Retention hyperkeratosis caused. Skin and venereal diseases (136 pages)
In animals, as in humans, there are many skin diseases determined by hereditary factors and hereditary predisposition. Such diseases include genodermatoses, scleroderma, atopic dermatitis, etc.
Genodermatoses.
Genodermatoses are hereditary skin diseases that combine many nosological forms, manifested by various pathological processes. In humans, the most common ichthyosis (vulgar, X-linked, ichthyosiform erythroderma), keratoderma, epidermolysis bullosa (O. L. Ivanov, 2002). In dogs and other animals from the group of genodermatoses, ichthyosis (ordinary, lamellar, X-linked) is more often recorded -chromosome, ichthyosiform bullous erythroderma), nasodigital hyperkeratosis, familial canine dermatomyositis, genetic pigmentation disorders (vitiligo, lentigo, etc.), epidermolysis bullosa (Emmanuel Bonsignore).
Ichthyoses– hereditary diseases characterized by a diffuse disorder of keratinization such as hyperkeratosis and manifested by the formation of scales on the skin. There are ichthyosis vulgaris, recessive X-linked ichthyosis, lamolar ichthyosis, and epidermolytic ichthyosis.
Ichthyosis vulgaris is characterized by diffuse damage to the skin of the trunk and limbs, functional failure of endocrine organs and an immunodeficiency state.
The type of inheritance is recessive-dominant.
Symptoms. The skin is dry. Rough to the touch. Retention hyperkeratosis is identified, caused by a defect in the synthesis of keratogealin, a lack of filaggrin synthesis.
Various dog breeds are susceptible to ichthyosis, especially terriers (Yorkshire, Jack Russell, bull terrier, Westie).
The severity of skin changes varies. Skin changes are most pronounced on the extensor surfaces of the limbs, paw pads, and tip of the nose. Skin lesions are diffuse or local in nature. An accumulation of desquamated scales and then hard crusts are noted. The paw pads are often affected. As a result, movement becomes difficult. Skin lesions have an unpleasant rancid odor. The animal loses its natural appearance and becomes ugly.
Diagnosis is made by clinical signs.
In skin biopsy material, histological examination reveals orthokeratotic hyperkeratosis.
Treatment . Ineffective. The use of special shampoos and synthetic retinoids (tigazon, neotigazon, etc.) is indicated, approximately 0.5-1.0 mg/kg per day for 2-3 months. and more.
Nasodigital hyperkeratosis – characterized by significant thickening of the nose or paw pads. This disease is a type of ichthyosis vulgaris.
With nasodigital hyperkeratosis, the paw pads become very keratinized, movement is difficult, and lameness appears. Mostly dogs of the Irish Terrier and Dogue de Bordeaux breeds are affected at an early age.
Diagnosis is made by clinical signs. To clarify the diagnosis, histological examination of biopsy material from the affected areas is possible.
Treatment . Aimed at softening compacted areas using water procedures or the use of gels. Sometimes they resort to surgical intervention.
Ichthyosis recessive X-linked – a disease caused by a gene mutation accompanied by the absence of the enzyme steroid sulfatase in epidermal cells and leukocytes. The disease is characteristic only of the male sex.
Pathogenesis. Deficiency of the enzyme steroid sulfatase leads to the accumulation of cholesterol sulfate in the blood serum and stratum corneum, increasing cell cohesion and slowing down the process of normal desquamation of the epidermis. Cholesterol sulfate inhibits hydroxymethylglutamyl coenzyme A reductase, a key enzyme in epidermal steroid synthesis.
Symptoms. In humans, the disease is characterized by damage to the skin in the first months of life or from birth. The scales on the skin are large and dark. Hyperkeratosis is especially pronounced in the area of the extensor surfaces of the elbow and knee joints. Histologically, retention hyperkeratosis is detected. X-linked ichthyosis is also characterized by cataracts, cryptorchidism and small testicles are possible. Severe cholesterolemia is detected in the blood serum. Apparently X-linked ichthyosis develops in animals in the same way.
Ichthyosis lamellar – caused by a lack of synthesis of transglutaminase 1. The disease manifests itself at birth and develops throughout life.
"Familial" canine dermatomyositis – inflammation of the skin and muscles is more common in young Collie and Sheltie breeds. Against the background of hereditary predisposition, provoking etiological factors are viruses, injuries, ultraviolet radiation, etc.
