Actinic keratosis

from Wikipedia, the free encyclopedia
Classification according to ICD-10
L57.0 Actinic keratosis
ICD-10 online (WHO version 2019)

The actinic keratoses , also actinic precancer or solar keratosis or light keratosis (from Greek ακτίς ( Aktis , "beam", actinic : caused by radiation (see also actinometer )) and Greek κέρας ( keras , "Horn")) is a light-induced skin change. It is chronic damage to the cornified epidermis caused by long-term, intensive exposure to sunlight ( UV radiation ) , typically with reddish, firmly adhering scales on the skin. The skin damage progresses slowly, but after years it can turn into a form of skin cancer: squamous cell carcinoma , also called spinalioma . Actinic keratosis is therefore an optional precancerous condition . Histologically , it corresponds to an intraepithelial precancerous lesion . It occurs mainly in people in the second half of life in places that have been exposed to sunlight particularly often. These are primarily the face, back of the hand, forehead, bald head, nose, ear, but also forearms and décolleté.

Epidemiology

Actinic keratosis on the scalp of a 52 year old man

People with fair skin type are most frequently affected , preferably over the age of 50. People who spend a lot of their leisure time or work outdoors are at higher risk for actinic keratosis. The Medical Advisory Board "Occupational Diseases" at the Federal Ministry of Labor and Social Affairs has recommended that a new occupational disease with the legal definition "Squamous cell carcinoma or multiple actinic keratoses of the skin due to natural UV radiation" be included in Appendix 1 of the Occupational Diseases Ordinance . Actinic keratosis has been recognized as an occupational disease under number 5103 since January 1, 2015 . The prevalence of the disease for 2008 in Germany was given as 11.5% among 60 to 70 year olds. In 2011, they accounted for 8.3% of the hundred most common outpatient dermatological therapies in Germany. In a Dutch study of 2061 people with an average age of 72 years, a prevalence of 28% in women and 49% in men was found. The risk factors identified included light skin, frequent sunburns in childhood, baldness and male gender.

Clinical picture

The appearance of actinic keratosis on the skin is very diverse. Clinically, it is classified according to different systems, with the Olsen classification (Olsen grade I to III) being the most common. Early actinic keratosis appears as single or a few, millimeter-sized, rough, blurred skin changes (lesions), which are red in color and can be felt better than seen (Olsen grade I). Advanced lesions become whitish or reddish in color due to an increase in corneal cells ( hyperkeratosis ), harden and spread (Olsen grade II). Later, the lesions look like warty, bumpy skin growths that are firmly attached to the subsurface (grade III). They feel rough like coarse sandpaper. Individual lesions do occur, but mostly large areas of skin are affected, such as the entire hairless scalp, an appearance of the disease known as field cancerization. Actinic keratosis can be recognized microscopically by a malformation ( dysplasia ) of the tissue with disorganized growth, impaired differentiation and atypical epidermal skin cells ( keratinocytes ). These have irregular, enlarged cell nuclei. The epidermal horny layer stratum corneum is thickened. At the genetic level, mutations in the p53 gene have often been identified in actinic keratosis tissue . These mutations are typical changes caused by UVB light, mainly point mutations (CC to TT; C to T) in susceptible areas of the gene. These can inactivate the tumor suppressor p53, which means that it is no longer used as a guardian of cell division and programmed cell death ( apoptosis ) and the modified cells have a selection advantage over healthy cells. In the further course of the disease, a single changed cell can develop into an entire monoclonal field derived from it (field cancerization). Mutations in p53 have also been identified in more than 90% of squamous cell carcinomas that can result from actinic keratosis.

