Fortunately, pathology of the optic nerve, the conductor of electrochemical signals from the retina to the visual cortex of the brain, is relatively rare in ophthalmological practice; According to medical and statistical data, the share of such pathology in the total flow of eye diseases does not exceed 1-1.5%. However, every fifth (according to other sources, every fourth) of such cases ends in irreversible blindness due to optic nerve atrophy.
Atrophy - “optic neuropathy”, organic degeneration of the neural fibers of the optic nerve due to a pronounced deficiency of its nutrition and blood supply - can be either complete or partial. In the latter case, there is a profound decrease in all visual functions, including disturbances in color perception, narrowing of visual fields, etc.; During ophthalmoscopy, the optic disc extending into the macular region of the retina (the “yellow spot”, most sensitive to light) looks paler than usual.
Causes of optic nerve atrophy
The etiological causes of optic neuropathy can be various chronic or acute eye diseases, pathology of the central nervous system, ophthalmic trauma, general intoxication, severe systemic diseases (endocrine, autoimmune, etc.).
Among the actual ophthalmopathic factors, under the influence of which optic nerve atrophy can begin, glaucoma of various forms is in the lead; pigmentary retinal (retinal) dystrophy; all kinds of blockages of the retinal arteries and drainage veins (for example, occlusion of the central retinal artery); severe myopia; uveitis, retinitis, neuritis, orbital vasculitis and other inflammations. In addition, the optic nerve can be involved and atrophy during the development of oncopathology, in particular, with primary orbital cancer, meningioma or glioma of the optic nerve, neuroma or neurofibroma, osteosarcoma, sarcoidosis.
Diseases of the central nervous system that provoke or “trigger” atrophic processes in the optic nerve include mainly pituitary tumors, chiasms (compressing the optic chiasm), infectious and inflammatory processes of the meninges (encephalitis, meningitis, arachnoiditis) and general brain abscess, demyelinating diseases (eg, multiple sclerosis), traumatic brain injuries and wounds in the maxillofacial area, especially with direct mechanical damage to the optic nerve.
In some cases, systemic atherosclerosis, chronic malnutrition and exhaustion, vitamin deficiencies and anemia, poisoning with toxic substances become the provoking background and pathogenic soil of optic neuropathy (the most striking examples are frequent methyl poisoning when consuming surrogate alcoholic beverages, as well as intoxication with nicotine, insecticides, and drugs ), massive blood loss (for example, with extensive internal hemorrhages), diabetes mellitus and other endocrinopathy, lupus erythematosus, Wegener's granulomatosis and other autoimmune disorders.
Optic nerve atrophy can be a complication and outcome of severe infections, the causative agents of which in various cases are bacteria (syphilis, Koch’s tuberculous mycobacterium), and viruses (measles, rubella, influenza, herpes, even “ordinary” adenoviral ARVI), and parasites (intracellular toxoplasmosis, intestinal ascariasis, etc.).
In some cases, the optic nerve is atrophied already at birth (as a rule, this occurs with severe chromosomal pathology with gross skeletal and cranial deformations, for example, with acro-, micro- and macrocephaly, Crouzon's disease and other genetically determined anomalies of intrauterine development.
Finally, there is a fairly large proportion of cases (up to 20%) when the direct causes of optic nerve atrophy cannot be established.
Classification of optic nerve atrophy
As shown above, optic neuropathy can be either congenital or acquired. In accordance with this, hereditary forms are distinguished, classifying them according to the type of inheritance: autosomal dominant, autosomal recessive, mitochondrial.
Autosomal dominant optic atrophy can be expressed in varying degrees and in some cases is observed in combination with congenital deafness. Autosomal recessive atrophy is part of the structure of a number of chromosomal syndromes (Wolfram, Kenny-Coffey, Jensen, Rosenberg-Chattorian syndromes, etc.).
Mitochondrial atrophy occurs when mitochondrial DNA is mutated (Leber's hereditary optic neuropathy).
Acquired optic neuropathy can also develop for various reasons and in different types. Thus, primary atrophy is based on long-term mechanical compression of the neural optic canal, while the optic disc when examining the fundus may appear intact, undamaged, with normatively clear boundaries.
