Actinic keratoses

Actinic keratoses are caused by chronic UV damage that has occurred over the course of a lifetime. The main cause is therefore UV rays, in particular sunlight. UV rays are rich in energy and, if they penetrate into the skin, can set unwanted chemical reactions into motion and thus result in changes in the composition of the DNA of the cells. This cell damage is normally corrected by the repair mechanisms of the body's own immune system.

Over the course of the years or decades, however, precisely these repair mechanisms can also be negatively affected by UV rays so that individual damaged skin cells continue to divide unhindered and result in a thickening of the horny layer.

Other factors

• Fair skin type: With fair-skinned persons who easily get sunburned, natural sun protection is only present to a limited extent. They have an increased risk to develop actinic keratoses compared to people with darker skin.
• Too much sun: People who were exposed to the sun over a long period of time in their jobs or in their leisure time (e.g. farmers, sailors, roofers, bricklayers, marathon runners) are frequently affected. Over the last few years, the number of patients with actinic keratoses has been increasing rapidly, as leisure activities have changed considerably over the course of the decades (e.g. extensive sunbathing on holiday).
• Old age: The development of actinic keratoses is very slow over several decades. Consequently, it predominantly affects people aged 50 or older.
• Weak immune system: Patients whose immune system is weakened due to illness (e.g. HIV infections) or due to the intake of drugs (e.g. cortisone) have an increased risk of developing actinic keratoses. Patients whose immune system has been artificially suppressed after organ transplants are at particular risk.