Antipyretics for children are prescribed by a pediatrician. But there are emergency situations with fever when the child needs to be given medicine immediately. Then the parents take responsibility and use antipyretic drugs. What is allowed to be given to infants? How can you lower the temperature in older children? What medications are the safest?
Atopic dermatitis is a genetically determined chronic recurrent skin disease, clinically manifested by primary, often painful itching, age-related evolution of the clinical picture, hypersensitivity to many immune and non-immune stimuli.
Etiopathogenesis.
In the etiology of atopic dermatitis, the contribution of genetic factors is an established fact. An autosomal dominant mode of inheritance is assumed. If both parents have dermatosis, then the risk of developing atopic dermatitis in a child is 70-80%; if only the mother or father is sick, the risk of developing the disease is reduced to 30-60%.
In the pathogenesis of atopic dermatitis, leading importance is attached to immune mechanisms.
Among the exogenous factors that have a provoking effect in atopic dermatitis are inhalant food substances, external irritants of a physical nature, animal and plant origin, and negative emotions.
External irritants include wool, fur, latex, synthetic fibers, detergents, nickel, cobalt, lanolin, antibiotics and even topical corticosteroids. In case of drug intolerance in patients, the cause-significant allergens are antibiotics - penicillin and its semisynthetic derivatives, sulfonamides, local anesthetics, non-steroidal anti-inflammatory drugs, B vitamins. The importance of psycho-emotional stress in worsening the condition of patients is known.
Epidemiology.
In Ukraine, the incidence ranges from 3-10 per 1000 children. Females are more often affected - 65%, males - 35% less often.
The risk of developing atopic dermatitis in patients in the future respiratory symptoms allergies is 40-60% (hay fever - 40%, seasonal rhinitis- 25%, atopic asthma - 25%). The chronic course of blood pressure is characterized by seasonal (summer months) and off-season remissions. An exacerbation of the disease usually occurs at the ages of 7-8 and 12-14 years.
Clinical manifestations.
The first signs of atopic dermatitis usually appear between the ages of 2-3 months. up to 1.5-2 years. Initial changes appear on the cheeks in the form of “physiological hyperemia” or erythema, peeling on the scalp, which later spread to the forehead, postauricular folds, chin, neck, and torso.
Typical for the infancy period are erythematous-squamous edematous foci with acute inflammatory small round red papules, microvesicles with serous contents, which quickly open, with the formation of “serous wells”. Exudate from dried vesicles forms yellowish-brown crusts. After 6 months of age and in the 2nd year of life, exudative phenomena decrease, and lichenoid and pruriginous components of the lesion begin to appear. The lesions become dry, infiltrative, scaly, small, superficial, barely noticeable polygonal papules appear on the forehead and upper chest. Inflammatory follicular papules develop on the trunk and limbs, sometimes pruriginous and occasionally urticarial rashes. By the end of the 2nd year of life, lesions usually become limited, occupying the extensor and flexion surfaces of the extremities, but a tendency to limit the lesions to the ankle, elbow, and cervical folds begins to appear; the damage to the face is less pronounced.
The second period of development of atopic dermatitis is characterized by the localization of the rash in the folds, the chronic inflammatory nature of the lesions with a more pronounced lichenoid syndrome, the development of secondary skin changes (dyschromia), the undulation of the course, reactions to many provoking influences with a decrease in nutritional hypersensitivity. The main localization of skin lesions is the elbow and popliteal folds, the flexor surfaces of the upper and lower limbs, neck, postauricular folds and perioral region, dorsum of hands and fingers, with a more common process - upper back, lateral surfaces of the torso. The face of most patients is free of rashes.
The most common efflorescences are inflammatory follicular and lichenoid papules, erythematous-infiltrative-squamous and lichenified lesions. Skin lesions, widespread at the beginning of the period, later become localized.
Lesions in the folds alternate diffuse changes skin of the face, neck, upper torso, upper limbs. On the cheeks they are less pronounced; the nasolabial triangle and forehead skin are involved in the process. Only a small proportion of patients retain pronounced changes in the elbow and popliteal folds, local perioral rashes, and lesions on the hands. The most characteristic rashes are polygonal lichenoid papules, lichenified lesions, and excoriations.
The main symptom of atopic dermatitis is itching, which persists for a long time even when the skin lesions disappear. The intensity of itching is high, especially in the lichenoid and pruriginous forms, and can acquire the character of a biopsy itch. During acute inflammatory rashes, burning, soreness, dryness and tightness of the skin often appear.
In patients with atopic dermatitis, it is naturally found functional disorders nervous system and vegetative-vascular dystonia. Manifestations of respiratory atopy in the form of asthmatic bronchitis, atopic rhinitis, bronchial asthma noted in almost 25% of patients. Eye lesions (conjunctivitis, bilateral “atopic cataracts”) are among the manifestations associated with atopic dermatitis. Characteristic lesions of the gastrointestinal tract are in the form of hypo- or hyperacid states of gastric secretion, gastritis, duodenitis, inflammatory diseases biliary tract, pancreatitis, intestinal dysbiosis.