Prognosis and prophylaxis

There is the possibility of spontaneous regression of actinic keratosis, for which rates of 18–63% are given after 7–17 months (weighted 15%), with 15–53% of the regressed skin changes being present again after one year. However, actinic keratosis usually persists for years. The overall risk of developing squamous cell carcinoma from actinic keratosis appears to be around ten percent per patient and ten years on average. A risk of 20% is given for patients with more than 20 lesions. Squamous cell carcinoma develops from actinic keratosis on average within 24 months. It cannot be determined in advance which lesion will change; this can happen even with Olsen grade I lesions. It is estimated that about 60% of squamous cell carcinomas result from actinic keratoses. Actinic keratoses, even those of mild severity, should therefore be detected and treated at an early stage in order to prevent the development of pale skin cancer. With appropriate clothing or the use of highly effective UVB / UVA sun filters, actinic keratosis and possibly a subsequent skin cancer can be prevented.

treatment

Due to the high risk of developing pale skin cancer, actinic keratosis as an early skin tumor disease should be taken seriously and treated efficiently as early as possible. Treatment should be done by an experienced dermatologist. Various options are available here. Small keratoses can be removed surgically (under local anesthesia), with a laser or superficially with liquid nitrogen ( cryosurgery ). Photodynamic therapy (PDT) is often used for large-area treatments . Here, the skin areas are first pretreated with a finished medicinal product based on 5-aminolevulinic acid or its methyl ester (MAOP) and then irradiated with cold red light after an exposure time. In contrast to the (cryo) surgical removal of actinic keratosis, PDT does not leave any scars. If necessary, it can be repeated after a few months. Other large-area procedures are creams or ointments with imiquimod , 5-fluorouracil (5-FU), diclofenac or ingenol mebutate . In a Dutch comparative study with 624 patients, each with five or more individual skin defects on an area of ​​25-100 square centimeters, a cream with five percent of the active ingredient 5 was found out of four investigated therapies (5-FU, imiquimod, PDT, ingenol mebutate) -Fluoruracil (5-FU) as the best and cheapest method.

Differential diagnosis

Foci on the trunk can occasionally be confused with other precancerous stages (e.g. Bowen's disease ) or with a certain type of skin cancer, the basalioma . There is also a risk of confusion with the rare discoid lupus erythematosus . In addition, squamous cell carcinoma, which can result from actinic keratosis, can look similar. During the transition from actinic keratosis (e.g. due to persistent damage by light) to such a squamous cell carcinoma, the clinical picture of actinic keratosis changes only slightly, since it hardly seems to grow. Histologically, on the other hand, the transition to squamous cell carcinoma is clearly recognizable by the basement membrane of the skin, which is broken by malignant epithelial cells, and an ingrowth into the dermis that carries the blood vessels .

Veterinary medicine

Actinic keratosis in a domestic cat

Actinic keratoses also occasionally occur in animals, such as domestic dogs and house cats . This mainly affects parts of the body with little pigmentation and white and light hair, such as the outside of the auricle . It manifests itself in skin thickening and plaques with thick, clinging scales . Therapy is with acitretin , mild cases can also be treated with a combination of β-carotene and glucocorticoids .

See also

literature

Guidelines

Others

  • Peter Fritsch: Dermatology and Venereology. 2nd Edition. Springer-Verlag, 2004, ISBN 3-540-00332-0 .
  • Thomas B. Fitzpatrick, Klaus Wolff (ed.): Atlas and synopsis of clinical dermatology: common and threatening diseases. 3. Edition. McGraw-Hill, New York / Frankfurt am Main 1998, ISBN 0-07-709988-5 .
  • RG Glogau: The risk of progression to invasive disease . In: J Am Acad Dermatol . 42, No. 1, Pt. 2, 2000, pp. 23-24. PMID 10607353 .
  • Chiara Noli and Fabia Scarampella: Actinic Keratosis. In: Practical Dermatology in Dogs and Cats. 2nd Edition. Schlütersche, Hannover 2005, ISBN 3-87706-713-1 , p. 317.
  • Dr. med. Dirk Hasselmann: Actinic Keratosis. In: Light Skin Cancer - And How To Put It In The Shade. 2nd edition 2018 . ISBN 978-3-7407-4964-4