Patients experience skin depigmentation, skin rashes, and signs of seborrhea. Muscle damage manifests itself in a tense gait, stiffness of movement, and myopathy.
The disease is differentiated from lupus erythematosus, demodicosis, dermatophytosis, and epidermolysis bullosa. Histological examination reveals vacuolization of the basal cells of the epidermis and multifocal muscle necrosis.
For treatment, etiotropic therapy, the use of glucocorticoids and other agents are indicated.
Epidermolysis bullosa .
Epidermolysis bullosa refers to hereditary dermatoses, subdivided into epidermolysis bullosa simplex, epidermolysis bullosa
bullous confluent, epidermolysis dystrophies stratified basal. The disease occurs in poodles and German pointers.
Skin lesions appear in the form of erosions, ulcerations and scabs located on the inner surface of the ears and other areas of the skin. The diagnosis is confirmed by the results of histological studies of skin biopsy material. Vacuolization is detected at the level of the basement membrane and dermoepidermal separations.
Treatment Not effective.
Genetic pigmentation disorders include anomalies: white fur, blue or heterochromic iris, albinism, vitiligo, depigmentation, etc.
Prevention of genodermatoses consists of limiting or preventing the mating of animals with such a congenital anomaly.
Albinism– a congenital disease characterized by the absence of pigment in the skin, hair, and iris of the eyes. The disease belongs to the group of genodermatoses.
The pathogenetic essence of the disease is the blocking of an enzyme that is necessary for normal melanin synthesis. Under these conditions, melanocytes are present in the skin, hair, and eye membranes in normal quantities, but there is no melanin in them, so they do not have their normal color.
Hair, skin without pigmentation, eye color blue (Blue Doberman syndrome). There are no other characteristic signs for this disease.
The term "phakomatoses" comes from the Greek word "pha-kon" - nevus.
Phakomatoses- diseases characterized by combined nevoid tumors, hamartomas of several organs (skin, nervous system, etc.). These are monogenic defects. The effect of the gene is manifested even in intrauterine development, when differentiation is disrupted at the embryonic stage. This action usually continues postnatally. All phakomatoses are characterized by a progressive course.
Inheritance is predominantly autosomal dominant.
Skin symptoms do not determine the severity of the disease, but are of great diagnostic value.
Tuberous sclerosis (Pringle-Bourneville disease, epiloya)
Inheritance is autosomal dominant, both sexes are affected, expressivity is highly variable, and incomplete penetrance is possible. Population frequency is 1:30,000. Classic triad: skin lesions, epilepsy and mental retardation. The course is progressive, but slow.
Skin lesions:
1) facial pseudoadenomas (hamartomas with angiomatous proliferation, the presence of vascular, connective tissue elements, pilosebaceous structures);
2) achromatic leaf-shaped spots;
3) periungual fibromas;
4) connective tissue nevi in the form of shagreen plaques. Facial pseudoadenomas usually appear at 4-8 years of age or a little later, do not fester and do not disappear, unlike acne vulgaris, they are clearly demarcated and more dense.
In adults, they can form something like rhinophyma. Clinically: closely grouped, symmetrical numerous hemispherical nodules of a reddish color with a yellowish or brown tint. Localization: nose, adjacent cheeks, nasolabial and chin folds.
Achromatic leaf-shaped spots - the earliest symptom (maybe from birth) - clearly visible in a Wood's lamp. They often have irregular jagged outlines. Number - 4-6, described up to 22 - on the back, lower back, buttocks, sometimes chest, limbs. Diameter - several centimeters.
Periungual fibromas appear with age and not for everyone. They are growing hamartomas, consisting of collagen fibers and vessels, usually multiple.
Connective tissue nevi appear due to the proliferation of fibrous tissue - on the skin of the forehead, eyelids, lower back, etc. They protrude slightly, yellowish in color with a rough surface. The diameter can be quite large (up to 10-15 cm).
Neurofibromatosis (Recklinghausen's disease)
Population frequency 1:3000. It is usually not transmitted beyond 2-3 generations.
There are 2 forms: peripheral and central (tumor-like symptoms of central nervous system damage) neurofibromatosis. From birth there are “coffee spots”, and neurofibromas, bone changes, and diencephalic disorders are formed later.