Secondary atrophy may be a consequence of swelling of the optic nerve head, which, in turn, is one of the consequences of pathology of the retina or the nerve itself. The degeneration and displacement of specialized, functional neural tissue by neuroglial tissue has more pronounced and obvious ophthalmoscopic correlates: the observed optic disc in this case is usually increased in diameter, its boundaries lose clarity. In glaucoma, the axial symptom of which is chronically increased intraocular fluid pressure, developing collapse of the lamina cribrosa of the sclera leads to atrophy of the optic nerve.
The observed tint of the optic disc has significant diagnostic significance. Thus, initial, partial and complete atrophy of the optic nerve looks different during ophthalmoscopy: in the initial stage there is a slight blanching of the disc with the usual coloring of the nerve itself, with partial atrophy the optic nerve disc turns pale in individual segments and, finally, complete atrophy is observed as total and uniform blanching of the optic disc in combination with a narrowing of the blood vessels supplying the fundus of the eye.
There are also ascending and descending forms of atrophy (with ascending, the atrophic process in the nerve is initiated by damage to the retinal tissue, with descending, it begins in the fibers of the optic nerve itself). Depending on the extent of the process, atrophy is divided into unilateral and bilateral; by the nature of development - stationary (stable) and progressive, which can be diagnosed through regular ophthalmological observations over time.
Skin thickening, or hyperkeratosis
Diabetes mellitus
Human papillomavirus (HPV)
Fungus
Menopause
Climax
16720 16 August
IMPORTANT!
The information in this section cannot be used for self-diagnosis and self-treatment.
In case of pain or other exacerbation of the disease, diagnostic tests should be prescribed only by the attending physician. To make a diagnosis and properly prescribe treatment, you should contact your doctor. Thickening of the skin: causes of occurrence, what diseases it occurs with, diagnosis and treatment methods.
Definition
Hyperkeratosis is an abnormal thickening of the top layer of skin (epidermis) as a result of excessive sun exposure, exposure to chemicals, frequent friction or pressure. In addition, hyperkeratosis can occur against the background of certain diseases.
Thickening of the skin occurs in the stratum corneum of the epidermis, which is the end point of the differentiation process of keratinocytes - cells containing the protein keratin. It is in the stratum corneum that keratinocytes lose water and their nucleus and turn into scales of the stratum corneum - corneocytes.
Normally, corneocytes are gradually exfoliated, due to which the skin is renewed.
With hyperkeratosis, accelerated differentiation of keratinocytes occurs, and the physiological exfoliation of horny scales from the skin surface, on the contrary, slows down.
Types of hyperkeratosis
Depending on the origin, acquired and hereditary hyperkeratosis are distinguished.
According to clinical manifestations.
- Calluses are a common type of hyperkeratosis. There are several types of calluses, but they all appear due to thickening of the skin in places most susceptible to mechanical stress. Moreover, such skin changes can be associated both with increased physical activity and with various chronic diseases, which is typical for elderly patients.
- Horny (tilotic) eczema manifests itself as hyperkeratosis of the palms and soles.
- Psoriasis is an autoimmune inflammatory disease in which hyperkeratotic scaly plaques form on the skin.
- Actinic keratosis usually appears as small, reddish, scaly bumps that appear after excessive sun exposure. Actinic keratosis is a serious condition with a high probability of malignancy and requires mandatory consultation with a doctor.
- Seborrheic keratosis is characterized by small brown or black patches, usually located on the face, neck, shoulders and back. This is one of the most common benign skin tumors in adults.
- Follicular hyperkeratosis (“goose bumps”) is characterized by blockage of the mouths of the follicles with keratinized epidermal cells.
- Epidermolytic hyperkeratosis is a rare hereditary disease that appears immediately at birth. Newborns have reddish skin, sometimes covered with small blisters.
Possible causes of skin thickening
Skin hyperkeratosis can occur in people who neglect regular skin care procedures, as a result of which dead cells of the stratum corneum accumulate and form keratomas - benign neoplasms.
Our skin is constantly exposed to adverse external factors, such as chlorinated water and detergents, and UV radiation. As a result, the protective lipid layer of the skin is damaged, and moisture begins to rapidly evaporate from its surface, and corneocytes lose their ability to physiologically exfoliate.
In diabetes mellitus, hyperkeratosis becomes a consequence of metabolic disorders and deterioration of skin microcirculation.
Wearing tight or uncomfortable shoes, especially with flat feet, congenital foot pathologies, and obesity, can cause thickening of the skin on the feet.
The development of cervical hyperkeratosis (leukoplakia) is promoted by the human papillomavirus.
