Keratoacanthoma

Introduction to keratoacanthoma Keratoacanthoma (keratoacanthoma), also known as sebaceous soft palate or pseudocancer soft palate, is a proliferative lesion of the keratinized epithelium of the follicle. More common in men, middle-aged and older people are better. The clinical manifestation is that the horny plug of the center of the lesion is bulged to form a solid papule or nodule. Keratoacanthoma grows more rapidly, but it resolves on its own. After the scar, the scar should be treated early. The disease was first reported by Sirjonathanhutchinson in 1889 as "crateriformulceroftheface". Single keratoacanthoma was identified as an independent disease after 1950 and was clinically and histologically separated from its similar squamous cell carcinoma. basic knowledge The proportion of sickness: 0.003%-0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: lupus erythematosus leukemia leprosy kidney transplantation burn

The cause of keratoacanthoma

(1) Causes of the disease

Genetic factors (15%)

Genetics is a phenomenon in which the traits of the parents are expressed in the next generation, and the genetic material is passed from the previous generation to the offspring. The development of keratoacanthoma is also related to genetic factors.

Long-term sun damage (25%)

Since the disease begins in the exposed area, its incidence is consistent with an increase in ultraviolet radiation, and it is considered that the keratoacanthoma is secondary to long-term sun damage.

Chemical pathogenic substances (25%)

Chemical pathogenic substances such as tar, bitumen, and grass leaf fat may also be associated with the development of keratoacanthoma.

Virus infection (25%)

HPV type 25 was found in some lesions, so there is also a claim that keratoacanthoma is associated with viral infection.

(two) pathogenesis

The pathogenesis of this disease is still unclear. Many people have the same report on the expression of P53 tumor protein in immunohistochemical study and the same report in the literature. It is considered that keratoacanthoma is a degenerative squamous cell carcinoma. Inflammatory cell infiltration in the keratoacanthoma is mostly similar to the inflammatory infiltrating cells of squamous cell carcinoma, and CD4+ T lymphocytes activated by interleukin 2 and adhesion molecules, suggesting that they have the same association.

The pathological manifestations are:

Early

It can be seen that the epidermis sag is crater-like, which is full of horny, hyperplasia of the epidermis, and the epidermis protrudes irregularly into the dermis. These epidermal processes are unclearly demarcated from the surrounding interstitial and contain atypical cells and many mitotic phases in the dermis. Inflammatory cell infiltration can be seen inside.

2. Developmental stage

Large and irregular epidermal depressions can be seen in the central part of the lesion, which are filled with horny skin. The epidermis on both sides stretch like lip-like or arch-like walls on both sides of the depression. The epidermis of the basal part is irregularly hyperplasia, and a certain degree of atypical Sexual, but lighter than earlier lesions.

3. Regression period

The epidermal hyperplasia stopped, the crater-like epidermis depression gradually flattened, the keratin disappeared, and most of the cells in the basal part were keratinized.

Keratoacanthoma prevention

Avoid long-term exposure to sunlight in the life, do not touch chemical pathogenic substances such as tar, asphalt, grass leaf fat, etc., to prevent viral infection. Early detection, early diagnosis, early treatment.

Antagonistic acanthoma Complications lupus erythematosus leukemia leprosy kidney transplantation burn

It has been reported to be associated with lupus erythematosus, leukemia, leprosy, kidney transplantation, photochemotherapy, burns and radiation therapy.

Symptoms of keratoacanthoma common symptoms pruritus nodules papular sclerosis scaly epithelial horn suppository valgus periosteal reaction crescentic osteolytic defect

Can be divided into 4 types, that is, single, multiple, rash and marginal eccentric keratoacanthoma.

1. Single keratoacanthoma (solitary keratoacanthoma)

Skin lesions grow rapidly, from 1mm rash or pimples to 25mm in 3-8 weeks, hemispherical, dome-shaped, skin-colored nodules, smooth crater surface visible on the surface of the nodules The skin lesions are smooth and bright and the surrounding boundary is clear. The surface is visible with capillary vessels. Atypical keratoacanthoma is common, some are similar to seborrheic keratosis or benign acanthoma, others are nodular proliferative appearance, crater The sag, giant keratoacanthoma refers to a diameter greater than 2cm, often invading the nose and eyelids. The keratoacanthoma is rare, has tenderness, is destructive crater-like center, often causes end phalanx damage, and the underarm damage is often unnatural. Regression, and early bone damage caused by it, characterized by crescent-shaped osteolytic defects under radiation, without sclerosis or periosteal reaction, single keratoacanthoma occurs in the exposed area, such as the middle The back of the hand and the arm, other such as the buttocks, thighs, penis, ears and head can also be affected, the female hand has less back damage, the calf damage is common, the oral mucosa is rare, more common in middle-aged and older, male is less common The disease Interesting characteristics are about 2 to 6 weeks of rapid growth, followed by 2 to 6 weeks of stability, and finally disappeared after 2 to 6 weeks, leaving a slight depressed scar, but some damage takes 6 months It will not be fully regressed until one year, and it is estimated that about 5% of the damage can recur.