"Coffee stains"- small lentigines-like spots and soft neurofibromas. Typical localization is axillary folds, perineum. Then they appear larger spots(up to 2-3 cm), there may be diffuse pigmentation (for example, on the back). Rashes practically do not occur on the extremities (usually on the torso, neck). In adults, new spots do not appear; in old age, some of them may disappear.
In the second decade and later, skin tumors and tumors of the nerve trunks appear (any location is possible).
Treatment is symptomatic. Avoid stimulants and physical therapy.
Angiomatous phakomatoses
Sgerdge-Weber-Krabbe syndrome: unilateral vascular nevus on the face from birth, damage to the vessels of the eyes and intracranial on the affected side.
Klipiel's syndrome-Trenaunay: unilateral telangiectatic nevus, varicose veins on one limb.
Pigmentation disorders
Albinism
A disease in which melanin is absent or produced in insufficient quantities in the skin, hair, sclera, and retina. The number of melanocytes remains normal.
The main reason is tyrosinase deficiency.
Total albinism. X-linked and autosomal recessive inheritance is possible. The frequency of occurrence in the population is 1:10,000. The skin is dry, pink, sweating is reduced, hypothyroidism is possible. The eyes are red, the hair is colorless. Characterized by decreased visual acuity, refraction, photophobia, and blepharocononctivitis. Due to increased sensitivity to UV rays, solar dermatitis develops, leading to superficial skin atrophy, telangiectasia, and later to keratosis. Possible degeneration into cancer. Possible combination with deaf-muteness, mental retardation, epilepsy, polydactyly, etc.
Subtotal albinism. The frequency of occurrence is 1:20,000 (among Indians - 1:10,000). Inheritance is autosomal recessive, rarely autosomal dominant. It is based on impaired differentiation of melanoblasts.
Partial albinism. There is no pigment in certain areas of the skin. In the midline of the forehead - autosomal dominant inheritance with incomplete penetrance, frequency of occurrence - 1:20,000.1:25,000. At the back of the head - autosomal recessive. There are no other defects. There may be isolated ocular albinism.
Epidermolysis bullosa
Epidermolysis bullosa is a group of diseases associated with mutations. Different forms of this disease are associated with different gene mutations. Some of these forms are inherited autosomal dominantly, some - autosomal recessively.
Pathogenesis is poorly understood. All forms of epidermolysis bullosa are characterized by disturbances at the level of the basement membrane.
The clinical picture is highly variable . In the vast majority of cases, the disease manifests itself from the first days of life: minimal mechanical effects on the skin lead to the formation of blisters and erosions.
There are simple and dystrophic forms of epidermolysis bullosa. In simple forms, the basement membrane is not damaged and erosions heal without scarring. In dystrophic forms, detachment of the epidermis occurs at the border between the basement membrane and the dermis. Damage to connective tissue leads to the formation of scars.
Treatment is predominantly symptomatic. It is fundamentally important to prevent trauma to the skin and mucous membranes as much as possible: gentle skin care, proper professional guidance, etc.
When erosions occur, external epithelizing agents are used. To improve the condition of the connective tissue of the skin, high doses of vitamin E and cyclic retinoids are indicated. For bacterial complications of the disease, various antimicrobial agents are used. If the child is lagging behind in physical development, general strengthening drugs and anabolic steroids are prescribed. With the development of various scar complications (contractures, etc.), surgical correction is used.
Ichthyoses
Ichthyoses(from Greek ichthy- fish) - a group of diseases characterized by a violation of keratinization. The most common are vulgar, X-linked, lamellar and epidermolytic ichthyoses.
These diseases are based on mutations of genes responsible for ensuring the process of keratinization. Ichthyosis is characterized by retention hyperkeratosis, caused by delayed exfoliation of horny scales. The inheritance of ichthyoses is different: autosomal dominant, autosomal recessive or X-linked.
The most common is ichthyosis vulgaris. The first manifestations of the disease are usually detected at the age of 3-12 months. Men and women get sick with the same frequency. As a rule, the disease is most active during puberty. In adulthood, only dry skin and slight flaking usually persist.
