| Actinic keratosis | |
|---|---|
| Classification and external resources | |
Actinic keratosis on the lip |
|
| ICD-10 | L57.0 |
| ICD-9 | 702.0 |
| DiseasesDB | 29438 |
| MeSH | D055623 |
Actinic keratosis (also called "solar keratosis"[1] and "senile keratosis"[1]) is a premalignant condition[2] of thick, scaly, or crusty patches of skin.[3]:719[4] It is more common in fair-skinned people. It is associated with those who are frequently exposed to the sun,[5] as it is usually accompanied by solar damage. Since some of these pre-cancers progress to squamous cell carcinoma,[4] they should be treated. Untreated lesions have up to twenty percent risk of progression to squamous cell carcinoma[6].
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 between 2 and 6 millimeters in size, and can be dark or light, tan, pink, red, a combination of all these, or have the same pigment as the surrounding skin. It may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, backs of hands, forearms, or lips.
Contents |
Actinic keratoses may be divided into the following types:[1]
See also:
Actinic keratosis is very common, affecting half of the global population. It is seen more often in fair-skinned individuals, and prevalence can vary with geographical location and age. People who take immunosuppressive drugs, such as organ transplant patients, are 250 times more likely to develop actinic keratoses which may lead to skin cancer[7].
Preventive measures recommended for AK are similar to those for skin cancer:
According to an article in the Journal of Investigative Dermatology (2005) 125, 93–97; doi:10.1111/j.0022-202X.2005.23733.x, entitled "Human Papillomavirus-DNA Loads in Actinic Keratoses Exceed those in Non-Melanoma Skin Cancers", actinic keratosis can contain a significant amount of infectious human papillomavirus. Verbatim: "HPV presents in significantly higher viral loads in actinic keratosis (AK), which are the precursor lesions of squamous cell carcinoma (SCC), than in SCC. Viral loads of 1 HPV-DNA copy per less than 50 cells were measured in 40% of AK. The higher viral loads in AK are likely to reflect enhanced HPV-DNA replication. This may be because of intense keratinocyte proliferation and differentiation in AK favoring amplification of commensalic HPV. Active HPV replication and presumably enhanced gene expression may in turn stimulate keratinocyte proliferation and contribute to carcinogenesis in these early stages of NMSC development. HPV-E6 proteins were recently shown to inhibit UV-induced apoptosis by abrogation of Bak in response to UV damage (Jackson and Storey, 2000) and to bind a protein required for repair of single strand DNA breaks (Iftner et al, 2002). Thereby, accumulation of UV-induced mutations and oncogenic transformation might be facilitated in cases of active HPV infection."
Doctors can usually identify AK by doing a thorough examination; in principle AK is a clinical diagnosis. 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.
Actinic keratosis usually shows focal parakeratosis with associated loss of the granular layer, and thickening of the epidermis. The normal ordered maturation of the keratinocytes is disordered to varying degrees, there may be widening of the intracellular spaces, and they may also have some cytologic atypia, such as abnormally large nuclei. The underlying dermis often shows severe actinic elastosis and a mild chronic inflammatory infiltrate[6].
Various modalities are employed in the treatment of actinic keratosis:
Regular follow-up after the treatment is advised by many doctors. The regular checks are to make sure no new bumps have developed and that old ones haven't become thicker.
In 2007, Australia biopharmaceutical company Clinuvel Pharmaceuticals Limited began clinical trials with a melanocyte-stimulating hormone called afamelanotide (SCENESSE®)[11] (formerly CUV1647)[12] for mitigation of photodynamic therapy side effects in organ transplant patients.[13][14]
Another Australian biopharmaceutical company, Peplin,[15] is also developing a topical treatment for actinic keratosis. Formed in 1998 they are currently developing Ingenol Mebutate, which is the first in a new class of compounds and which is derived from Euphorbia peplus, or E. peplus, a rapidly growing, readily-available plant, commonly referred to as petty spurge or radium weed. The sap of E. peplus has a long history of traditional use for a variety of conditions, including the topical self-treatment of various skin disorders, such as skin cancer and pre-cancerous skin lesions. The company has recently redomiciled to the USA and is about to enter phase III trials with Ingenol Mebutate.
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||