The cause of hyperkeratosis can be chronic fungal infection, as well as herpes zoster.
It is believed that symptoms of thickened and dry skin may be caused by a deficiency of vitamins A, E, D and C.
Hyperkeratosis often results from a lack of the hormone estrogen in women during menopause.
Diseases and conditions in which hyperkeratosis develops
- Diabetes.
- Obesity.
- Flat feet.
- Ichthyosis.
- Psoriasis.
- Eczema.
- Menopause.
- Fungal skin infection.
- Shingles.
- Erythroderma.
- Atopic dermatitis.
- Seborrheic keratosis.
Which doctors to contact for hyperkeratosis
Most often, the first consultation regarding skin thickening is addressed to a dermatologist. After a thorough examination, collecting complaints, finding out the patient’s medical and family history, conducting laboratory and instrumental studies, a consultation with an infectious disease specialist may be required.
Diagnosis and examinations for thickening of the skin
A thorough history taking, taking into account all the patient’s complaints, examination and additional diagnostic methods will help determine the cause of hyperkeratosis.
- Clinical blood test with a detailed leukocyte formula to identify inflammatory processes in the body.
Symptoms of atrophy
One of the main signs of incipient optic nerve atrophy is an uncorrectable decrease in visual acuity and quality: neither glasses nor contact lenses can compensate for the decrease in visual functions caused by the atrophic process in the nerve. Rapidly progressive optic atrophy can result in complete, incurable blindness within months or even days. With partial atrophy, organic degradation and increasing functional failure of the visual organs stop at a certain level and stabilize (the reasons for such stabilization often also remain unclear).
Visual fields are narrowed, as a rule, due to loss of peripheral (“side”) vision – the so-called tunnel vision syndrome. Color vision disorders concern mainly red-green and yellow-blue gradients of the general spectrum. Scotomas may appear, i.e. blind spots in the field of relatively intact vision.
Quite typical for optical neuropathy is the so-called. pupillary defect: weakening of the pupil's reaction to light while maintaining overall consistency of pupillary reactions. The pupillary defect can be unilateral or detected in both eyes simultaneously. Whatever symptoms accompany optic nerve atrophy, they should only be detected during a professional ophthalmoscopic examination and interpreted by a qualified ophthalmologist.
Diagnosis of CHAZN
In addition to visual ophthalmoscopy, any information relating to the premorbid (pre-morbid) period of the patient’s life can acquire decisive diagnostic significance: pharmacological group and dosages of previously taken medications, previous intoxications and common diseases, self-destructive habits (smoking, alcohol abuse, unhealthy lifestyle), experienced TBI (traumatic brain injury), background residual pathology of the central nervous system, etc. Direct examination includes the statement or exclusion of exophthalmos (“bulging”, anterior displacement of the eyeball), study of pupillary and corneal reflexes, mobility of the eyeball, general acuity and visual fields (visimetry , perimetry), diagnostics of color perception.
As stated above, one of the most informative diagnostic criteria is the appearance of the optic disc during ophthalmoscopy of the fundus: color, clarity of boundaries, diameter, uniformity, deformation, excavation (“pitting”) of the optic disc surface, Kestenbaum’s symptom (reduction in the usual number of small capillaries by disk), caliber, shade and linearity/tortuosity of the retinal arteries and veins. You may also need an additional tomographic study in one mode or another (laser scanning, optical coherence tomography), an electrophysiological study to measure sensitivity thresholds and lability of the optic nerve. In case of atrophy caused by glaucoma, it is mandatory to measure and control IOP (intraocular pressure), incl. in daily and load modes.
Volumetric orbital oncopathology is diagnosed using plain radiography. If a detailed study of circulation and hemodynamics in the vascular system is necessary, fluorescein angiography (one of the methods of contrast radiography) and/or Doppler ultrasound is prescribed. For the purpose of clarifying diagnostics, consultants of related specialties are involved, primarily neurologists, oncologists, neurosurgeons, and in the presence of systemic vasculitis - rheumatologists, etc.; Imaging methods for studying the skull and brain (radiography, CT, MRI) are prescribed.
Occlusions of retinal vessels (arteries, veins) require the involvement of a vascular surgeon. If infectious symptoms are present, laboratory tests (ELISA, PCR) are prescribed.
Optic atrophy should be differentiated from peripheral cataracts (clouding of the lens) and amblyopia (“lazy eye syndrome”).
