Actinic keratosis is an occupational disease, which is mainly induced by sunlight, ultraviolet rays, radioactive heat, asphalt or coal, and its extracts. The lesions are more common in sun-exposed parts of middle-aged men and older, such as the face, auricles, and back of hands. Mainly manifested as a rough surface with visible keratinizing scales. Peel off the scales, you can see that the underlying base surface is ruddy, bumpy, and papillary. Treatment generally takes external medicine and surgical treatment. 20% can develop secondary squamous cell carcinoma.
What is keratinization
The process of keratin formation in the stratum corneum is called keratinization, which is the process of transforming cellular proteins into keratin with completely different physical and chemical properties. The keratinization process includes fibrillary degeneration of cytoplasm and decomposition and disappearance of cytoplasm and nucleus. Actinic keratosis (actinic keratosis) is a disease mainly caused by hyperkeratosis of the epidermis caused by long-term sunlight or ionizing radiation stimulation, also known as solar keratosis or senile keratosis. It is the most common type of epithelial precancerous skin lesions. It is more common in middle-aged men and more exposed parts. The main clinical manifestations are brown-red or yellow flat papules or plaques. A few can transform into squamous cell carcinoma, but metastasis is extremely rare. Single patients can be treated with local medication or physical therapy. Early surgical resection is recommended when the malignant transformation is suspected.
What are Actinic Keratoses?
Actinic keratoses, (Greek: aktis = ray; keratosis = cornification of the skin), also called sun damage, are usually small, often rough to the touch corned spots of the skin. The color varies from skin to brown. These skin abnormalities arise on parts of the body exposed to (sun) light, such as the face and the backs of the hand. Actinic keratoses are mainly seen in old age, but partly due to the changed leisure activities, due to sun holidays and tanning beds, actinic keratoses are increasingly observed at a younger age. People who have lived in the tropics for a long time, people with a light skin type, and people who have taken immunosuppressant drugs for a long time are more at risk of getting actinic keratoses. It can occur, with increasing age, it can reach up to 80% in people with light skin type (blond hair and blue eyes) between the ages of 60 and 69 years. Actinic keratoses can be regarded as a chronic effect of (too much) ultraviolet radiation and they must be seen as possible precursors of skin cancer.
Actinic keratosis pathology outlines
Histopathology can be divided into 3 types: hypertrophic atrophic carcinoid in situ. Hypertrophic type: hyperkeratosis of the middle epidermis is obvious, and hypokeratosis can be seen. There is a disorder of spine cell arrangement between spine hypertrophy and atrophy, and vacuolar degeneration. Mitosis is more common but atypical with abnormal cells. Atrophic epidermis: atypical cells and dyskeratosis cells with loose spinous processes can be seen in the basal layer. Carcinoma-in-situ type: thickening of the epidermis, disordered arrangement of epidermal cells and atypical cells, and a clear boundary between epidermis and dermis. The superficial layer of the Type III dermis has obvious elastic degeneration, with medium density infiltration dominated by lymphocytes.
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How do actinic keratoses develop?
Sunlight or artificial light has both positive and negative sides for humans. The production of vitamin D in the skin can be mentioned as a good property. Many people also experience sunbathing as pleasant. The negative sides can be divided into direct effects and long-term effects. A direct effect is, for example, the sunburn reaction. The long-term effects of ultraviolet rays include premature aging of the skin. The skin becomes dry, with wrinkles, pale yellow to brown in color and leathery to the touch. The skin becomes blotchy and bruises easily. Actinic keratoses, therefore, develop after prolonged exposure of the skin to sunlight and/or tanning beds, usually with increasing age, and are therefore also called solar (sol = sun) keratoses. The development of these actinic keratoses depends on the skin type and the total amount of ultraviolet radiation that a person has received on the skin in the course of life. The whiter the skin, the more chance one has of developing this skin lesion.
What are the symptoms of keratoses?
Preferred places are the backs of the hands, the forearms, the face, and the bare scalp. In the beginning, the skin abnormality can be felt (as a rough spot) rather than seen. Sometimes they are slightly painful to the touch. The size can vary from a few millimeters to a few centimeters. Over the years, skin cancer can develop in these spots. Often multiple spots are present and the skin shows other signs of prolonged exposure to sunlight, such as blotchy discoloration, wrinkles, and thinning of the skin.
