Actinic keratosis is a widespread (especially among the elderly) disease with a slow, steadily progressive course, the occurrence of which is provoked by exposure to direct sunlight on the skin. The primary element is an oval peeling spot localized in open areas of the skin, which quickly transforms into a keratoacanthoma – a benign neoplasm located in the epidermis and upper layers of the dermis. The patients’ well-being is not disturbed. Both self-resolution of the process and rebirth into cancer are possible. Diagnosis is based on biopsy data. Treatment is hardware–cosmetic or radical-surgical.
L57.0 Actinic (photochemical) keratosis
The disease, known as actinic keratosis, statistically occurs in every fourth person over 45 years old and accounts for about 14% of all visits to a dermatologist. In clinical dermatology, it is also called “solar keratosis” or “senile acanthoma”. Despite the obvious cause of the disease – prolonged hyperinsolation – the disease is out of season. Actinic keratosis has a cumulative component: for ten years, being exposed to constant exposure to sunlight, the skin asymptomatically “accumulates” their negative influence. And only with age, against the background of weakening immunity, the first symptoms of the disease appear. At the same time, a person may not sunbathe, have no contact with the sun for a long period of time – the primary elements will still appear on the exposed areas of the skin.
Sometimes the root cause of rashes is taking antibiotics, which increases skin sensitization, wearing tight clothes, causing friction in some areas of the dermis, hormonal restructuring of the body. By their nature, the primary elements of actinic keratosis are nothing more than a thickening of the stratum corneum of the epidermis. The possibility of their degeneration into malignant forms of skin cancer determines the relevance of acquaintance with this disease.
There is one reason that causes actinic keratosis – it is prolonged hyperinsolation, constant ultraviolet irradiation with a certain wavelength of the solar spectrum (from 280 to 320 nm). But there are many factors involved in the occurrence and development of the disease. First of all, the climate. People living high in the mountains, in the equatorial, subequatorial, tropical zone, where there are almost 365 sunny days a year, and the temperature in summer reaches >35 ° C, have the highest incidence index of actinic keratosis. The risk of pathology is aggravated by working outdoors.
The second important factor is age. The very term “senile acanthoma” indicates that it is a disease of the elderly. Everyone over 50 is at risk. The third risk factor is the light color of the skin, hair and eyes. Blondes with a minimum number of pigment cells, acting in this case as a kind of protection against hyperinsolation, are sick three times more often than owners of dark skin, black hair and brown eyes. A kind of “predictor” of the appearance of actinic keratosis in old age are freckles in young people. Not the least role in the occurrence of the disease belongs to sunburn, which repeatedly “prepare” the skin for the onset of the disease; heredity, stress and severe somatic ailments, forcing patients to take hormones, immunosuppressants, chemotherapy.
Actinic keratosis has not manifested itself in any way for decades. The skin all this time does not change its structure under the influence of ultraviolet light, it accumulates the negative influence of the sun in its layers. This is called the latent, latent period of the disease. With age, against the background of weakening immunity, the surface layer of the skin begins to gradually change. Some of the cells of the epidermis become undifferentiated, a focus of preinvasive cancer is formed from them, which does not grow through the base of the epithelium, but “crawls” along the basal layer.
In the process of this spread, atypical cells replace the normal epithelium, the epidermis loses its protective function, and keratinization processes accelerate in it. Over time, the “x” hour comes, when atypical cells violate the integrity of the basement membrane, penetrate into the dermis, where they create a new focus of an already malignant tumor. Up to the moment of violation of the integrity of the basal layer of the epidermis, the disease can suddenly self-resolve.
Actinic keratosis is classified exclusively by pathomorphological changes in the layers of the skin. According to the localization of the active process in the epidermis and dermis, it is customary to distinguish typical variants of the disease:
- Hypertrophic actinic keratosis, when atypical large-nuclear cells appear in the epidermis, producing light and dark keratin. It is the alternation of keratin layers that is a diagnostic sign of actinic keratosis.
- Pigmented actinic keratosis is called the accumulation of a large number of melanin cells, staining the localization site in a dark brown color in the basal layer of the epidermis.
- Lichenoid actinic keratosis is characterized by active processes at the border of the basal layer of the epidermis and the upper layers of the dermis, where lymphocytic infiltrates from dermal cells form on the “pitted” keratosis basal layer of the epidermis.
