The importance of early diagnosis and treatment of actinic keratosis (original) (raw)
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Pathobiology of actinic keratosis: Ultraviolet-dependent keratinocyte proliferation
Journal of the American Academy of Dermatology, 2013
Actinic keratoses are proliferations of transformed neoplastic keratinocytes in the epidermis that are the result of cumulative ultraviolet (UV) radiation from sun exposure. They are commonly found on sites of sun-exposed skin such as the face, balding scalp, and back of the hand. Although UV exposure does exert certain beneficial effects on the skin, excessive exposure to UV radiation induces multiple cascades of molecular signaling events at the cellular level that produce inflammation, immunosuppression, failure of apoptosis, and aberrant differentiation. Cumulatively, these actions result in mutagenesis and, ultimately, carcinogenesis. This article provides a brief overview of the key mediators that are implicated in the pathobiology of actinic keratosis. Three evolutionary possibilities exist for these keratoses in the absence of treatment: (1) spontaneous remission, which can be common; (2) remaining stable, without further progression; or (3) transformation to invasive squamous cell carcinoma, which may metastasize. Because the effects of UV radiation on the skin are complex, it is not yet fully clear how all of the mediators of actinic keratosis progression are interrelated. Nonetheless, some represent potential therapeutic targets, because it is clear that directing therapy to the effects of UV radiation at a number of different levels could interrupt and possibly reverse the mechanisms leading to malignant transformation. ( J Am Acad Dermatol 2013;68:S10-9.)
Actinic keratosis - review for clinical practice
International journal of dermatology, 2018
Actinic keratosis (AK) is a lesion that arises as a result of excessive exposure to solar radiation and appearing predominantly on Fitzpatrick phototype I and II skin. Given that some AKs evolve into squamous cell carcinoma, these lesions are considered premalignant in nature, occurring mostly in elderly men and immunosuppressed individuals chronically exposed to ultraviolet (UV) radiation. There are several mechanisms for the formation of AKs; among them are oxidative stress, immunosuppression, inflammation, altered proliferation and dysregulation of cell growth, impaired apoptosis, mutagenesis, and human papillomavirus (HPV). Through the understanding of these mechanisms, several treatments have emerged. Among the options for AK treatment, the most commonly used include 5-fluorouracil (5-FU), cryotherapy, diclofenac, photodynamic therapy (PDT), imiquimod (IQ), retinoids, and ingenol mebutate (IM). There have been recent advances in the treatment options that have seen the emergent...
Actinic keratosis treatment as a key component of preventive strategies for nonmelanoma skin cancer
The Journal of clinical and aesthetic dermatology, 2010
Actinic keratosis is responsible for more than eight million visits to dermatologists and primary care physicians annually. Actinic keratosis, the result of chronic sun damage to the skin, is closely linked to nonmelanoma skin cancer, both histologically and pathophysiologically. Clinical evidence shows that not only does actinic keratosis have the potential to progress and transform into nonmelanoma skin cancer, but it also may in fact be an early stage of cancer. The treatment of actinic keratosis is evolving from a "treat-as-you-go" strategy to a more preventive approach to curtail the potential emergence of nonmelanoma skin cancer. As the interrelationship between actinic keratosis and nonmelanoma skin cancer, squamous cell carcinoma, and basal cell carcinoma continues to strengthen, treating actinic keratosis as part of a preventive strategy to reduce nonmelanoma skin cancer is coming to the forefront. The following review of the relationship between actinic keratosis...
The importance of treating the field in actinic keratosis
Journal of the European Academy of Dermatology and Venereology, 2017
Actinic keratoses (AKs) are intraepithelial atypical proliferations of keratinocytes that develop in skin that has undergone long-term exposure to ultraviolet radiation. Given the ageing population and an increasing prevalence of AK, the socioeconomic burden of AK is likely to rise over the coming years. Areas of subclinical (non-visible) sun damage in the periphery of visible AK lesions contain the same genetic changes as those found in the lesions themselves, and are known as areas of field cancerization. AK lesions and the field are associated with an increased risk of skin cancer, including invasive squamous cell carcinoma. Although effective in clearing visible AK, lesion-directed therapies do not address field cancerization and can lead to high recurrence rates. In contrast, field-directed therapies, such as ingenol mebutate, imiquimod and diclofenac, can clear both visible and subclinical AK lesions and reduce the development of new lesions in the treated field. Additionally, preclinical studies suggest that field therapy may prevent or delay the recurrence of non-melanoma skin cancer. AK treatment guidelines now recognize the importance of treating the field in patients with AK, and adaptation of treatment guidelines into clinical practice is warranted. Physician and patient education around the consequences of leaving the field of cancerization untreated is necessary in order to reduce the increasing burden associated with AK.