Diagnostics. The diagnosis, in the vast majority of cases, is made on the basis of the clinical picture of the disease. To identify a specific trigger for atopic dermatitis, skin prick tests with various types of allergens are used. In patients with extensive skin lesions and severe white dermographism, in vitro tests (RAST or ELISA - determination of specific IgE antibodies) are performed instead of skin tests. A scoring system has been developed to assess the severity of atopic dermatitis and assess disability clinical symptoms in SCORAD scores (scoring of atopic dermatitis). In the hemogram of patients, eosinophilia is most common (6-10%). A biochemical blood test reveals hypoalbuminemia, changes in globulin fractions, increased sialic acid, seromucoid, and sometimes the appearance of C-reactive protein. In the immunogram of patients, the content of T-lymphocytes is reduced due to T-suppressors and T-killers, disimmunoglobulinemia (increased content of IgE and IgG, inhibition of IgA synthesis), as well as an increase in the level of CEC.
Treatment of atopic dermatitis.
Treatment of patients with atopic dermatitis has the main goal of reducing readiness for allergic reactions and eliminating clinical symptoms of skin lesions. The whole range of therapeutic and health measures, including the organization of the correct regime and rational nutrition of the child, the use of various pharmacological drugs, physiotherapeutic procedures; herbal and reflexology, sanatorium-resort treatment can be defined in a broad sense as nonspecific hyposensitization.
Patients should take baths with starch, bran, and special products (Trixera - softening baths, Exomega - shower oil). Soap and gel must have a neutral pH. It is necessary to control the temperature and humidity in the apartment, and regularly clean the home. Sanitation of foci of chronic bacterial, viral and helminthic protozoal infections with specific drugs is necessary. Normalization of intestinal microflora is achieved by prescribing drugs containing microbes that are antagonists of opportunistic flora (bactisubtil, biosporin, acylact, biobakton, bifidumbacterin, lactobacterin, bificol, linex, primadolyx, lactofiltrum, hilak-forte, normaze), agents with antibacterial activity ( metronidazole, chlorquinoldol), nitrofuran preparations, herbal medicine (St. John's wort, yarrow, pomegranate, calendula).
Correction of digestion and absorption processes is carried out using diet therapy, gastrointestinal enzymes (acidin-pepsin, abomin, pepsidil, pancreatin, cholenzyme, pankurmen, mezim-forte), herbal medicine (wormwood, immortelle, green tea), restoration of liver function and the colloidal state of bile - correct mode nutrition, prescription of hepatoprotectors (Legalon, Hepabene, Essentiale), dietary fiber (wheat bran, oat decoction), sorbents (Enterosgel), mineral water. Correction of the pathophysiological and pathochemical effects of allergic (immunopathological) reactions is achieved by antimediator therapy (mast cell membrane stabilizers, Ngistamine receptor blockers), the use of antioxidants and antihypoxants (vitamin E, etimizol, dimephosphone, xidifon).
Intap (1 capsule 4 times a day for 3-4 weeks or in microenemas) and the H1-histaminolytic ketotifen (zaditen) have properties to prevent the destruction of mast cells and the release of allergy mediators during long-term use. It is prescribed from the age of 6 months. up to 3 years, 0.5 mg 2 times a day; at the age of over 3 years - 1 mg 2 times a day with food, for a maximum duration of at least 2 months.
Antihistamines are used to control itching and allergic inflammation of the skin, their effectiveness is due to the critical role of histamine in the mechanisms of development of most clinical symptoms of atopy.
Therapeutic measures for severe and torpid forms may include systemic corticosteroids. Metypred or triamcinolone are preferable at a daily dose of 1-5 mg/kg (30-40 mg per day) with gradual withdrawal. There is also an alternative method of treatment - a double daily dose is prescribed every other day.
In cases of extreme torpidity, the selective immunosuppressant cyclosporine is used in the form of capsules or solution at a dose of 5 mg/kg. A course of extracorporeal detoxification, in particular in the form of plasmapheresis, may be useful for severe blood pressure.
In cases of repeated detection of changes in laboratory parameters (immunograms), immunomodulatory therapy is indicated for patients. Preference should be given to drugs with a pluripotent mechanism of action: sodium nucleinate, ribomunil, bronchovax, some interferon drugs (leukinferon), replacement immunotherapy agents such as titrated donor immunoglobulin (anti-influenza, anti-staphylococcal), native plasma. In all other situations, to restore the functional activity of immunocompetent cells, a regime of antigenic sparing, elimination of the syndrome of endogenous intoxication, stimulation of nonspecific resistance using adaptogens (dibazol, methyluracil, eleutherococcus, Chinese schisandra), some methods of physiotherapy (general ultraviolet radiation, UHF on the sternum or solar plexus) is sufficient ).