- Proliferative actinic keratosis occurs against the background of elastosis (colloidal dystrophy of the deep layers of the dermis), is associated with the germination of epidermal cells into the skin and the formation of foci of hyperkeratosis.
- Atrophic actinic keratosis is localized in the upper layers of the dermis, thinning and destroying them locally, by forming specific “lacunae” and cracks.
- A distinctive feature of acantholytic actinic keratosis is elastosis with the formation of epithelial-connective tissue foci in the depth of the dermis over already existing “lacunae” and “cracks”. These local tumor-like formations grow to the surface of the skin.
- Bowenoid (bovenoid) variant of actinic keratosis is the initial stage of cancer, characterized by the accumulation of dysplastic atypical cells both in the epidermis and in the upper layers of the dermis. Atypical cells are in a so-called “dynamic equilibrium”: how many atypical cells appear, as many of them die.
According to non-standard primary manifestations, atypical forms of actinic keratosis are distinguished:
- Bullous actinic keratosis, which is based on infiltration of the dermis by neutrophils with the formation of mini-abscesses in the papillary layer.
- Pagetoid actinic keratosis, when atypical pagetoid (pre-melanoma) cells appear in the upper layer of the epidermis.
The disease begins unexpectedly, with the asymptomatic appearance of flaky, slightly infiltrated reddish spots of small size, up to 1 cm in diameter, with clear boundaries in open areas of the skin. Most often, the skin of the back of the nose is involved in the process, where telangiectasia can be seen against the background of the spot. This is an erythematous form of the disease. If the process is localized on the forehead and upper eyelid, the primary element is a plaque with thick horny scales (skin horn), this is a hypertrophic, or horny variant of the disease. The diameter of such plaques is up to 4 cm, when they are removed, mini-bleeding and soreness appear, and sometimes an erosive surface or an island of atrophy is exposed.
Manifestations depend on the form of actinic keratosis, the connection of the primary element with the epidermis, dermis. In the pagetoid form of the disease, the rash resembles a seborrheic wart due to its shape and brown color. This is how the pigmented, or papillomatous form of the disease manifests itself. Actinic keratosis is often localized on the lower lip, where cracks and erosions occur – this is actinic cheilitis. The neck, shoulders, hands, forearms, auricles, cheeks, and the scalp also suffer from the appearance of a rash. Sometimes rashes are localized on the back and upper third of the abdomen – depending on the exposed parts of the body that are most often exposed to sunburn.
The rash that appears may spontaneously disappear in one place, but immediately pour out in another, or it may regress completely. It depends on the patient’s immunity and on the amount of “negative” solar energy accumulated in the skin. If the disease progresses, it is very slow. Actinic keratosis requires constant attention, because in a few years its malignancy is possible: an inflammatory rim appears around the plaques, soreness and itching.
Actinic keratosis is diagnosed based on clinical signs and histological examination. The differential diagnosis is confirmed only by biopsy. It is necessary to distinguish actinic keratosis from the manifestations of:
- benign lichen;
- senile lentigo;
- lupus erythematosus;
- verrucose nevus;
- red lichen planus;
- dermatophytosis of the trunk;
- Bowen’s diseases;
- squamous cell and basal cell skin cancer;
- malignant melanoma;
- radiation dermatitis.
The method of treatment for each patient with actinic keratosis is selected individually by a dermatologist based on a complete clinical and laboratory examination. In benign senile keratosis, hardware methods of removing formations are used. The most atraumatic, painless and effective is laser coagulation, the most popular and affordable is the cryodestruction method. With a hint of rebirth, a consultation with a dermatooncologist and surgical intervention is indicated.
It is difficult to prevent the appearance of actinic keratosis. We are all children of the sun. We are biologically dependent on it, we like to sunbathe, walk, travel, do outdoor sports. However, in order not to get problematic skin with a tendency to local cancer degeneration by the age of 40, it is necessary to know the measure in communicating with the Luminary: to sunbathe at the proper hours for this (from 10 am to 14 pm); use creams to protect the skin from ultraviolet radiation, including, if necessary, in winter; wear comfortable sunscreen clothes and be very critical of artificial tan all year round. At the first signs of the growth of a mole or any other “plaque”, an urgent consultation with a dermatologist is needed, since it is almost impossible to predict the further development of the disease.