Actinic keratosis: review of the literature and new patents
Recent patents on inflammation & allergy drug discovery, 2013
Actinic Keratoses (AK) are considered a worldwide problem with continuously increasing incidence. They clinically present as rough or scaly plaques and are histologically characterized by a proliferation of atypical keratinocytes limited to the epidermis. AK are considered as an early step in the continuum of transformation from normal skin to invasive squamous cell carcinoma (SCC). These lesions develop on a background of field cancerization in which chronically UV- damaged-areas accumulate molecular changes, but remain clinically normal for prolonged periods. The presence of certain clinical features of AK, such as large size, ulceration, or bleeding, suggests an increased risk of disease progression. The risk is also increased by evidence of extensive solar damage, advanced age, and immune-suppression. Many treatment modalities are available, although recent developments have focused on the management of the whole actinically damaged field. In this regard, several topical drugs h...
Seminars in Cutaneous Medicine and Surgery, 1999
Actinic keratoses (AKs) are primarily induced by ultravlolet (UV) radiation and are often identified as premalignant lesions. In our opinion, AKs are proliferations of transformed, neoplastic keratinocytes confined to the epldermls that may eventually extend Into the dermis, at which point they are termed squamous cell carcinoma (SCC). In contrast to AKs, SCCs have the potential to metastaslze and kill. Thls process is analogous to that of evolving carcinoma of the uterine cervlx that has been termed cervlcal IntraepltheUal neoplasla (CIN), a time-tested and reliable classification that provides cllnlclans wlth accurate Information on whlch to base treatment declslons regardlng cervlcal neoplasms followlng blopsy testlng. A slmllar classlficatlon scheme could provlde guldance to cllnlclans for the dlagnosls and treatment of evolvlng SCC of the skln and as such, we propose a slmllar classlficatlon uslng the termlnology keratinocytlc Intraepldermal neoplasla (KIN). Thls system Is more refiectlve of the hlstology and natural hlstory of SCC and ellmlnates amblgulty In the termlnology of leslons currently referred to as AKs. The KIN classlficatlon defines features by whlch Indlvldual specimens can be objectively graded and specific treatment recommendations are made based on the grade of the leslon. We propose that the term keratlnocyftc Introeplderreal neoplaslo (KIN) be used to define and descrlbe evolvlng SCC of the skln and that the term actlnlc (solar) keratosls be ellmlnated. Copyright 9 1999 by W.B. Saunders Company HISTORICAL PERSPECTIVE AK was first identified as "keratoma senilis" by Freudenthal in 19267 and later more fully described and renamed actinic keratosis by Pinkus in 1958. 8 Actinic keratosis literally means a keratotic (thickened, scaly) growth caused by damage induced by a ray, presumably electromagnetic irradiation. AKs have historically been characterized as being precancerous. 9 Although it is true that these lesions, because they are
Proliferative Actinic Keratosis
International Journal of Dermatology, 1994
Background. Solar/actinic keratoses (AKS) are premalignant lesions, usually less than 1 cm in diameter, that appear on chronically sun-damaged skin. Methods. We describe four patients with a form of AK that enlarged and recurred despite standard treatment. Histologic examination revealed a single and multilayered sheet of anaplastic cells along the undersurface of the epidermis extending down hair follicles and present over a large area. Results. Three of the patients developed either a squamous cell carcinoma (sec) or basal cell carcinoma (BCC) within the area encompassed by the AK. Conclusions. These cases represent an insidious, proliferative form of AK with an Increased tendency to develop into skin cancer. Int J DermatoM994; 33:341-345 Gase Reports Case T: A 59-yeat-old white man was seen with a 10-yeat history of a scaly, erythematous macule on the left nasolabial fold (Fig. 1). In 1983, the initial biopsy of the lesion revealed actinic keratosis (AK). This lesion had then been treated with liquid nitrogen and 5-fluorouracil cream on several occasions over a 5-year period. Curettage was performed 5 years after the initial biopsy. A histologic report of curettings from the area was read as "actinic keratosis." The lesion in the left nasolabial fold tecutred 1 year after curettage. A shave biopsy revealed keratinizing basal cell carcinoma (BCC). Mohs' micrographic surgery was performed on the BCC, but no attempt was made to eradicate the AK completely. Microscopic study of the Mohs' micrographic sections revealed keratinizing BCC and AK with atypical keratinocyte proliferation and atypia, extending as a sheet of cells at the undersurface of the epidermis (Fig. IA). These cells showed no tendency to differentiate (Figs. lAand IB). Eleven months postoperatively, an erythematous macule was noted on the border of the Mohs' surgical scar. Shave biopsy revealed AK with cicatrix. No further treatment was undertaken, but the lesion was followed. A second biopsy, 1 year later, in the same area revealed hypertrophic AK; sec could not be ruled out (Fig. IC). Mohs' micrographic surgery
Are actinic keratoses really squamous cell cancer? How do we know if they would become malignant?