Topical therapy for atopic dermatitis includes: suppression or elimination of itching, elimination of biologically active substances and destructive substances, elimination of bacterial and mycotic infections, improvement of microcirculation and metabolism in the affected areas, elimination of lichenification, reduction or elimination of dryness.
When treating the acute stage of the disease, lotions and wet-dry dressings, creams and gels with vitamins A, E, topical corticosteroids with weak or moderate activity are used, but it should be remembered that the maximum possible surface for treatment with steroids is no more than 20% of the body surface and duration of use in children - 14 days with return to indifferent therapy; dilute corticosteroids and do not use them under occlusive dressings; Do not use in the area of lips, scrotum, diaper rash.
For children with allergic dermatoses, the safest steroids for a short period are those containing mometasone furoate, methylprednisolone aceponate, hydrocortisone butyrate (Elocom, Advantan, Lokoid) and non-steroidal cream Elidel. If complicated by a bacterial or fungal infection - solutions of aniline dyes, creams or ointments pimafucort, triderm, triacutan, bactroban, baneocin, fusidine, etc. At the stage of the chronic process, preparations of naphthalan, tar, fenistil-gel, psilo-balm, actovegin, solcoseryl, ozokerite, paraffin applications, local baths for hands, feet, sapropels, DARDIA cream (Lipo Balm), soft shampoos of the Freederm series, products for Trixer baths, exomega. After a bath, shower, sauna, emollient creams containing polyunsaturated fatty acids, vitamin E (exomega cream and milk), Trixer creams, and bepanthen are recommended.
Spa treatment: SPA resorts.
Prevention atopic dermatitis. Primary prevention aimed at preventing the development of the first manifestations of atopic dermatitis in children early age, should be carried out in pregnant women at risk (those with a family predisposition to atopy or patients with atopic dermatitis). Secondary prevention involves timely diagnosis disorders of the immune and nervous systems, diseases of the digestive system, their adequate therapy.
No. 2, 2001 - »» SKIN DISEASES: DIAGNOSIS, TREATMENT, PREVENTIONYu.V. SERGEEV, Academician of the Russian Academy of Natural Sciences, Doctor of Medical Sciences, Professor MODERN APPROACHES TO DIAGNOSIS, THERAPY AND PREVENTION
The problem of atopic dermatitis (AD) is becoming increasingly important in modern medicine. Increase in incidence in the last decade, chronic, with frequent relapses, course, lack of effectiveness existing methods treatment and prevention today place this disease among the most pressing medical problems.
According to modern concepts, atopic dermatitis is a genetically determined, chronic, recurrent skin disease, clinically manifested by primary itching, lichenoid papules (papulovesicles in infancy) and lichenification. The pathogenesis of AD is based on altered reactivity of the body, caused by immunological and non-immunological mechanisms. The disease often occurs in combination with a personal or family history of allergic rhinitis, asthma or hay fever.
The term “atopy” (from the Greek atopos - unusual, alien) was first introduced by A.F. Sosa in 1922 to determine hereditary forms of increased sensitivity of the body to various environmental influences.
According to modern concepts, the term “atopy” is understood as a hereditary form of allergy, which is characterized by the presence of reagin antibodies. The causes of atopic dermatitis are unknown, and this is reflected in the lack of generally accepted terminology. “Atopic dermatitis” is the most common term in world literature. Its synonyms are also used - constitutional eczema, Besnier's prurigo and constitutional neurodermatitis.
Etiology and pathogenesis of atopic dermatitis remain largely unclear. The theory of the allergic genesis of atopic dermatitis is widely accepted, which associates the occurrence of the disease with congenital sensitization and the ability to form reagin (IgE) antibodies. In patients with atopic dermatitis, the content of total immunoglobulin E is sharply increased, which includes both antigen-specific IgE antibodies to various allergens and IgE molecules. The role of the trigger mechanism is played by ubiquitous substances penetrating through the mucous membrane. allergens.
Among the etiological factors leading to the development of the disease, sensitization to food allergens is indicated, especially in childhood. This is due to congenital and acquired disorders of the digestive tract, improper feeding, early introduction of highly allergenic foods into the diet, intestinal dysbiosis, disruption of the cytoprotective barrier, etc., which contributes to the penetration of antigens from food gruel through the mucous membrane into the internal environment of the body and the formation of sensitization to food products.
Sensitization to pollen, household, epidermal and bacterial allergens is more common in older age.
However, the reagin type allergic reaction not the only one in the pathogenesis of atopic dermatitis. Greatest interest in last years attract disturbances in cell-mediated immunity. It has been shown that patients with AD have an imbalance of Th1/Th2 lymphocytes, impaired phagocytosis, other nonspecific immune factors, and skin barrier properties. This explains the susceptibility of patients with AD to various infections of viral, bacterial and fungal origin.