The severity of clinical manifestations varies. Skin lesions with vulgar ichthyosis diffuse, most pronounced on the legs and forearms. Characterized by dry skin, fine-plate peeling, and follicular hyperkeratosis. A constant symptom is hyperlinearity of the skin of the palms and soles. In half of the cases, ichthyosis vulgaris is combined with an atopic disease (usually atopic dermatitis).
X-linked ichthyosis most often affects men (the gene is localized in one of the sex chromosomes). The disease manifests itself in the first months of life. Tight, large dark brown scales appear on the child’s skin. Large horny layers often form. Typical localization is the skin of the scalp, neck, torso, buttocks, and extensor surface of the limbs. The skin of the palms, soles, and face is not affected. Unlike vulgar ichthyosis, there is no improvement in the course of the disease with age.
Lamellar ichthyosis (an autosomal recessive type of inheritance) manifests itself at birth. The skin of a newborn is in a state of erythroderma and is covered with a yellowish-brownish film resembling collodion. The eyelids and lips are turned out (these symptoms persist throughout life). After a few days, peeling develops, and in some children (rarely) the skin may even clear completely. In most cases, the disease persists throughout life. In adulthood, hyperkeratosis usually intensifies and manifestations of erythroderma become less noticeable. Lamellar ichthyosis is often combined with dementia.
Epvdermolytic ichthyosis (Broca's bullous congenital erythroderma). The appearance of flabby blisters against the background of the bright red skin of the newborn is characteristic. Nikolsky's symptom positive. The bubbles quickly open with the formation of erosions. Often the condition is aggravated by the addition of a secondary bacterial infection. At the age of 3-5 years, the severity of hyperkeratosis increases, and the number of blisters decreases. Typical localization of rashes is the neck, large folds, the back of the hands and feet. The scales are dark in color, linear in shape, tightly attached to the skin.
Treatment of ichthyosis depends on the type of disease and the severity of its course. For congenital ichthyosis, no later than the 10th day of life, systemic glucocorticosteroids are prescribed in a dose of 1.5 to 3.5 mg/kg body weight per day (prednisolone). The duration of the course is at least 1 month, then a gradual reduction in the dose of the drug is necessary.
For all clinical forms of ichthyosis, systemic retinoids are effective. However, these drugs have a number of side effects. Therefore, their use in mild forms of ichthyosis is not justified. In such cases, external use of this group of drugs is possible.
In addition to topical retinoids, fattening and emollient agents are prescribed externally. Salt, soda, butter-milk and starch baths are indicated. For all forms of ichthyosis, sanatorium treatment is recommended (a humid and warm climate has a beneficial effect) and sea bathing.
Skin changes are most pronounced on the extensor surfaces of the extremities, especially in the area of the elbows and knees, while the neck and flexor surfaces of the elbow and knee joints, as well as the axillary fossae, are not affected. Follicular keratosis is also characteristic in the form of small dryish nodules localized at the mouths of disseminated hair follicles. The skin of the face in childhood is usually not affected; in adults, peeling of the skin of the forehead and cheeks is observed. On the palms and soles there is a network-like skin pattern with changes in dermatoglyphics and slight mealy peeling.
Depending on the type and degree of formation of scales, several clinical variants of vulgar ichthyosis are distinguished: xeroderma - an abortive variant of ichthyosis, the most easily occurring, characterized by dryness, slight roughness of the skin, mainly extensor surfaces, limbs. The skin is easily irritated, especially when washed with soap and water, and is prone to eczematization; simple ichthyosis, in which the lesion covers the entire skin.
- The scales are small, their central part is tightly attached to the base;
- Ichthyosis brilliantis is distinguished by the transparency and tenderness of the scales, located in the form of a mosaic, mainly on the limbs;
- white ichthyosis - white, asbestos-like scales, giving the impression of floured skin;
- Ichthyosis serpentine - the scales are large grayish-brown, reminiscent of a snake's cover.
Currently, all of them are regarded as vulgar ichthyosis of varying severity. Histologically, retention hyperkeratosis is revealed, caused by a defect in the synthesis of keratohyalin. The proliferative activity of the epidermis is not impaired. The process of cell rejection is disrupted, which may be due to the cementing effect of glycosaminoglycans.