Clinics in Dermatology, 2017
Actinic Keratosis (AK) is a very common skin disease, caused by chronic sun exposure. AKs have historically been characterized as being "precancerous" or "premalignant." It is true that these lesions do not possess metastatic potential, because they are confined to the epidermis but it is not accurate to deem them "premalignant." AK qualifies as a malignant neoplasm because it also fulfills criteria for malignancy in classic pathology, namely, the capability, or potential, to kill by either destruction of tissue locally or by metastasis widely. In this context AK is considered now by many a carcinoma in situ, and can persist or progress to invasive squamous cell carcinoma (iSCC), which rarely metastasizes. Through this controversy, that certainly speaks to an issue we have been debating for at least a century, we'd like to start a really and constructive debate to reach a unanimous conclusion considering the various theories and the various points of view of the literature. Are actinic keratoses really squamous cell cancer? How do we know if they would become malignant? We are going to write about a very debated subject: is the actinic keratosis a cancer or a precancerous lesion? The data in the literature are conflicting, we are trying to come to a conclusion. Actinic Keratosis (AK) is a very common skin disease, caused by chronic sun exposure. Over 75% of AKs arise on chronically sun-exposed areas 1 , consequently
Actinic Keratosis: Rationale and Management
Dermatology and Therapy, 2014
Actinic keratoses (AKs) are common skin lesions heralding an increased risk of developing squamous cell carcinoma (SCC) and other skin malignancies, arising principally due to excessive ultraviolet (UV) exposure. They are predominantly found in fair-skinned individuals, and increasingly, are a problem of the immunosuppressed. AKs may regress spontaneously, remain stable or transform to invasive SCC. The risk of SCC increases for those with more than 5 AKs, and the majority of SCCs arise from AKs. The main mechanisms of AK formation are inflammation, oxidative stress, immunosuppression, impaired apoptosis, mutagenesis, dysregulation of cell growth and proliferation, and tissue remodeling. Human papilloma virus has also been implicated in the formation of some AKs. Understanding these mechanisms guides the rationale behind the current available treatments for AKs. One of the main principles underpinning the management of AKs is that of field cancerization. Wide areas of skin are exposed to increasing amounts of UV light and other environmental insults as we age. This is especially true for the head, neck and forearms. These insults do not target only the skin where individual lesions develop, but also large areas where crops of AKs may appear. The skin between lesions is exposed to the same insults and is likely to contain as-yet undetectable preclinical lesions or areas of dysplastic cells. The whole affected area is known as the 'field'. Management is therefore divided into lesion-directed and field-directed therapies. Current therapies include lesiondirected cryotherapy and/or excision, and topical field-directed creams: 5-fluorouracil, imiquimod, diclofenac, photodynamic therapy and ingenol mebutate. Combining lesion-and field-directed therapies has yielded good results Electronic supplementary material The online version of this article (and several novel therapies are under investigation. Treatment is variable and tailored to the individual making a gold standard management algorithm difficult to design. This literature review article aims to describe the rationale behind the best available therapies for AKs in light of current understanding of pathophysiology and epidemiology. A PubMed and MEDLINE search of literature was performed between
Actinic keratosis: a clinical and epidemiological revision
Anais Brasileiros de Dermatologia, 2012
Actinic keratoses are benign intraepithelial skin neoplasms constituted by atypical proliferation of keratinocytes that may evolve to squamous cell carcinoma. They develop in photoexposed skin areas; they are induced mainly by ultraviolet radiation and are considered cutaneous markers of chronic exposure to sunlight. They develop mainly in adults and older, fair skinned individuals, and are the fourth most common cause of dermatologic consultation in Brazil. Damage to the apoptosis pathway in photoexposed epithelium favors cellular proliferation and the permanence of the lesions. In this revision, the authors assemble the main epidemiological data regarding this disease and suggest that strategies to identify risky phenotypes, early diagnosis, adequate treatment, clinical follow-up, stimulus to skin self examination, photoeducation and photoprotection should be promoted with the aim of avoiding the progression to malignancy and also the prevention and the diagnose of concomitant neoplasms also induced by ultraviolet radiation.