The immunogenesis of AD is determined by the characteristics of a genetically programmed immune response to an antigen under the influence of various provoking factors. Prolonged antigen exposure, Th2 cell stimulation, production of allergen-specific IgE antibodies, mast cell degranulation, eosinophilic infiltration, and inflammation exacerbated by keratinocyte damage due to scratching all lead to chronic inflammation in the skin of AD, which plays a critical role in the pathogenesis of cutaneous hyperreactivity.
The hypothesis of intradermal absorption of staphylococcal antigens, which cause a slow, supportive release of histamine from mast cells either directly or through immune mechanisms, is also of interest. Disturbances in the autonomic system may play a major role in pathogenesis. nervous system.
Characteristics of atopic dermatitis are white dermographism and a perverted reaction to intradermal administration of acetylcholine. Behind these skin changes lies, obviously, a basic biochemical defect, the essence of which is still largely unclear. In patients with atopic dermatitis, altered reactivity is also explained by unstable adrenergic influences. This instability is considered to be a result of congenital partial blockade of beta-adrenergic receptors in the tissues and cells of patients with atopy. As a result, a significant disturbance in the synthesis of cyclic adenosine monophosphate (cAMP) was noted.
An important place in the pathogenesis of atopic dermatitis is given to endocrinopathies, various types metabolic disorders. The role of the central nervous system is great, which has been and is currently recognized and is reflected in the neuro-allergic theory of the origin of atopic dermatitis.
All of the above explains why atopic dermatitis develops against the background of various and interdependent immunological, psychological, biochemical and many other factors.
Clinical manifestations atopic dermatitis are extremely diverse and depend mainly on the age at which the disease manifests itself. Beginning in infancy, atopic dermatitis, often with remissions of varying duration, can last until puberty, and sometimes does not go away until the end of life. The disease develops in attacks that often occur seasonally, with symptoms improving or disappearing in the summer. In severe cases, atopic dermatitis occurs without remission, sometimes giving a picture similar to erythroderma.
Skin status of an asymptomatic atopic patient The skin of those suffering from atopic dermatitis, especially during the period of remission or “dormant course,” is characterized by dryness and ichthyosiform peeling. The frequency of vulgar ichthyosis in atopic dermatitis varies from 1.6 to 6%, according to different phases of the disease. Hyperlinearity of the palms (folded palms) is observed in combination with ichthyosis vulgaris.
The skin of the trunk and extensor surfaces of the limbs is covered with shiny, flesh-colored follicular papules. On the sides of the shoulders, elbows, sometimes in the area shoulder joints Horny papules are identified, usually regarded as Keratosis pilaris. In older age, the skin is characterized by dyschromic variegation with the presence of pigmentation and secondary leukoderma. Often, patients have whitish spots of Pityriasis alba in the cheek area.
During the period of remission, the only minimal manifestations of atopic dermatitis may be barely flaky, weakly infiltrated spots or even cracks in the area of the lower edge of the earlobe attachment. In addition, such signs may be cheilitis, recurrent seizures, a median fissure of the lower lip, as well as erythemosquamous lesions of the upper eyelids. Periorbital darkening and pale facial skin with a sallow tone may be important indicators of atopic personality.
Knowledge of minor symptoms of skin manifestations of atopic predisposition is of great practical importance, since it can serve as the basis for the formation of high-risk groups.
Phases of atopic dermatitis
During atopic dermatitis, depending on the clinical characteristics in different age periods, three phases of the disease can be divided into three phases: infant, childhood and adult. The phases are characterized by the originality of reactions to the stimulus and are distinguished by a change in the localization of clinical manifestations and a gradual weakening of the signs of acute inflammation.
Infant phase usually begins from the 7-8th week of a child’s life. During this phase, the skin lesions are acutely eczematous in nature.
The rash is localized mainly on the face, affecting the skin of the cheeks and forehead, leaving the nasolabial triangle free. At the same time, changes gradually appear on the extensor surface of the legs, shoulders and forearms. The skin of the buttocks and torso is often affected.
The disease in the infantile phase can be complicated by pyogenic infection, as well as yeast infections, which are often accompanied by lymphadenitis. Atopic dermatitis takes a chronic, relapsing course and worsens with dysfunction gastrointestinal tract, teething, respiratory infections and emotional factors. During this phase, the disease may resolve spontaneously. However, more often atopic dermatitis passes into the next, childhood phase of the disease.
Child phase begins after 18 months of age and continues until puberty.
Rashes of atopic dermatitis in the early stages of this phase are represented by erythematous, edematous papules, prone to the formation of continuous lesions. Subsequently, lichenoid papules and foci of lichenification begin to predominate in the clinical picture. As a result of scratching, the lesions become covered with excoriations and hemorrhagic crusts. The rashes are localized mainly in the elbow and popliteal folds, on the sides of the neck, upper chest and hands. Over time, in most children, the skin clears of the rash, and only the popliteal and elbow bends remain affected.