The nail plates become dry, brittle, rough, deformed, and the hair may become thinner and thinner. Clinical manifestations of ichthyosis weaken during puberty. The disease lasts a lifetime, worsening in winter. There is functional insufficiency of the endocrine system (thyroid, gonads) in combination with an immunodeficiency state, a pronounced tendency to allergic diseases with low resistance to pyococcal and viral infections. Conjunctivitis, retinitis, pharyngitis with subatrophic lesions of the nasopharynx, otitis media, rhinosinusitis, chronic mesotympanitis are common.
Treatment by a cosmetologist-dermatologist in Moscow
The cosmetologist-dermatologist at our clinic "EVROMED S" in Moscow uses the latest methods of treating dermatological pathologies.
Drug treatment- new generation drugs that specifically target the source of the problem. Correctly contribute to the rapid resolution of pathological skin processes, relieve pain, itching, restore metabolic processes, and strengthen the immune system.
Hardware therapy— effective hardware technologies help to quickly and permanently get rid of aesthetic problems. Mesotherapy, laser treatment, cryotherapy are just a few techniques that are successfully used in the Moscow clinic.
Radio wave surgery— to remove tumors we use the safest technology of non-contact tissue excision. It guarantees rapid healing of the skin, absence of scars and scars, and reduces the risk of papillomas appearing in the same place.
The key to the success of any treatment is an individual approach to each patient. Dermatologist in Maryino draws up a therapy program in accordance with the characteristics of the patient’s skin and the history of his past diseases. Thus, maximum treatment efficiency and long-term effect of aesthetic procedures are achieved.
You can obtain more detailed information about treatment and its cost by phone or during a personal consultation with a cosmetologist-dermatologist.
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| № | Service name | Price |
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| 1. | Dermatologist consultation with examination | 1000 rub. |
| 2. | Secondary appointment with a dermatologist | 800 rub. |
| 3. | Molluscum contagiosum removal | 500 rub. |
| 4. | Removal of moles, papillomas, on the body (radio wave method) from 0.5 to 1 cm | 500 rub. |
| 5. | Intravenous ultraviolet irradiation of blood ("Matrix-ILBI") | 1200 rub. |
| 6. | Removal of moles, removal of papillomas, in the face, neck, décolleté (radio wave method) from 0.5 to 1 cm | 1500 rub. |
| 7. | Removal of moles, papillomas, warts in the face, neck, décolleté (radio wave method) over 1 cm | 1300 rub. |
| 8. | Removal of kandil 1 unit (radio wave method) | 1000 rub. |
| 9. | Wart removal | 1000 rub. |
| 10. | Course of treatment for psoriasis: skin, scalp, palmoplantar form (without the cost of medications) | 2000- rub. |
| 11. | Course of treatment of onychomycosis (fungal infections) (without the cost of medications) | 3000 rub. |
| 12. | Course of treatment for microsporia of the scalp and smooth skin (without the cost of medications) | 2000 rub. |
| 13. | Treatment course for lichen versicolor (without the cost of medications) | 2000 rub. |
| 14. | Removal of formations on the sole, on the palm | 1000-1500 rub. |
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Dyskeratosis is a process of keratinization of certain areas of the skin, with its thickening, roughening and related symptoms. The essence of the problem is discussed in this article.
What is dyskeratosis of the skin?
Dyskeratosis means a disorder of the process of keratinization (keratinization) in certain areas of the epidermal layer of the skin, which is externally expressed in abnormal thickening and coarsening. This is a sign of diseases with similar names - keratoses,.
When the skin functions normally, the formation of new horny plates occurs as dead, old ones are peeled off. If this cycle is broken, the following events occur:
- pathologically active formation of horny substance begins in the cells, which includes fatty acids and a special substance keratohyalin;
- old cells stop dying in time, forming thick layers on the surface of the epidermis.
As a result of dyskeratosis (or hyperkeratosis), the cells enlarge, acquire a rounded shape and are separated from other cells of the epidermis. In this case, tonofibrils - thin protein fibers that retain the shape of epithelial cells, break away from desmosomes - special structures that firmly connect cells to each other, and tightly surround the nucleus.
More often, such processes are observed on the scalp, face, elbows, buttocks, feet, side and back surfaces of the arms, and thighs.
The most severe psychological trauma is caused by abnormal keratinization of the epidermis on the face and head due to the inability to hide the pathology that disfigures the appearance.