Actinic keratosis clinical presentation
01. Diseases in susceptible and prevalent parts are more common in sun-exposed parts of middle-aged men and older, such as face, auricles, back of hands, etc. In male patients, skin lesions can occur on the bald area, auricle and lower lip, while females are more common on the extended side of the forearm.
02. The clinical symptom damage is limited to brown-red or yellow spots or plaques, with clear borders, from the needle tip to more than 2cm in diameter, most of which are several millimeters indefinite. It can be slightly higher than the leather surface, but there is no obvious raised edge. The surface is rough with keratinizing scales visible. Forcibly peeling off the scales, you can see that the underlying base surface is ruddy, bumpy, and papillary. Sometimes the skin lesions can be horn-like protrusions, forming a skin corner lesion that develops slowly and has no symptoms. There may be telangiectasia around the skin lesions.
Complications: 20% can develop secondary squamous cell carcinoma. When the lesions are combined with inflammation, erosion, and ulcers, it is a sign of secondary squamous cell carcinoma.
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Auxiliary examination of Actinic Keratosis
According to the pathological morphology of the disease, it can be divided into the following types:
- Hyperkeratosis with occasional incomplete keratosis. The granular layer thickened or disappeared focally. The spinous layer is thick, all the spinous cells are arranged in disorder, some cells are pleomorphic, and their nuclei are anaplastic. There are some dyskeratosis cells in the middle of the epidermis. The nuclei of basal cells are often tightly packed. There are still atypical basal cell populations that branch irregularly to the upper dermis. The epidermal ridge extends downward irregularly. The thickened collagen fibers and expanded capillaries of the dermal papilla are perpendicular to the skin surface.
- In addition to the above changes, the lichen type also sees liquefaction and degeneration of basal cells and infiltration of subcutaneous inflammatory cells. Gel-like bodies can also be seen in the upper dermis.
- Atrophic epidermal atrophy, mild hyperkeratosis, atypical cells mainly in the basal layer, with large nuclei, deep staining, and densely arranged. Sometimes atypical cells may proliferate into the dermis in a band or tube shape or surround the hair follicle and the upper part of the sweat duct, like a tube cuff, but it is clearly separated from the normal epithelium.
- The type of carcinoma in situ is similar to epidermal carcinoma in situ but does not invade terminal hair follicles and sweat gland ducts.
- The pigmented epidermis has a significant increase in pigment, especially in the basal layer. Melanin can be found in atypical cells, or only in melanocytes and their dendrites. There are a lot of melanocytes in the upper dermis.
- The spinous process decomposing type is located immediately above the atypical cells in the basal layer of the epidermis, and there are fissures or cavities, and there are a few spinous process decomposing cells. There are different degrees of atypical cells above the fissure, but there are fewer cells than the basal layer. Anaplastic cells often expand to the upper dermis in a bud-like or tubular shape toward the basal layer. The loosening of spinous processes can be seen in the basal layer of hair follicles and sweat ducts in the upper dermis.
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Diagnosis and treatment of actinic keratoses
Usually, the diagnosis can be made with the naked eye. If the abnormality is agitated, for example, because there is redness, non-healing wounds, or excessive cornification on the spot, a further examination can be done by taking a small skin sample ( biopsy ) in order to be able to make the diagnosis with more certainty.
What is the treatment for actinic keratoses?
Treatment of actinic keratoses is necessary because over time, especially with longer existing or changing abnormalities, there is a markedly increased risk of local skin cancer. Actinic keratoses can be treated in several ways by
- freezing with liquid nitrogen
- First, scrape away the spots with a sharp spoon and then burn away (electro-coagulation)
- Removal by chemical peel
- However, sometimes it is necessary to cut out the deviation. This is usually done on an outpatient basis under local anesthesia
- A cream, containing a substance that destroys restless tissue (5-fluorouracil), can also be used, especially when it comes to large areas of skin. This cream should be used until the skin is superficially damaged (about 3 weeks). Thereafter, the skin heals without scarring and the actinic keratoses often stay away for a long time
- Applying a vitamin A-like substance ( tretinoin ) in a cream to the skin. This cream works slowly and must be applied daily for a long time and is often only effective for starting abnormalities
- A new form of treatment, especially for extensive abnormalities, is treated with laser (CO2)
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Early treatment for actinic keratoses
Actinic keratosis may transform into skin cancer, so it should be treated early.