Adult phase occurs at puberty and in clinical symptoms is close to rashes in late childhood.
The lesions are represented by lenoid papules and foci of lichenification. Wetting occurs only occasionally.
Favorite localizations are the upper torso, neck, forehead, skin around the mouth, flexor surface of the forearms and wrists. In severe cases, the process can take on a widespread, diffuse nature.
When highlighting the phases of atopic dermatitis, it is necessary to emphasize that not everyone has a disease with a natural alternation of clinical manifestations; it can begin from the second or third phase. But whenever the disease manifests itself, each age period is characterized by its own morphological characteristics, presented in the form of three classical phases.
Table 1. Main clinical signs of atopic dermatitis
- itchy skin;
- typical morphology and location of the rash;
- tendency towards a chronic relapsing course;
- personal or family history of atopic disease;
- white dermographism
Other manifestations of atopy, such as respiratory allergy, are detected in most patients with atopic dermatitis. Cases of a combination of respiratory allergies with atopic dermatitis are distinguished as cutaneous and respiratory syndrome, major atopic syndrome, etc.
Drug allergies, reactions to insect bites and stings, food allergies, and urticaria most often plague patients with AD.
Skin infections. Patients with atopic dermatitis are susceptible to infectious skin diseases: pyoderma, viral and fungal infections. This feature reflects the immunodeficiency state characteristic of patients with atopic dermatitis.
From a clinical point of view, pyoderma is of greatest importance. More than 90% of patients with atopic dermatitis have skin infections Staphylococcus aureus, and its density is most pronounced in places where lesions are localized. Pyoderma is usually represented by pustules localized in the area of the extremities and trunk. In childhood, pyococcal infection can manifest itself in the form of otitis and sinusitis.
Patients with atopic dermatitis, regardless of the severity of the process, are prone to viral infection, more often a virus herpes simplex. In rare cases, generalized “eczema herpetiformis” (Kaposi's varioliform rash) develops, reflecting a deficiency of cellular immunity.
Older people (after 20 years) are susceptible to fungal infections, usually caused by Trichophyton rubrum. In childhood, infection by fungi of the genus Candida predominates.
The diagnosis of atopic dermatitis in typical cases does not present significant difficulties (see Table 1). In addition to the main diagnostic signs of atopic dermatitis, additional signs are of great help in the diagnosis, which include the skin status of an asymptomatic atopic patient described above (xerosis, ichthyosis, hyperlinearity of the palms, cheilitis, seizures, Keratosis pilaris, Pityriasis alba, pallor of the facial skin, periorbital darkening, etc.), eye complications and susceptibility to infectious skin diseases.
On this basis, international diagnostic criteria have been developed, including the identification of basic (mandatory) and additional diagnostic signs. Their different combination (for example, three main and three additional) is sufficient to make a diagnosis. However, our experience shows that the diagnosis, especially in the early stages and with a latent course, must be made on the basis of minimal signs and confirmed modern methods laboratory diagnostics. This makes it possible to carry out preventive measures in a timely manner and prevent the disease from manifesting itself in extreme forms.
To assess the severity of the skin process and the dynamics of the disease, the Scorad coefficient has currently been developed. This coefficient combines the area of affected skin and the severity of objective and subjective symptoms. It has become widely used by practitioners and researchers.
Special methods of additional examination, which, however, require special interpretation, play a significant role in diagnosis. Among them, the most important are a specific allergological examination, a study of the immune status, and a stool test for dysbacteriosis. Other examination methods are carried out depending on the patient’s concomitant diseases.
Specific allergological examination. Most patients with atopic dermatitis show sensitization to a wide range of tested allergens. Skin testing allows you to identify a suspected allergen and implement preventive measures. However, involvement of the skin in the process does not always allow this examination; difficulties may arise both in carrying out such reactions and in interpreting the results obtained. In this regard, immunological studies have become widespread, making it possible to determine sensitization to certain allergens using a blood test.
Immunological examination. IgE antibodies. Serum concentration of IgE is increased in more than 80% of patients with atopic dermatitis and is often higher than in patients respiratory diseases. The degree of increase in total IgE correlates with the severity (prevalence) of the skin disease. At the same time high levels IgE is determined in patients with atopic dermatitis when the disease is in remission. The pathogenetic significance of total IgE in the inflammatory response remains unclear, since about 20% of patients with typical manifestations of atopic dermatitis have normal level IgE. Thus, determining the level of total IgE in serum helps in diagnosis, but it cannot be fully relied upon when making the diagnosis, prognosis and management of patients with atopic dermatitis.
PACT (radioallergosorbent test), MAST, ELISA methods for determining the content of specific IgE antibodies in vitro.
Our experience in using these methods in AD shows their high diagnostic value. An effective preventive program is built on their basis (see Table 2).