Classification
Dyskeratosis is divided into benign and malignant forms, characteristic of,.
According to the mechanism of development, pathology is divided into two types:
- proliferative, which is characterized by abnormally active production of keratin;
- retention hyperkeratosis, caused by a delay in the desquamation of keratinized skin plates.
Among the types of dyskeratosis, there are acquired ones, which developed during the patient’s life due to internal disorders and diseases, and hereditary ones, which are caused by changes at the gene level.
In addition, according to clinical signs, course and causes, hyperkeratoses are divided into:
- diffuse (spreading over large areas of skin);
- follicular (occurs only in areas where there are hair follicles);
- warty;
- keratoderma (general name for dermatoses, which are characterized by disruption of keratinization processes).
How to identify it in yourself
In order to associate unpleasant and painful manifestations on the skin with the development of dyskeratosis, one should understand what the general signs are for different types of the disease and the specific ones characteristic of a particular type of pathology.
Basic symptoms:
- , strongly ;
- the volume of secretions from the sweat glands decreases;
- areas are formed covered with keratinized plates, forming layers of different thicknesses - from 2 – 3 to 30 mm;
- keratinization of hair follicles is observed if hyperkeratosis of the scalp is diagnosed;
- nodules and skin bumps of different sizes are formed;
- appear, often deep, painful, on the feet, elbows, palms and even on the head;
- the process is accompanied by bleeding, ulcers, (damage), and can cover a large area, spreading to the entire body;
- limited lesions may look like warts or calluses on the soles.
Specific manifestations of dyskeratosis in various diseases:
| Type of keratosis | Specific signs |
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| Follicular |
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| Lichen pilaris as a type of keratosis pilaris |
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| Hereditary types of keratosis pilaris, including Kirle and Darier-White disease |
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| Lenticular (hereditary form) |
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| Disseminated (hereditary) |
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| Hyperkeratosis of the feet |
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| Subungual (often of fungal origin -) |
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| Seborrheic |
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| Actinic |
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| Porokeratosis of Mibelli |
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| Senile | The appearance on different parts of the body (usually on open ones) of dry or greasy flat plaques of a yellow-brown color with uneven outlines, 1–3 cm in size, similar to warts. The disease can last a very long time and cause no discomfort other than occasional mild itching. Sometimes inflammation and bleeding of plaques begins to develop, followed by tissue damage (erosion). This sign indicates the probable transition of the pathology to a malignant form. It degenerates into cancer in rare cases. |
What disorders may this symptom indicate?
Dyskeratosis is not a disease, but a clear symptom of unfavorable factors acting from the outside (exogenous) and provoking this condition or certain internal (endogenous) pathologies that usually occur in a chronic form, that is, for a long time.
Exogenous causes
- Prolonged intense pressure on the feet when wearing tight shoes. This occurs due to the fact that excessive compression of tissues, like external aggression, activates protective mechanisms in the form of abnormally rapid cell division against the background of disruption of the process of exfoliation of dead cells.
- Obesity, in which excess weight increases the load on the feet many times over.
- Diseases of the joints (lower limbs), curvature of the bones of the feet, lameness, flat feet, overload of the ankle joint. These diseases and conditions disrupt the correct distribution of load on the feet, resulting in areas where excessive pressure occurs and, as a result, hyperkeratosis in certain areas.
- Long-term treatment with glucocorticosteroids. Hormonal drugs accelerate the process of cell renewal, which provokes the development of keratosis.
- Frequent and prolonged sun exposure. Ultraviolet radiation excessively dries out the skin, causing various pathological changes in the epidermis.
- Frequent contact with aggressive chemical environments (occupational keratosis).
Endogenous (internal) causes
Abnormal thickening of the stratum corneum of the skin with a disorder of the process of keratinization and exfoliation is observed in the following diseases:
- Diabetes mellitus. Disruption of metabolic processes causes dulling of skin sensitivity, disruption of the blood supply to the epidermis, and increased dryness of the skin. These unfavorable factors are the basis for the development of dyskeratosis.
- Genetic disorders of keratin production.
- Diseases that cause abnormal changes in the structure and functions of the epidermis, which include: molluscum contagiosum, .
- Erythroderma is a skin disease with widespread redness and peeling.
- Fungal skin diseases.