Skin xerosis. Solving the problem externally
Xerosis is caused by impaired sebum and sweating, a deficiency of amino acids contained in the stratum corneum of the skin, and dehydration. Most often, xerosis appears on the skin of the feet due to an initially small number of sebaceous glands, slow turnover of epithelial cells and a pronounced violation of the protective functions of the skin.
The main cause of dryness is a lack of moisture in the stratum corneum of the skin; with a long-term process, peeling, a feeling of tightness, irritation, microcracks and itching appear.
Dryness occurs due to insufficient care, poor circulation, which is facilitated by constitutional features, wearing tight clothes and tights, tight shoes, insufficient moisture intake, and also due to alkalization of the skin with hygiene products and the use of harsh abrasive products. The problem with dryness most often manifests itself in the autumn-winter period due to the fact that with the onset of cold weather, the feet are constantly in contact with warmer and coarser woolen fabrics and synthetics, and this prevents sufficient air penetration; In addition, seasonal vitamin deficiency affects it. At the same time, problems can also arise in the summer, which is associated with prolonged exposure to the sun and walking barefoot. With proper and regular care, an aesthetically pleasing appearance is achieved. The main causes of skin xerosis and options for their correction are presented in Table 1.
The main pathogenetic mechanisms of increased skin dryness are:
1) a decrease in barrier function due to the failure of the lipids of the stratum corneum, a violation of their structure and location, which causes defects in the intercellular lipid layers, which leads to an increase in transepidermal moisture loss;
2) a decrease in the ability to retain moisture due to a lack of hygroscopic substances inside corneocytes, the so-called natural moisturizing factor (NMF), which consists of free amino acids and their derivatives, lactic acid, urea and other components that create the hydrolipid mantle of the skin [5];
3) disruption of moisture transport from the dermis to the epidermis and stratum corneum.
All this leads to dehydration of the epidermis and the development of a clinical picture of xerosis [1–3].
The group of chronic dermatoses, accompanied by dryness, hyperkeratosis and peeling, includes a large number of skin diseases. These include such common diseases as psoriasis, eczema, atopic dermatitis with lichenification, squamous-hyperkeratotic forms of mycoses, and rare nosological forms - ichthyosis, keratoderma, etc. Xerosis is also characteristic of age-related changes or can be caused by concomitant somatic pathologies - diseases thyroid gland, diabetes mellitus (DM), vitamin deficiency, metabolic disorders.
The process of development of dehydration at the cellular level is presented in Figure 1, and the stages of clinical manifestations during the development of skin xerosis with possible correction methods are shown in Figure 2. It should be noted that these phases can be traced for all manifestations of dry skin, both in chronic dermatoses and for somatic diseases.
Xerosis of the skin of the feet in diabetes is one of the provoking factors of diabetic foot syndrome. Statistics show that the appearance of diabetic foot signs is associated with the stage of decompensation in individuals suffering from type 2 diabetes; manifests itself in 90% of patients [4]. This condition occurs due to angio- and neuropathy of the feet, i.e. destruction of nerves and blood vessels, while tissue nutrition deteriorates, their protective function decreases, and this leads to trophic changes and thereby increases the risk of developing gangrene or ulcers even with minimal injuries. Such patients complain of discomfort in the legs, stabbing and burning pain when the legs are at rest, at night, as well as severe pain when walking. Over time, the sensitivity of the feet noticeably decreases, the color of the skin of the lower extremities changes - it becomes pale or with a slight brownish pigmentation, at the same time dryness, peeling of the skin, cracks, microvesicles with serous contents, as well as thickening of the stratum corneum of the skin of the feet appear. All this shows that xerosis of the skin in diabetes, both due to general dehydration and autonomic diabetic neuropathy with impaired innervation and regulation of the sweat glands, is not only a cosmetic problem, but also one of the links in the development of diabetic foot syndrome.
Dry skin to one degree or another occurs in 85% of patients at the appointment. Therefore, practicing doctors encounter such patients every day, sometimes they make up the majority of adult dermatological appointments. Advances in pharmacology, in particular combined anti-inflammatory drugs with exfoliating components, have significantly improved the quality of life of patients, and their availability and variety in pharmacy chains make it possible to make choices and experiment with treatment methods. Over time, new issues have arisen in the treatment of dermatoses accompanied by hyperkeratoses, namely, the duration of use of combined and monosteroids, anti-relapse and preventive therapy, care for hyperkeratotic conditions and peeling, the correction of which is initially difficult due to genetic “breakage” or due to concomitant diseases.