Web links

Commons : Actinic keratosis  - Collection of images, videos and audio files

Individual evidence

  1. ↑ a b C. Holmes, P. Foley, M. Freeman, A. h. Chong: Solar keratosis: epidemiology, pathogenesis, presentation and treatment. In: Australasian Journal of Dermatology . 2007 May; 48 (2): pp. 67-74. PMID 17535191
  2. ^ GJ Goodman, R. Marks, TS Selwood, MW Ponsford, W. Pakes: Non-melanotic skin cancer and solar keratoses in Victoria. clinical studies II. In: Australasian Journal of Dermatology . December 25, 1984 (3): pp. 103-106, PMID 6534368 .
  3. ↑ Recognition as an occupational disease - 3rd ordinance amending the occupational diseases ordinance - Federal Ministry of Labor and Social Affairs (accessed March 10, 2015)
  4. ↑ a b c I. Schaefer, M. Augustin, C. Spehr, M. Reusch, T. Kornek: Prevalence and risk factors of actinic keratoses in Germany - analysis of multisource data. J Eur Acad Dermacol Venereol. 2013 Jan 24.
  5. ↑ a b S. C. Flohil, RJ van der Leest, EA Dowlatshahi, A. Hofman, E. de Vries, T. Nijsten: Prevalence of actinic keratosis and its risk factors in the general population: the Rotterdam Study. J Invest Dermacol. 2013 Aug; 133 (8): pp. 1971-1978.
  6. ↑ Stockfleth et al. (12/2011): Field cancerization is more likely than single isolated lesions. In: "Guidelines for the management of actinic keratosis". http://www.ensas.ee/docs/management_of_actinic_keratoses.pdf . (Accessed 08/2013)
  7. ↑ a b c V. Ratushny, MD Gober, R. Hick, TW Ridky, JT Seykora: From keratinocyte to cancer: the pathogenesis and modeling of cutaneous squamous cell carcinoma. In: Journal of Investigative Dermatology . 2012; 122 (2): pp. 464-472. PMID 22293185
  8. ^ A b A. Ziegler, AS Jonason, DJ Leffell, JA Simon, HW Sharma, J. Kimmelman, L. Remington, T. Jacks, DE Brash: Sunburn and p53 in the onset of skin cancer. In: Nature . 1994 Volume 372 (6508): pp. 773-776. PMID 7997263
  9. ^ DE Brash, A. Ziegler, AS Jonason, JA Simon, S. Kunala, DJ Leffell: Sunlight and sunburn in human skin cancer: p53, apoptosis, and tumor promotion. In: J Investig Dermacol Symp Proc. April 1996; 1 (2): pp. 136-142. PMID 9627707
  10. ↑ BJ Braakhuis, RH Brakenhoff, CR Leemans: Gene expression profiling in head and neck squamous cell carcinoma. Curr Opin Otolaryngol Head Neck Surg. April 2010; 18 (2): pp. 67-71. PMID 20084003
  11. ↑ BJM Braakhuis, MP Tabor, JA Kummer, CR Leemans, RH Brakenhoff: A genetic explanation of Slaughter's concept of field cancerization: Evidence and clinical implications. In: Cancer Res . 2003; 63: pp. 1727-1730.
  12. ↑ RN Werner, A. Sammain, R. Erdmann, V. Hartmann, E. Stockfleth, A. Nast: The Natural History of Actinic keratosis: A Systematic Review. In: Br J Dermatol . September 2013, pp. 502-518, PMID 23647091
  13. ↑ E. Stockfleth: Actinic keratosis. 2009. Cancer Treat. Res. 146; Pp. 227-239.
  14. ^ A. Fuchs, E. Marmur: The kinetics of skin cancer: progression of actinic keratosis to squamous cell carcinoma. In: Dermatologic Surgery . September 2007; 33 (9): pp. 1099-1101. PMID 1776060
  15. ↑ Jansen MHE et al .: Randomized Trial of Four Treatment Approaches for Actinic Keratosis. N Engl J Med. 2019 Mar 7; 380 (10): 935-946. doi: 10.1056 / NEJMoa1811850
  16. ↑ Actinic Keratosis - Ointment Beats Laser