2. Multiple keratoacanthoma (multiple keratoacanthoma)

This keratinized acanthosis is often called Ferguson Smith type multiple self-healing keratoacanthoma. It is clinically and histologically the same as isolated lesions, and the number of lesions varies from 3 to 10, limited to In a certain part, the disease occurs in the face, the trunk and the genitals, and is more common in young men.

Another type of familial generalized keratoacanthoma has been reported, called Ferguson smith type of self-healing squamous epithelioma. This type differs in that it is intensely itchy and lasts for many years. It is easily misdiagnosed as nodular pruritus.

3. Eruptive keratoacanthomas (eruptive keratoacanthomas)

This type of keratoacanthoma is characterized by a generalized dome-shaped skin color papular rash, 2 to 7 mm in diameter, and a large number of rashes, but the palmar sputum is not tired, the oral mucosa can be involved, and some are characterized by intense itching. It can be seen that the bilateral valgus valgus and the narrow mouth are small, and some damages, especially the shoulder and the arm, are linearly arranged. This type has higher incidence of immunosuppression than other types of keratoacanthoma. Lupus erythematosus, leukemia, leprosy, kidney transplantation, photochemotherapy, burns and radiation therapy, the summer condition deteriorated, again indicating that ultraviolet rays are related to the onset of the disease.

4. Edge eccentric acanthoma (keratoacanthoma sentrifugum marginatum)

This type is not common. It was first reported by Miedzinski and Kozakewicz in 1962. It is characterized by the progressive expansion of the lesion to the surrounding area, while the central cure, leaving atrophy, the lesion diameter is 5 ~ 30cm, usually involving the back of the hand and the anterior region, this type and huge The difference in isolated keratoacanthoma is that this type has no self-healing tendency.

Examination of keratoacanthoma

Laboratory inspection:

Detection of tumor cell blood group antigen: keratinized acanthoma cell membrane blood group antigen positive, which is helpful for the differentiation of squamous cell carcinoma.

Other auxiliary inspections:

Histopathology: The structure of the disease is as important as the characteristics of the cells. Therefore, it is best to remove the entire lesion, at least from the center of the lesion including its side, preferably on both sides. The histological changes at the bottom of the lesion are important for distinguishing squamous cell carcinoma.

The tissue images of various types of keratoacanthoma are basically the same. Early damage to the epidermis is like a crater, which is full of horny matter, the epidermis of the bottom is hyperplasia, and the epidermis protrudes irregularly to the dermis. These epidermal processes are indistinguishable in many places and the surrounding interstitial, and atypical cells, fibrils and horns are visible in the epidermis. There is considerable infiltration in the dermis. When the lesion is further developed, the epidermis is enlarged like a crater, which is filled with keratin. The epidermis on both sides are arched, and the epidermis at the bottom can proliferate upward and downward. Some atypical cells are still visible in the hyperplastic epidermis. However, the damage was lighter in the early days, the angle beads increased, and the center was mostly completely keratinized. The bottom of the tumor is clearly defined.

Diagnosis and differentiation of keratoacanthoma

According to the characteristics of clinical manifestations of skin lesions, histopathological features can be diagnosed.

The early stage of the disease is similar to squamous cell carcinoma in both clinical manifestations and pathological changes. It is difficult to distinguish between the two, but the disease develops faster than squamous cell carcinoma, usually without ulceration, and can be self-healing. These can be used as clinical identification. The typical keratoacanthoma cell membrane contains a free peanut agglutinin binding site, which can be stained by peanut agglutinin. Although the squamous cell membrane also contains the same binding site, it can not be agglutinated by peanuts because it is covered by sialic acid. Immunostaining, this grouping method is helpful for differential diagnosis. In addition, blood group antigens can be found in keratoacanthoma cells, but not in squamous cell carcinoma nests, or only in patchy form. Reference value.

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