Table 2. Etiological structure of allergies in patients with atopic dermatitis [according to RAST)
| Allergens (allergen code "Pharmacia") | Quantity positive RAST, % |
||
| Pollen | |||
| q | 1 | Spring grass | 31,3 |
| 3 | Cocksfoot | 40,9 | |
| 4 | Meadow fescue | 40,0 | |
| 5 | Paradise grass | 34,7 | |
| 6 | Timothy grass | 40,0 | |
| 8 | Meadow bluegrass | 40,5 | |
| 12 | Rye | 20,2 | |
| w | 1 | Ambrosia | 5,26 |
| 5 | Wormwood | 37,8 | |
| 6 | Common wormwood | 36,0 | |
| 7 | Daisy | 24,3 | |
| 8 | Dandelion | 27,7 | |
| 9 | Plantain | 10,4 | |
| 10 | Weed pigweed | 8,33 | |
| 15 | Quinoa | 0 | |
| f | 1 | Maple | 12,8 |
| 2 | Alder | 39,3 | |
| 3 | Birch | 44 | |
| 4 | Hazel | 29,8 | |
| 7 | Oak | 21,5 | |
| 12 | Goat willow | 16,2 | |
| 14 | Poplar | 8,7 | |
| 15 | Ash | 9,7 | |
| 16 | Pine | 3,3 | |
| Household | |||
| d | 1 | Dermatophagus pteron. | 14,1 |
| 2 | Dermatophagus farinae | 10,3 | |
| h | 1 | House dust N1 | 26 |
| 2 | House dust N2 | 30 | |
| 3 | House dust N3 | 25 | |
| Epidermal | |||
| e | 1 | Epidermis of a cat | 33,3 |
| 2 | Dog epidermis | 15 | |
| 3 | Horse epidermis | 10,8 | |
| 4 | Epidermis of a cow | 12,3 | |
| 10 | goose feather | 1,85 | |
| 70 | goose feather | 1,7 | |
| 85 | Chicken fluff | 3,2 | |
| 86 | duck feather | 5,4 | |
| Food | |||
| f | 1 | Egg white | 7,8 |
| 2 | Milk | 2,2 | |
| 3 | Cod fish) | 13,8 | |
| 4 | Wheat | 24,4 | |
| 5 | Rye | 22 | |
| 6 | Barley | 14,8 | |
| 7 | Oats | 14,3 | |
| 9 | Rice | 11,4 | |
| 11 | Buckwheat | 17,1 | |
| 12 | Peas | 10,1 | |
| 20 | Almond | 2,6 | |
| 23 | Crabs | 0 | |
| 25 | Tomatoes | 7,7 | |
| 26 | Pork | 9,3 | |
| 31 | Carrot | 11,4 | |
| 33 | Oranges | 6,7 | |
| 35 | Potato | 13,9 | |
| 47 | Garlic | 12,3 | |
| 48 | Onion | 7,8 | |
| 511 | (75) | Egg yolk | 5,5 |
| 530 | Cheddar cheese | 1,4 | |
| 531 | Cheese "Roquefort" | 3,3 | |
| Fungal | |||
| m | 1 | Penicillium mold | 26,8 |
| 2 | Cladosporium | 24,4 | |
| 3 | Aspergillus | 24,4 | |
| 4 | Mucor racemosus | 21,1 | |
| 5 | Candida olba | 22,5 | |
| 6 | Alternaria alternata | 26,3 | |
| Fungal | |||
| R | 1 | Roundworms | 12,5 |
| 2 | Echinococcus | 0 | |
| 3 | Schistosomes | 8,7 | |
The study of cellular immunity makes it possible to differentiate the immune-dependent form of atopic dermatitis from the immune-independent one and conduct an in-depth additional examination in order to clarify the pathogenetic mechanism. Assessment of immune status makes it possible to identify immunodeficiency states and conduct controlled immunocorrective therapy. In a series of studies we have conducted, we have proven the existence of four clinical and immunological variants of the course of AD, which makes it possible to carry out immunocorrective therapy taking into account the characteristics of the immune response of a particular patient.
Treatment
When starting treatment for atopic dermatitis, one should take into account the age stage, clinical manifestations and concomitant pathology. Clinical and laboratory examination of the patient allows us to establish the leading pathogenetic mechanism, identify risk factors, and outline a treatment plan. preventive measures acceptance. The plan must include stages of course treatment, changing medications, consolidating treatment and relapse prevention.
In cases where atopic dermatitis is a manifestation of atopic syndrome (accompanied by asthma, rhinitis, etc.) or is caused by dysfunction of other organs and systems, correction of identified concomitant diseases should be ensured. For example, in childhood, dysfunctions of the gastrointestinal tract play an important role, in puberty - endocrine dysfunctions, etc.
Dietary therapy can bring significant improvement, including preventing severe exacerbations.
Types of diet therapy
An elimination diet, that is, a diet aimed at eliminating diagnosed allergens, usually does not present difficulties in older children and adults. As the first step of the dietary regimen, it is recommended to eliminate eggs and cow's milk, regardless of whether they were the trigger. It is significant that in patients with atopic dermatitis there is often no correlation between skin testing (or PACT) and nutritional history.