Currently, there is a reassessment of the importance of cosmeceuticals in the therapy and care of the skin of patients with xerosis, chronic dermatoses, and diabetes. There are a number of modern lines of medical cosmetics for skin care for hyperkeratosis, which have proven themselves, are widely available for everyday use and often have a pronounced softening, exfoliating and moisturizing effect. Basic drugs, most often based on topical steroids, have high expectations in terms of their antiproliferative, resolving, antipruritic, anti-inflammatory, antibacterial and healing effects. But such properties, while maintaining a softening, moisturizing and exfoliating effect, are also inherent in classic dermatropic components with metabolic, hydrating and softening effects: urea, various acids, panthenol, complexes of oils, alkaloids and flavonoids.
To successfully combat dry feet, you first need to find out the cause of its occurrence. Diagnosis of dry skin involves excluding fungal infections, various endocrinopathies, skin diseases, and identifying the causes of xerosis. If the cause is any disease, then it is necessary to first cure it or correct the condition, and then deal with the manifestations. In some cases, with a severe inflammatory reaction, the prescription of glucocorticosteroid or combination creams with the parallel use of care products is required. But sometimes the use of moisturizers, which have pronounced effectiveness in treating dryness of various origins, high organoleptic properties, a high safety profile and good tolerability, leads to the desired result. At the same time, it has been clinically proven that anti-inflammatory drugs in combination with emollients are more effective than monotherapy with glucocorticosteroids. Thus, one of the main tasks when the skin barrier function is impaired is protection and hydration. Examples of products that effectively solve these problems are foot balms Balzamed and Balzamed intensive (Esparma GmbH, Germany), which are recommended for daily care of dry and sensitive skin of the feet, prone to redness, irritation, the formation of chafing and calluses, especially in patients with diabetes. .
Balzamed balms provide the skin of the feet with sufficient hydration and nutrition, preventing the formation of chafing and calluses, the appearance of peeling, redness and irritation on the skin of the feet. Balzamed balms contain a balanced composition of vital vitamins, moisturizing components and softening vegetable oils.
Balzamed and Balzamed intensive balms contain the following components:
Vitamin A, which protects against excessive keratinization and increases the skin's resistance to infections, protects it from the formation of microcracks, slows down the aging process, improves its elasticity and general condition.
Vitamin E (tocopherol acetate) is an antioxidant, binds free radicals, protects skin cells from metabolic damage caused by metabolic disorders, as well as from external environmental influences, helps reduce skin itching.
Vitamin F increases skin elasticity, regulates moisture content, and promotes rapid healing of microcracks.
Provitamin B5 (panthenol) accelerates the healing of small wounds, maintains water balance and skin resistance to external environmental influences, stimulates the regeneration of skin and mucous membranes, normalizes cellular metabolism, accelerates mitosis and increases the strength of collagen fibers, has a regenerating and anti-inflammatory effect.
Lactic acid promotes exfoliation and hydration, faster cell renewal.
Urea increases the absorption of water by keratinized areas of the skin, actively moisturizes dry skin and increases its permeability to vitamins, and also protects against external environmental influences; easily penetrates into the deep layers of the epidermis and serves as a conductor for other active components; has keratolytic, wound healing and bacteriostatic effects.
Avocado and jojoba oils contain vitamins A, B, D, E and K, soften, moisturize and nourish the skin, have a protective effect, restore skin elasticity, and prevent premature aging.
Zinc stearate, which is part of Balzamed intensive, stabilizes the skin of the feet and promotes healing.
Thus, the components included in the balms Balzamed and Balzamed intensive have a pronounced anti-inflammatory, antipruritic, exfoliating and antimicrobial effect, help restore damaged skin, increase the regenerative and barrier functions of the skin, prevent the feeling of dryness and irritation, relieve itching, promote hydration and restoration of affected areas of the epidermis. These drugs can be used both in complex therapy with anti-inflammatory glucocorticosteroid drugs, and independently, as a means of daily skin care.
In order to achieve maximum positive results, it is recommended to apply the foot balm daily to the damp skin of the feet, especially to areas subject to pressure and friction, rubbing in with light massaging movements.
Regular care of the skin of the feet using Balzamed will prevent the appearance of peeling, redness and irritation on the feet, the formation of corns and calluses, give elasticity and firmness to the skin, and prevent premature aging.
