Actinic keratosis

Actinic keratosis, also actinic precancer or solar keratosis or light - keratosis (from Greek ακτίς ( aktis, " beam ", actinic: caused by radiation ( see also actinometer ) ) and of Greek κέρας ( keras, " horn " ) ) is a through many years of intense exposure to sunlight ( UV radiation) caused chronic damage to the cornified epidermis, typically reddish, adherent scales on the skin. The skin damage progresses slowly, but can go years into a form of skin cancer: squamous cell carcinoma or squamous. Actinic keratosis is therefore a facultative precancerous condition. Histologically, it corresponds to a precancerous intraepithelial lesion. It occurs mainly in people in the second half of life in places that were most frequently exposed to the sun unprotected. Most notably are the face, back of the hands, face, bald head, nose, ear, and also forearms and chest.

Epidemiology

The most commonly affected are people with light skin type, preferably beyond the age of 50. People who reside in your spare time or work-related lot of time outdoors are at increased risk for actinic keratosis. Actinic keratosis is a recognized by the Federal Ministry of Labour and Social occupational disease. The prevalence of the disease was reported for Germany with 11.5 % among 60-70 year olds. In 2011, 8.3 % of the most common outpatient diagnosis and therapy in dermatology accounted for actinic keratosis. In a Dutch study of 2061 individuals with a mean age of 72 years with a prevalence of 28% among women and 49 % in men was found. Risk factors include, among others, light skin, frequent sunburns in childhood, baldness, and male gender were identified.

Clinical picture

The appearance of actinic keratosis on the skin is very diverse. Clinically it is classified according to different systems, the classification by Olsen ( Olsen Grade I to III) is most common. Early actinic keratosis appears as a single or a few millimeter-sized, rough, ill-defined lesions ( lesions), the rich reddish color and to feel better as you can see ( Olsen grade I ). Advanced lesions become discolored due to a proliferation of corneal cells hyperkeratosis whitish or reddish, harden and may spread ( Olsen grade II ). Later, the lesions appear as warty nodular skin growths that are anchored firmly to the ground ( grade III). They feel rough like coarse sandpaper. Individual lesions occur, but most are large areas of skin affected as the entire hairless scalp, a process called field cancerization of the disorder. Microscopically, the actinic keratoses to a malformation of the tissue dysplasia with disorganized growth, impaired differentiation and atypical epidermal skin cells keratinocytes recognizable. These have irregular, enlarged nuclei. The epidermal stratum corneum stratum corneum is thickened. At the genetic level, mutations in the p53 gene were frequently identified in the tissues of actinic keratosis. These mutations are typically caused by UVB light changes, mainly point mutations (CC to TT, C to T) in susceptible regions of the gene. This can cause inactivation of the tumor suppressor p53, which eliminates this as a guardian of cell division and programmed cell death apoptosis and get the modified cells a selective advantage over healthy cells. In the further course of the disease may result from a single altered cell a whole, monoclonal -derived from their field to develop ( field cancerization ). Mutations of p53 have also been identified in more than 90 % of squamous cell carcinomas, which can arise from actinic keratosis.

Prognosis and prophylaxis

There is the possibility of spontaneous regression of actinic keratosis, are given for the rate of 18-63 % after 7-17 months (weighted 15 %), with 15-53 % of the reformed skin lesions after one year were available again. Usually, an actinic keratosis remains exist for years. The overall risk of development of squamous cell carcinoma from an actinic keratosis appears to be on average about ten percent per patient per decade. For patients with more than 20 lesions, a risk of 20% is given. The development of a malignant squamous cell carcinoma from an actinic keratosis occurs on average within 24 months. This is not pre- identify which lesion will change, this can even happen at Olsen grade I lesions. It is estimated that about 60 % of squamous cell carcinoma arising from actinic keratoses. Actinic keratosis is also easier severities should therefore be detected and treated early to prevent the development of melanoma skin cancer. Appropriate clothing or the use of highly effective UVB / UVA sun filter of actinic keratosis and possibly a subsequent skin cancer can be prevented.

Treatment

Due to the high risk of development of melanoma skin cancer actinic keratosis should be taken seriously as an early tumor disease of the skin and treated as early as possible efficiently. Treatment should be done by an experienced dermatologist. Various options are available here. Small keratoses can surgically ( local anesthesia ), are removed with laser or superficially with liquid nitrogen ( cryosurgery ). In particular for large-scale treatments offers due to the high cure rates and good cosmetic result photodynamic therapy (PDT ) on. It is recognized in the guidelines as a first treatment choice. Here, the skin can be treated initially with a finished product on the basis of 5 -aminolevulinic acid or its methyl ester ( MAOP ) and irradiated after a contact with cold red light. The PDT leaves no scars, in contrast to ( cryo- ) surgical removal of actinic keratosis. If necessary it can be repeated after a few months.

A study published in 2006 from the United States showed that destructive treatment methods are effective and given the local cost of regulation represent the standard of care in the U.S.. Corresponding data from Europe are lacking. The primary destructive, läsionsgerichteten therapy methods are, however, the problem of field cancerization not fair and not detect subclinical lesions. Here is the advantage of surface effective methods, such as topical imiquimod, 5-fluorouracil (5- FU), diclofenac, Ingenolmebutat and photodynamic therapy.

Differential Diagnosis

Herd on the fuselage can be (for example, Bowen's disease ), or confused with a certain form of skin cancer, basal cell carcinoma which occasionally with other cancer precursors. Likelihood of confusion also with the rare discoid lupus erythematosus. In addition, particularly squamous cell carcinoma, which can result from an actinic keratosis, look similar. In the transition to an actinic keratosis (eg due to persistent damage by light ) in such a squamous cell carcinoma, the clinical picture of actinic keratosis changed little since she hardly seems to grow. Histologically, however, the transition to squamous be clearly seen at the partially of malignant epithelial basement membrane of the skin and ingrowth into the blood vessel leading dermis.

Veterinary Medicine

Even in animals, such as domestic dogs and domestic cats are uncommon actinic keratoses. Above all pigment- poor parts of the body with white lights and hair are affected, such as the outside of the ear. It manifests itself in skin thickening and plaques with thick adherent scales. The sessions are held with acitretin, mild cases can be treated with a combination of β -carotene and glucocorticoids.