When prescribing a hypoallergenic diet during an exacerbation, it is necessary first of all to exclude extractive nitrogenous substances: meat and fish broths, fried meat, fish, vegetables, etc. Completely exclude chocolate, cocoa, citrus fruits, strawberries, black currants, melon, honey, pomegranates, nuts, mushrooms, and caviar from the diet. Also exclude spices, smoked meats, canned and other products containing additives of preservatives and dyes that have a high sensitizing ability.
A hypochloride diet (but not less than 3 g of sodium chloride per day) plays a special role in atopic dermatitis.
Due to reports of impaired fatty acid metabolism in patients with atopic dermatitis, a dietary supplement containing fatty acids is recommended. Suitable for adding to the diet vegetable oil(sunflower, olive, etc.) up to 30 g per day in the form of salad dressings. Vitamin F-99, containing a combination of linoleic and linolenic acids, is prescribed, either in high doses (4 capsules 2 times a day) or in medium doses (1-2 capsules 2 times a day). The drug is especially effective in adults.
General treatment. Drug treatment should be carried out strictly individually and may include tranquilizers, antiallergic, anti-inflammatory and detoxification agents. It should be noted that a large number of methods and means have been proposed for the treatment of atopic dermatitis (corticosteroids, cytostatics, intal, allergoglobulin, specific gmposensitization, PUVA therapy, plasmapheresis, acupuncture, fasting-dietary therapy, etc.). However, the most important in practice are medications that have an antipruritic effect - antihistamines And tranquilizers.
Antihistamines are an integral part of the pharmacotherapy of atopic dermatitis. Drugs in this group are prescribed to relieve symptoms of itching and swelling due to skin manifestations, as well as atopic syndrome(asthma, rhinitis).
When carrying out treatment with first-generation antihistamines (suprastin, tavegil, diazolin, fercarol), it is necessary to remember that rapid addiction develops to them. Therefore, medications should be changed every 5-7 days. In addition, it must be taken into account that many of them have a pronounced anticholinergic (atropine-like) effect. As a consequence - contraindications for glaucoma, prostate adenoma, bronchial asthma (increased sputum viscosity). Penetrating the blood-brain barrier, first-generation drugs cause a sedative effect, so they should not be prescribed to students, drivers and anyone who must lead an active lifestyle, as concentration is reduced and coordination of movements is impaired.
Currently, considerable experience has been accumulated in the use of antihistamines second generation - loratodine (Claritin), astemizole, ebostin, cetirizine, fexofenadine. Tachyphylaxis (addiction) does not develop with second-generation drugs; there is no atropine-like side effect when taken. Nevertheless, a special place in the treatment of blood pressure is given to Claritin. Today it is the safest and most effective antihistamine and the most commonly prescribed in the world. This is due to the fact that Claritin is not only devoid of the side effects of first-generation antigen drugs, but even with a significant (up to 16 times) increase in the daily dose does not cause virtually any side effects characteristic of a number of second-generation antigen drugs (minor sedation, increase in QT interval, ventricular fibrillation, etc.). Our many years of experience using Claritin have shown it high efficiency and portability.
Systemic administration of corticosteroids is used to a limited extent and for common processes, as well as unbearable, painful itching that cannot be relieved by other means. Corticosteroids (preferably metypred or triamcinolone) are given for several days to relieve the severity of the attack with a gradual reduction in the dose.
If the process and phenomena of intoxication are widespread, intensive therapy is used using infusion agents (hemodez, rheopolyglucin, polyion solution, saline solution, etc.). Methods of extracorporeal detoxification (hemosorption and plasmapheresis) have proven themselves well.
Ultraviolet irradiation. In the treatment of persistent atopic dermatitis, a very useful auxiliary method may be light therapy. Ultraviolet light requires only 3-4 treatments per week and, with the exception of erythema, has few side effects.
When a secondary infection occurs, broad-spectrum antibiotics are used. Erythromycin, Rondomycin, Vibramycin are prescribed for 6-7 days. In childhood, tetracycline drugs are prescribed from the age of 9 years. A complication of AD with a herpes infection is an indication for the administration of acyclovir or famvir in standard dosages.
Recurrent pyoderma, viral infection, mycosis are indications for immunomodulatory/immunostimulating therapy (tactivin, diucifon, levamisole, sodium nucleinate, isoprinosine, etc.). Moreover, immunocorrective therapy should be carried out under strict control of immunological parameters.
In the general therapy of patients with AD, it is necessary to include, especially in children, enzyme preparations (Abomin, Festal, Mezim-Forte, Panzinorm) and various dental medications (Bifidumbacterim, Baktisubtil, Linex, etc.). It is better to prescribe eubiotics based on the results of a microbiological study of stool for dysbacteriosis.
