Actinic Keratosis Clinical Trials, Diagnosis, and Treatment

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Actinic Keratosis

Actinic keratosis (also called solar keratosis, or AK) is a premalignant condition of thick, scaly, or crusty patches of skin. It is most common in fair-skinned people who are frequently exposed to the sun, because their pigment isn't very protective. It usually is accompanied by solar damage. Since some of these pre-cancers progress to squamous cell carcinoma, they should be treated.

When skin is exposed to the sun constantly, thick, scaly, or crusty bumps appear. The scaly or crusty part of the bump is dry and rough. The growths start out as flat scaly areas, and later grow into a tough, wart-like area.

An actinic keratosis site commonly ranges in between 2 to 6 millimeters, and can be dark or light, tan, pink, red, a combination of all these, or the same pigment of one's skin. It may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, back of hands, forearms, lips etc.

Current Research

For current research articles click - here

Prevention

Preventative measures recommended for AK 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 15 and that also block both UVA and UVB light.
Using sunscreen even in winter sun exposure.
Wearing sun protective clothing such as hats, long-sleeved shirts, long skirts, or pants.
Avoiding sun exposure during noon hours is very helpful because ultraviolet light is the most powerful at that time.

Diagnosis

Doctors can usually identify AK by doing a thorough examination. A biopsy may be necessary when the keratosis is large and/or thick, to make sure that the bump is a keratosis and not a skin cancer. Seborrheic keratoses are other bumps that appear in groups like the actinic keratosis but are not caused by sun exposure, and are not related to skin cancers. Seborrheic keratoses may be mistaken for an actinic keratosis.

(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Actinic_keratosis)

Findings From Current Research

The Treatment of Actinic Keratoses with a Combination of 5-Fluorouracil and Imiquimod Creams

Authors: Price NM.

Department of Dermatology at USCF, San Francisco, CA, USA. nmp@pricen.net

BACKGROUND: 5-fluorouracil (5-FU) and imiquimod creams are accepted topical therapies for actinic keratosis (AK). Both are associated with a prolonged course of treatment with an inflammatory response that may preclude the treatment process. OBJECTIVES: To describe the treatment regimen and the extent of side effects in the use of the combined application of 5-FU and imiquimod creams in patients presenting with AKs and to demonstrate the convenience and ease of the methodology of this regimen. METHODS: The patients applied 5-FU and imiquimod creams to their lesions daily for one week each month over the course of 3 months. The patients were seen after the completion of each one-week course to evaluate their progress and side effects. RESULTS: There were 64 patients in the study, 48 of whom completed the study and demonstrated a clearing of their AKs by the end of the third course of treatment. All of the patients developed an inflammatory response at the sites of their AKs as well as at subclinical sites with no apparent AKs. Nearly all of these inflammatory reactions were confined to localized sites without involvement of the surrounding skin. CONCLUSIONS: Therapy with the combined application of 5-FU and imiquimod creams is a relatively rapid and convenient form of therapy as compared to the separate use of each medication.

Journal: J Drugs Dermatol. 2007 Aug;6(8):778-81.
Adapted from PubMed; click here to access full journal article.

Sun-Related Factors, Betapapillomavirus, and Actinic Keratoses: A Prospective Study

Authors: McBride P, Neale R, Pandeya N, Green A.

Cancer and Population Studies Unit, Queensland Institute of Medical Research, PO Royal Brisbane Hospital, Brisbane, Queensland, Australia 4029. penelope.mcbride@qimr.edu.au

OBJECTIVE: To examine prospectively the relationship among sun exposure, Betapapillomavirus, and development of actinic keratoses. DESIGN: Prospective, community-based cohort study. SETTING: Township of Nambour in Southeast Queensland, Australia. PARTICIPANTS: A total of 291 randomly selected adults aged 36 to 86 years with the presence or absence of Betapapillomavirus DNA in eyebrow hair follicle cells known at baseline in August 1996 and with subsequently documented sun exposure histories. MAIN OUTCOME MEASURES: Prevalence of actinic keratoses in March 2003 after 7 years of follow-up. RESULTS: Beyond the known determinants of multiple actinic keratoses, namely, advanced age, male sex, fair skin, and lifetime occupational sun exposure, Betapapillomavirus infection was associated with having more than 10 actinic keratoses (odds ratio, 1.8; 95% confidence interval, 0.7-4.4). However, Betapapillomavirus positivity led to a significant 13-fold increase in the risk of actinic keratoses among those 60 years or older, a nearly 6-fold increase in risk when combined with fair skin color, and a doubling in risk of actinic keratoses when combined with high sun exposure, recent or cumulative, compared with those who had neither Betapapillomavirus infection nor the respective risk factor of interest. CONCLUSIONS: Although the presence of Betapapillomavirus DNA in eyebrow hair follicle cells had only a small independent association with actinic keratoses, Betapapillomavirus infection in combination with key risk factors increased the risk of actinic keratoses, which is consistent with a potentiation by Betapapillomavirus of the effect of established causal factors.

Journal: Arch Dermatol. 2007 Jul;143(7):862-8.
Adapted from PubMed; click here to access full journal article.

Topical Therapy in the Treatment of Actinic Keratosis and Basal Cell Carcinoma

Authors: Newman MD, Weinberg JM.

Department of Dermatology, UMDNJ-Robert Wood Johnson Medical School, Newark, USA.