- Sexual infections (syphilis, gonorrhea).
- Disorders of the endocrine system.
- Neurological disorders. Depression and strong feelings lead to the loss of huge amounts of vitamin B, and its deficiency causes dry skin.
- , provoking para-oncological keratosis of the palms and soles.
- Deficiency of vitamins C, A, E and group B, responsible for skin health.
- Intestinal pathologies, liver and gallbladder diseases.
- Puberty and aging. These are conditions in which a sharp disturbance of the hormonal status in the body occurs.
- In adolescents, active hormone production provokes the production of keratin.
- In older people, on the contrary, a decrease in hormones in the body inhibits the processes of natural renewal and exfoliation of dead cells (senile dyskeratosis).
How to deal with this symptom
Basic principles
Basic principles of combating dyskeratosis:
- Accurate diagnosis and identification of the cause (external or internal) causing the disease.
- Elimination of all unfavorable factors contributing to the appearance or development of manifestations of hyperkeratosis.
- Treatment of symptoms and a specific type of dyskeratosis with special medications.
Treatment or correction of internal pathology, which is the main cause of the disease, can completely eliminate or significantly reduce the intensity of the manifestations of hyperkeratosis. Therefore, consultations with a dermatologist (dermatocosmetologist), endocrinologist, therapist (sometimes oncologist) are mandatory.
- Using medicated moisturizing creams.
- Vitamins of group B, necessarily A, E and C - in the form of tablets and as part of ointments - externally to correct the processes of exfoliation of dead cells and the synthesis of new ones (strictly as prescribed, negative manifestations are possible).
Some corrective measures
Treatment of dyskeratosis is always comprehensive, involving the use of internal and external medications, vitamins, and physiotherapy.
For example, in the follicular form, it is aimed at improving the functioning of internal organs and normalizing the hormonal state of the body. Prescribe softening, moisturizing ointments and external preparations with lactic and fruit acids that can gently exfoliate the stratum corneum.
Mechanical methods of skin cleansing (scrubs, peelings, use of pumice) are prohibited, which injure the top layer of skin, which often leads to the introduction of infectious agents, worsening of all symptoms and the development of pyoderma (pustular lesions). Manifestations of follicular dyskeratosis (not associated with genetic changes) often significantly decrease or completely disappear with age, which is associated with a decrease in sebum secretion and the rate of division of dermal cells.
Keratolytic ointments and creams are prescribed to soften and dissolve the keratinized layer of cells (only with the permission of a specialist):
- , giving results in palmoplantar punctate keratosis, congenital ichthyosis, unspecified types of thickening of the epidermis;
- (seborrheic dermatitis, acquired ichthyosis, keratoses) and Diprosalik;
- Tretinoin.
Important! When prescribing external Tretinoin, it should be borne in mind that it is absolutely contraindicated during pregnancy (an irreversible vascular network occurs). This applies to many retinoid medicated ointments.
- For scalp hyperkeratosis, Vaseline, glycerin, castor oil, and products with lactic acid are used.
- In severe cases of scalp hyperkeratosis, lenticular and disseminated forms of the disease, a specialist may prescribe glucocorticosteroids (hormonal agents) and aromatic retinoids.
- Foot hyperkeratosis is treated by a podiatrist or cosmetologist. If the cause of the disease is incorrect shoes, choose one in which the load on the foot will be evenly distributed over the entire area of the foot.
- In case of orthopedic disorders, they must be corrected by an otropedist. You should check the likelihood of fungal infection of the skin of the feet and the functioning of the endocrine system.
- Cracks in the feet are treated with Syntomycin ointment, moisturizing and greasy ointments with retinol solution. It is allowed to use foot baths with salt, with caution - pumice and mechanical grinding.
- With the development of hereditary types of pathology, cryo- and laser therapy procedures, electrocautery of individual lesions, and intralesional administration of hormones are often performed. Prescribe 5-fluorocil ointment 5% and fluorouracil, Etritinate.
- For actinic hyperkeratosis, the use of protective creams against solar radiation is mandatory.
It is important to remember that the use of effective means to reduce the external manifestations of the disease will not help cure it completely until the main cause of dyskeratosis is eliminated.
This video will talk about the treatment of dyskeratosis and hyperkeratosis of the skin with both drugs and folk remedies:
