines and AuditSubcommittee are: Ormerod (Chairman), Eedy, D. Mitchell, F. Humphreys, J. Peters,R. Bull, H. Bell, M. Kouimtzi and S. Guidelines stemmed from a consensus meeting held by the British Photo-biology Group (BPG) in 1999.

2 Following this meeting one of the authors ( )was invited to draw up Guidelines for the management of actinic keratoses bythe British Association of Dermatologists Therapy Guidelines and Audit Subcom-mittee. Relevant evidence was sought using the search terms solar keratosis and actinic keratosis in Medline from 1966 onwards. Additional and earlier litera-ture was reviewed on the basis of references within post-1966 publications. Allarticles of apparent relevance were reviewed independently of the nature of thepublication. The quality of the evidence elicited has been indicated. The NationalAmbulatory Medical Care Survey ( ) was used for further data on topicalchemotherapy. Papers were reviewed and discussed by the contributors to theBPG Workshop (see Acknowledgments). Recommendations are evidence basedwhere possible. Strength of recommendation is coupled with quality of of recommendation includes consideration of apparent cost-benefit andpractical considerations.

3 Quality of evidence reflects the nature of the trial struc-ture that provides data of Guidelines have been prepared for dermatologists onbehalf of the British Association of Dermatologists (BAD) andreflect the best data available at the time the report was pre-pared. Caution should be exercised in interpreting the data;the results of future studies may require alteration of the con-clusions or recommendations in this report. It may be neces-sary or even desirable to depart from the Guidelines in theinterests of specific patients and special circumstances. Just asadherence to the Guidelines may not constitute defence againsta claim of negligence, so deviation from them should notnecessarily be deemed Guidelines stemmed from a consensus meeting held bythe British Photobiology Group (BPG) in 1999. Following thismeeting one of the authors ( ) was invited to draw upguidelines for the management of actinic keratoses (AKs) bythe BAD Therapy Guidelines and Audit Subcommittee.

4 Medline(1966 2004) was the main source of references for thisreview. Relevant evidence was sought using the search terms solar keratosis and actinic keratosis . Additional and earlierliterature was reviewed on the basis of references within post-1966 publications. All articles of apparent relevance werereviewed independently of the nature of the publication. TheNational Ambulatory Medical Care Survey ( ) was usedfor further data on topical chemotherapy. Papers werereviewed and discussed by the contributors to the BPG Work-shop (see Acknowledgments).Definition and introduction to the guidelineActinic (syn. solar) keratoses are keratotic lesions occurring onchronically light-exposed adult skin. They represent focal areasof abnormal keratinocyte proliferation and differentiation thatcarry a low risk of progression to invasive squamous cell car-cinoma (SCC). A spectrum of histology is seen but the cardi-nal feature of an AK is epithelial dysplasia.

5 This may berestricted to the basal layer or may extend to full-thicknessatypia at which point differentiation from Bowen s disease canbe difficult. There is disorderly arrangement and maturation ofepithelial cells. Multiple buds of epithelial cells may occur at 2007 The Authors222 Journal Compilation 2007 British Association of Dermatologists British Journal of Dermatology2007156,pp222 230the membrane zone but no invasion is seen. Histological vari-ants of AK have been described, including hypertrophic, bow-enoid, lichenoid, acantholytic and are widely considered to be premalignant lesions withlow individual potential for invasive malignancy and higherpotential for spontaneous regression. They present as discrete,sometimes confluent, patches of erythema and scaling on pre-dominantly sun-exposed skin, usually in middle-aged andelderly individuals. They are often asymptomatic but mayoccasionally be sore or itch.

6 Lesions may be single or epidemiology, risk factors, disease associations and demo-graphics of the at-risk population are all pertinent to patientmanagement. They are discussed together with the availabletreatment suggests that most AKs are the result of chronic expo-sure to ultraviolet (UV) radiation. They occur predominantly onchronically sun-exposed skin, such as that of the face and dorsaof hands, in fair-skinned addition, UVB-specificp53 mutations have been demonstrated in AKs, providingmolecular evidence in support of a role for is ahigh prevalence in those receiving chronic immunosuppressionTable 1 Factors determining choice of active therapy from six main alternatives. The scoring is based on the authors evaluation of efficacy, easeof use, morbidity and cost-benefitCryosurgery 5-FU Diclofenac ImiquimodaCurettage PDTC ommentsMain characteristic of AKsLow number of AKs High number of AKs Thin AKs Thin lesions may not alwaysrequire treatmentHypertrophic AKs Histology may be excision may be preferredIsolated lesions failing torespond to other therapies Histology may be excision may be preferredConfluent recalcitrant AKs,failing other treatments Certain lesions within a resistantfield may require histologicalassessmentLocationScalp, ears, nose, cheeks,forehead.