Actinic keratosis (AK) is an evolving malignant cutaneous neoplasm. AK also is known as solar keratosis and squamous cell carcinoma (SCC) in situ, either solar keratotic type or keratinocytic intraepidermal neoplasia. AKs can be treated with destructive or topical therapies. This article reviews current and evolving topical therapeutic options for AKs, several of which have been shown to offer substantial benefit in the alleviation of these lesions. The topical therapies include 5-fluorouracil (5-FU), diclofenac sodium, colchicine, retinoids, and imiquimod. Topical treatment of basal cell carcinoma (BCC) with imiquimod also will be discussed.

Journal: Cutis. 2007 Apr;79(4 Suppl):18-28.
Adapted from PubMed; click here to access full journal article.

Immune-Mediated Changes in Actinic Keratosis Following Topical Treatment with Imiquimod 5% Cream

Authors: Torres A, Storey L, Anders M, Miller RL, Bulbulian BJ, Jin J, Raghavan S, Lee J, Slade HB, Birmachu W.

Dermatology Office, Loma Linda University Medical Center, Loma Linda, California, USA. abelt@aol.com

BACKGROUND: The objective of this study was to identify the molecular processes responsible for the anti-lesional activity of imiquimod in subjects with actinic keratosis using global gene expression profiling. METHODS: A double-blind, placebo-controlled, randomized study was conducted to evaluate gene expression changes in actinic keratosis treated with imiquimod 5% cream. Male subjects (N = 17) with >or= 5 actinic keratosis on the scalp applied placebo cream or imiquimod 3 times a week on nonconsecutive days for 4 weeks. To elucidate the molecular processes involved in actinic keratosis lesion regression by imiquimod, gene expression analysis using oligonucleotide arrays and real time reverse transcriptase polymerase chain reaction were performed on shave biopsies of lesions taken before and after treatment. RESULTS: Imiquimod modulated the expression of a large number of genes important in both the innate and adaptive immune response, including increased expression of interferon-inducible genes with known antiviral, anti-proliferative and immune modulatory activity, as well as various Toll-like receptors. In addition, imiquimod increased the expression of genes associated with activation of macrophages, dendritic cells, cytotoxic T cells, and natural killer cells, as well as activation of apoptotic pathways. CONCLUSION: Data suggest that topical application of imiquimod stimulates cells in the skin to secrete cytokines and chemokines that lead to inflammatory cell influx into the lesions and subsequent apoptotic and immune cell-mediated destruction of lesions.

Journal: J Transl Med. 2007 Jan 26;5:7.
Adapted from PubMed; click here to access full journal article.

Guidelines for the Management of Actinic Keratoses

Authors: de Berker D, McGregor JM, Hughes BR; British Association of Dermatologists Therapy Guidelines and Audit Subcommittee.

Bristol Dermatology Centre, Bristol Royal Infirmary, Bristol, UK. david.deberker@ubht.swest.nhs.uk

These guidelines stemmed from a consensus meeting held by the British Photobiology Group (BPG) in 1999. Following this meeting one of the authors (J.M.M.) was invited to draw up guidelines for the management of actinic keratoses by the British Association of Dermatologists Therapy Guidelines and Audit Subcommittee. Relevant evidence was sought using the search terms 'solar keratosis' and 'actinic keratosis' in Medline from 1966 onwards. Additional and earlier literature was reviewed on the basis of references within post-1966 publications. All articles of apparent relevance were reviewed independently of the nature of the publication. The quality of the evidence elicited has been indicated. The National Ambulatory Medical Care Survey (U.S.A.) was used for further data on topical chemotherapy. Papers were reviewed and discussed by the contributors to the BPG Workshop (see Acknowledgments). Recommendations are evidence based where possible. Strength of recommendation is coupled with quality of evidence. Strength of recommendation includes consideration of apparent cost-benefit and practical considerations. Quality of evidence reflects the nature of the trial structure that provides data of efficacy.

Journal: Br J Dermatol. 2007 Feb;156(2):222-30.
Adapted from PubMed; click here to access full journal article.

Measures of Cumulative Exposure from a Standardized Sun Exposure History Questionnaire: A Comparison with Histologic Assessment of Solar Skin Damage

Authors: Karagas MR, Zens MS, Nelson HH, Mabuchi K, Perry AE, Stukel TA, Mott LA, Andrew AS, Applebaum KM, Linet M.

Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA. margaret.karagas@dartmouth.edu

Ultraviolet radiation exposure is the dominant environmental determinant of all major forms of skin cancer; however, the nature of the association is incompletely understood. Existing instruments to capture sun exposure history tend to yield reproducible results, but the validity of these responses is unknown. To address this question, the authors examined the relation between responses to a standardized sun exposure instrument and histologic evidence of actinic damage in a population-based study of keratinocyte cancers from New Hampshire diagnosed from July 1, 1997, through March 31, 2000. A single study dermatopathologist histologically reviewed the adjacent skin of 925 skin cancer biopsies for the presence of solar keratoses and the extent of solar elastosis. The authors compared these measures with responses to a personal interview on history of sunburns, sunbathing, and time spent outdoors. Focusing on site-specific exposure, they found variables that estimated cumulative exposure related to histologic evidence of actinic damage. In contrast, measures of acute/intermittent exposure were generally unrelated to solar damage histologically. Findings suggest that cumulative, but not intermittent, measures of sun exposure derived from a personal interview appear to reflect a person's exposure history based on histologic evidence.

Journal: Am J Epidemiol. 2007 Mar 15;165(6):719-26. Epub 2007 Jan 4.
Adapted from PubMed; click here to access full journal article.

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