Skin xerosis is, as a rule, cyclical in nature with periods of deterioration, especially in the autumn-winter period, and therefore foot balms Balzamed and Balzamed intensive are the main links in both therapeutic and preventive care for the skin of the feet and allow you to completely cope with the problem of dry skin , including with such serious concomitant diseases as diabetes.
Treatment of partial optic atrophy
The principle of etiopathogenetic medicine requires the identification and maximum possible elimination of the causes of the disease; Since optic neuropathy is much more often a consequence and manifestation of other diseases than an autonomous and isolated pathology, the therapeutic strategy should begin with the treatment of the underlying disease.
In particular, for patients with intracranial (intracranial) oncological pathology, hypertension, established cerebral aneurysms, it is recommended, first of all, to undergo neurosurgical intervention in the appropriate direction.
Conservative treatment for optic nerve atrophy is focused on stabilizing and maintaining the functional status of the visual system to the extent possible in this particular case. Thus, various anti-edematous and anti-inflammatory measures may be indicated, in particular, retro- or parabulbar injections (administration of dexamethasone preparations, respectively, behind or next to the eyeball), droppers with solutions of glucose and calcium chloride, diuretics (diuretics, e.g. lasix). According to indications, injections of hemodynamic and optic nerve nutrition stimulants (trental, xanthinol nicotinate, atropine), intravenous nicotinic acid, aminophylline are also prescribed; vitamin complexes (B vitamins are especially important), aloe and vitreous extracts, tableted cinnarizine, piracetam, etc. For glaucomatous symptoms, drugs that reduce intraocular pressure are used (for example, instillation of pilocarpine).
Physiotherapeutic methods such as acupuncture, laser or electrical stimulation, various modifications of the electrophoresis technique, magnetic therapy, etc. are quite effective for optic nerve atrophy. However, if vision is reduced deeper than 0.01, any measures taken are, unfortunately, ineffective.
Treatment
Methods for moisturizing the skin are different and are largely determined by eliminating the source - the catalyst of the problem. If the cause is a specific disease, then treatment of dry skin of the body includes all the necessary measures that can stop the pathology, and hence remove its accompanying symptoms.
If the reason is different, then it is necessary to take measures to protect the skin from the negative influence of external irritants, which can be eliminated independently. It is necessary to keep the skin clean, but you should not overdo it with the amount of washing and taking baths and showers. Cosmetics for washing must be of high quality and match your skin type. You should use only high-quality, non-expired cosmetics. In winter, it is necessary to use protective creams. In everyday life, prefer clothes and shoes made from natural materials. This will protect against the occurrence of allergic reactions to artificial material and protect against thermal overheating of the skin. Anti-inflammatory agents must be used along with moisturizers. It is recommended to use anti-allergy medications or general health-improving medications internally, which will be prescribed by your dermatologist.
Forecast and prevention of optic nerve atrophy
The degree of cure and the possibility of rehabilitation for almost any ophthalmopathology depends decisively on how timely the patient applied and how skillfully, accurately and completely the diagnosis was established. If adequate treatment begins at the earliest stages of optic nerve atrophy, stabilization and, in some cases, partial rehabilitation of visual functions is quite possible. Their complete restoration today remains beyond the scope of available therapeutic options. With rapidly progressing atrophy, total blindness is a very likely outcome.
A preventive measure that is effective against optic nerve atrophy is “just” the timely treatment of any acute or chronic diseases, no matter what system of the body they concern: visual, nervous, musculoskeletal, immune, endocrine, etc. Of course, intoxication should be avoided, especially the voluntary poisoning with alcohol or nicotine described above. Any massive blood loss requires adequate compensation.
And, of course, even a slight tendency towards vision deterioration requires immediate consultation with an ophthalmologist.
Medical Internet conferences
Dry skin syndrome. Modern view of the problem
Sazonova S.A.
Scientific supervisor: candidate of medical sciences, associate professor Morrison A.V.
Federal State Budgetary Educational Institution of Higher Education Saratov State Medical University named after. V.I.Razumovsky Ministry of Health of the Russian Federation
Definition. Dry skin is a common skin condition in which there is a decrease in the function of the sebaceous and sweat glands, and, as a result, a decrease in moisture in both the dermis and epidermis. Dry skin syndrome can be the result of both exogenous factors (domestic and environmental conditions) and the manifestation of endogenous disorders (genetic, hormonal and immune). Although much of the literature refers to dry skin as “xerosis of the skin,” I believe that this term is most appropriate to describe dry skin as a mild form of ichthyosis vulgaris in the presence of a genetic predisposition.