7 Perioral Periorbital Topical therapies can be difficultto use near mouth and eyesConfluent scalp Pretreatment with 5% salicylic acidointment may improve outcomeBelow the knee Poor healing is a particular concernat this site. All modalities can leadto ulceration. Treatment may becombined with advice on elevationand compression bandagingwhere possibleBack of hands Courses of topical therapy may needto be extended and pretreatmentwith 5% salicylic acid ointmentmay improve outcomeCharacteristics of patient (rating may be considered in context of clinical need indicated by characteristic of AK and location)Medically dependentor senile Morbidity of treatment may dictatechoice of modalitySelf-reliant 5-FU may be repeated at sites ofrelapse or new lesions inprimary careOne-off treatment Lives far from hospital May favour treatment that allowsmonitoring in primary carePart of continuousmanagement plan 5-FU, 5-fluorouracil; PDT, photodynamic therapy; AKs, actinic keratoses ; , good treatment; , fair treatment, , can be useddepending on circumstances.

8 , rarely used in these is not currently licensed for use in the treatment of AKs. 2007 The AuthorsJournal Compilation 2007 British Association of Dermatologists British Journal of Dermatology2007156,pp222 230 Guidelines for the management of AKs, D. de organ transplant possible risk factorsinclude exposure to arsenic4,5and chronic sun bed 8 Incidence and prevalenceIn Ireland and the , 24%, 23% and 19% of individualsaged over 60 years were found to have at least one AK instudies from Galway, South Wales and Merseyside, 11 There was a linear increase in the prevalence withage (from 60 to 80 years) in men but not in women, and therate of new AKs was estimated to be 149 per 1000 were also present in 3 6% of men aged between40 and 49 history: spontaneous regression andmalignant transformationStudies indicate a high spontaneous regression rate in theorder of 15 25% for AKs over a 1-year period,10,12and a lowrate of malignant transformation, less than one in 1000 the less, mathematical models derived fromthis study predict that for an individual with an average of 7 7 AKs, the probability of at least one transforming within a10-year period is approximately 10%.

9 14 When 918 adults (mean age 61 years) with AKs but no pre-vious history of skin cancer were followed prospectively for5 years, the incidence rate for basal cell carcinoma (BCC) andSCC was estimated at 4106 and 3198 per 100 000 person-years, respectively, representing a substantial excess incidencecompared with the general data suggestthat even though the risk of malignant transformation for anygiven AK is very low, the probability of an individual with AKspresenting subsequently with skin cancer is none the less highcompared with the population at and diagnosisPatients with AKs may present to dermatologists in various cir-cumstances: they may be referred by the general practitioner(GP) because of diagnostic uncertainty or concern aboutmalignant risk or for further management , and AKs may bedetected incidental to referral for another problem, or detectedduring follow up of a skin cancer patient. Diagnosis is fre-quently made on clinical appearance alone but as the differen-tial diagnosis includes superficial BCC, Bowen s disease,invasive SCC and even amelanotic melanoma, a skin biopsymay be indicated in selected cases where there is clinicaldoubt or suspicion of invasive options are open to patients with AKs.

10 The natural his-tory of individual lesions studied in the suggests thattreatment is not universally required on the basis of prevent-ing progression into , others feel that preven-tion of SCC is the main reason for AKs have histological features within the spectrum ofin-situskin cancer. They can also represent a cause of symp-toms and disfigurement which may be the main determinantof treatment choices. Clinical judgement should discern whichlesions are more likely to represent a risk to the patient shealth, but where the likelihood is low, options include notherapy or palliation with emollient or keratolytic agent suchas low-strength salicylic acid active treatment is sought, many modalities of ther-apy are available (Table 1). Good-quality data on the outcomeof these different therapies are available in only a fewinstances. Treatment of an individual lesion may have a thera-peutic effect on surrounding skin, with an effect on overallprogression of actinic damage, but this potential benefit hasnot been quantified.


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