1. For the systemic treatment of multiple lesions, B-cis retinoic acid or etretinate aromatic retinoic acid can be taken orally, 0.5～1.0mg/(kg·d)
2. Local medication
- (1) External application of aminobenzoic acid preparations: 5ml of aminobenzoic acid, 60ml of ethanol, and 10ml of glycerin, add water to 100ml to make the preparation of aminobenzoic acid, once a day.
- (2) Anti-tumor drugs: For generalized patients or use anti-tumor drugs such as 20% podophyllum, 5% fluorouracil or 10% fluorouracil propanediol, etc., but after treatment, regular follow-up should be followed to observe whether there is recurrence. It has also been reported that after applying 1% fluorouracil solution for external application, and then applying 5% Triyansone Cream, it can significantly reduce side effects such as pain and inflammation. Or adding a small amount of steroid solution to 1% fluorouracil can have the same effect.
- (3) Apply 10.5% retinoic acid ointment, or use it in combination with 5% fluorouracil ointment, which is effective for intractable skin lesions.
3. Chinese medicine treatment
- (1) Crystal paste rubbing: The so-called crystal paste is to grind 15g of ore lime into fine powder and soak it with concentrated alkaline water (about 100m1). The alkaline water is 2 fingers higher than the lime surface. Take 50 glutinous rice and sprinkle on the ash. Soak for 1 day and night, take out the rice and mash it into a paste. Once every 2 days in winter. Apply crystal ointment to the skin lesions, do not damage the normal skin, it can be cured after removing the scabs.
- (2) Decolorization or black plucking stick therapy: warm and soften plaster and apply it to the skin lesion. After 3 to 5 days, remove the plucking paste and scrape off the softened keratin with a dull knife. If it does not heal, use it again until the skin lesion disappears. You can also use 5-fluorouracil ointment to rub externally after the skin lesions have become thinner for better curative effect.
4. Physical therapy: Carbon dioxide laser method, electrocautery method, liquid nitrogen freezing method can quickly remove skin lesions with few adverse reactions.
5. Surgical resection The skin lesions suspected of being cancerous or cancerous can be surgically removed. 6. X-ray irradiation treatment.
What can your doctor do?
Your doctor will first want to rule out that it is not a malignant skin lesion. If it is actinic keratosis, it can ‘freeze’ the lesions with the help of liquid nitrogen.
The dermatologist or skin doctor often applies photodynamic therapy. A special cream is applied to the actinic keratosis that makes the cells sensitive to light. After a few hours, a special lamp is used to shine on the actinic keratosis. That destroys the injuries. This treatment can be painful. You can also suffer from it the day after. Shortly after the treatment it may seem as if the skin condition has gotten worse, but that is getting better.
What can you do yourself with actinic keratoses?
It is important to prevent further damage to the skin by ultraviolet radiation as much as possible. This can be done by spending less time in the sun and by limiting the use of the tanning bed. You can discuss guidelines on this with the attending physician. The use of anti-sunscreen products with a high protection factor (factor 15 or higher), but especially wearing protective clothing and headgear is of great importance. It should be remembered that an anti-sunscreen is not intended to be in the sun longer; it is intended to protect the skin during the time you are in the sun. Always have new spots checked. In patients with many actinic keratoses, supervision by the doctor remains necessary.
What are the prospects?
Over the years, as mentioned, skin cancer can develop in the actinic keratoses. The forms of skin cancer that can develop are spinocellular carcinoma and less often, basal cell carcinoma. The chance of this occurring is estimated at 0.25% to 20%. Fortunately, these forms of skin cancer are usually not very aggressive, can be treated well and the chance of metastasis to other organs is small.