Clinical manifestations. Dry skin is characterized by pathological peeling, the presence of small cracks, thickening of the skin and its roughening (lichenification), decreased turgor and elasticity due to a lack of lipid content. Subjectively, patients may be bothered by: mild itching, a feeling of tightness and burning. With long-term itching, if it is accompanied by scratching and rubbing, dry skin can thicken and become pigmented. Often, dry skin is a prerequisite for the development of various inflammatory skin diseases such as atopic dermatitis, pyoderma, eczema, etc.
The classification according to the ethology and pathogenesis of dry skin syndrome can be divided into three main groups: • acquired; • associated with age-related changes; • constitutional.
First group
- these are patients with acquired dry skin. Firstly, these are people whose “dry” skin is caused by the direct influence of harmful environmental factors on the surface layers of the skin. These factors include: improper daily skin care (substances contained in soaps, shower gels and shampoos disrupt the functioning of the sebaceous glands) or adverse effects of climatic conditions (insolation: UVA and UVB rays lose the ability of collagen and elastic fibers to bind water), as well as contacts of chemically aggressive substances with the skin (when swimming in a pool with chlorinated water, the protective substances that ensure the normal condition of the epidermis are destroyed and washed away under the influence of chlorine).
Secondly, it should be noted that the clinical picture of some malignant diseases (lymphomagranulomatosis), infectious lesions (HIV/AIDS, viral hepatitis), mental disorders (psychogenic anorexia), endocrine pathology (diabetes mellitus), and renal failure may be accompanied by acquired dry skin. Dry skin syndrome is also a consequence of side effects from the use of certain pharmaceuticals. For example, externally applied retinoids, benzoyl peroxide, azelaic acid lead to severe dryness of the treated skin areas, and the use of vitamins (especially nicotinic acid), statins and diuretics leads to generalized dryness of the skin. [2] In addition, peeling, hyperemia and thinning of the skin can be the result of repeated aggressive cosmetic procedures: peeling, laser resurfacing, various types of masks (especially clay-based). Second group
(due to age-related changes): the condition of the skin is significantly influenced by physiological changes that occur in the body during certain age periods. During life, there are several peaks that are characterized by high dryness of the skin:
The first period begins on the 1st–2nd day of the child’s life, which is explained by the removal of caseous lubricant and a decrease in skin edema (physiological catarrh). Increased dryness of the skin can continue during the first 2–4 weeks of life and is observed in every third child.
The second period is for children aged 2 to 8 years, because they experience a period of minimal activity of sex hormones (estrogens, testosterone, progesterone, cortisol) and reduced production of sebum by the sebaceous glands.
The third age period is senile age. 75% of people over 70 years old have dry skin, which leads to the formation of microcracks. Dry skin is explained by involutive dystrophic processes occurring in the skin and a decrease in the level of sex hormones, which are responsible for stimulating the sebaceous glands.
Third group
(constitutional): dry skin is caused by genetic mutations that lead to structural and functional disorders in the superficial layers of the epidermis. These changes in the skin, as a rule, accompany patients from the moment of birth until old age, and the influence of harmful environmental factors and poor lifestyle can aggravate the severity of dry skin.
Mutations of the FLG gene, which is responsible for the synthesis of the filaggrin protein (from the English filaggrin - filament-aggregating protein) - a protein that promotes the aggregation of filaments, are well studied. Filaggrin deficiency leads to transepidermal water loss and disruption of the epidermal barrier. In addition, fillagrin differentiates to form amino acids (NMF - natural moisturizing factor), which can retain water in the epidermis.
Physiological conditions.
During pregnancy, many organs undergo changes, the skin is no exception. On average, 89% of women experience a change in hormonal levels during gestation, which is manifested by a decrease in the formation of the female hormone estrogen, which entails a decrease in the secretion of the sebaceous glands, so the skin is not sufficiently moisturized. The concentration of progesterone also decreases, resulting in a decrease in skin elasticity and flaking. The period of pregnancy is characterized by the possible development of hypothyroidism, which is characterized by brittle hair, nails and dry skin.
Conclusion. Dry skin syndrome can be caused by genetic mutations, associated with age-related physiological changes, and also acquired under the influence of harmful environmental factors and be a manifestation of hormonal and immune disorders. in organism.