In general, for children with AD, we always recommend the treatment and prophylactic triad of AD - membrane-stabilizing drugs (zaditen), enzymes and eubiotics.
Prescription also has a good effect antioxidants, especially aevita and vetorona.
External treatment carried out taking into account the severity of the inflammatory reaction, the extent of the lesion, age and concomitant complications of local infection.
In the acute stage, accompanied by weeping and crusting, lotions containing anti-inflammatory, disinfectant drugs (for example, Burov's liquid, chamomile infusion, tea) are used. After the symptoms of acute inflammation have been relieved, creams, ointments and pastes containing soothing and anti-inflammatory substances (naftalan oil 2-10%, tar 1-2%, ichthyol 2-5%, sulfur, etc.) are used.
Corticosteroid drugs are widely used in external therapy. The main, basic corticosteroids in the treatment of AD continue to be such drugs as celestoderm (cream, ointment), celestoderm with garamycin and triderm (cream, ointment) - includes anti-inflammatory, antibacterial and antifungal components.
In recent years, new non-fluorinated corticosteroids have been introduced to the pharmaceutical market. local use. These include Elokom and Advantan.
Currently, the greatest experience of use in dermatology among new drugs has been accumulated with Elokom (mometasone furoate 0.1%) both throughout the world and in the practice of Russian doctors. In this regard, I would like to highlight in more detail some of the features of Elokom. The unique structure of mometasone with the presence of a furoate ring ensures high anti-inflammatory effectiveness, not inferior to fluorinated corticosteroids. The long-term anti-inflammatory effect allows you to prescribe Elokom once a day. The low systemic absorption of Elokom (0.4-0.7%) gives doctors confidence in the absence of systemic complications (of course, subject to the basic rules for the use of GCS). It is known that during the entire period of use of Elokom in medical practice, and this is more than 13 years, there are no registered cases of complications from the HPA system. At the same time, the absence of a fluorine molecule in the structure of Elokom ensures high local safety of the drug (after all, it is the use of fluorinated and especially doubly fluorinated drugs that increases the risk of developing skin atrophy). Data from international studies indicate that the safety level of Elokom corresponds to hydrocortisone acetate 1%. The drugs Elokom and Advantan are recommended by the Ministry of Health of the Russian Federation and the Union of Pediatricians of Russia for the treatment of atopic dermatitis in children as an industry standard. An important advantage of Elokom is also the presence of three dosage forms - ointment, cream and lotion. This allows Elokom to be used at different stages of atopic dermatitis, on different areas of the skin and in young children (from two years old).
Ultraviolet irradiation. Light therapy can be a very useful adjuvant in the treatment of persistent atopic dermatitis. Ultraviolet light requires only 3-4 treatments per week and, with the exception of erythema, has few side effects.
PREVENTION
Primary prevention. Measures to prevent atopic dermatitis must be carried out even before the birth of the child - in the antenatal period (antenatal prevention) and continue in the first year of life (postnatal prevention).
Antenatal prevention should be carried out jointly with an allergist, doctors of the gynecological department and children's clinic. Significantly increase the risk of developing an allergic disease due to high antigenic loads (toxicosis in pregnant women, massive drug therapy of a pregnant woman, exposure to occupational allergens, one-sided carbohydrate nutrition, abuse of obligate food allergens, etc.).
In the early postnatal period, it is necessary to try to avoid excessive drug therapy and early artificial feeding, which lead to stimulation of immunoglobulin synthesis. A strict diet affects not only the child, but also the breastfeeding mother. If there is a risk factor for atopic dermatitis, proper care of the newborn’s skin and normalization of the gastrointestinal tract are necessary.
Secondary prevention. In all cases, an anti-relapse program for atopic dermatitis should be built taking into account factors similar to those in rehabilitation: medication, physical, mental, professional and social. The proportion of each aspect of secondary prevention varies across different phases of the disease. The prevention program should be drawn up taking into account a comprehensive assessment of the patient’s condition and continuity with previous treatment.
Correction of identified concomitant diseases, as well as leading pathogenetic mechanisms, is an important part of anti-relapse treatment.
Patients should be warned about the need to follow preventive measures that exclude exposure to provoking factors (biological, physical, chemical, mental), to follow a preventive elimination-hypoallergenic diet, etc. The preventive pharmacotherapy proposed and tested by us using membrane-stabilizing drugs (zaditen, ketotifen, intal) is effective. Their prophylactic (preventative) administration during periods of expected exacerbation of blood pressure (spring, autumn) in long 3-month courses helps prevent relapses.
For staged anti-relapse therapy of atopic dermatitis, sanatorium-resort treatment in the Crimea, on the Black Sea coast of the Caucasus and the Mediterranean is recommended.
Social and everyday adaptation, professional aspects, psychotherapy and auto-training are also of great importance.
An important role is played by cooperation between the patient or his parents and the attending physician. Conversations should be held about the nature of the disease, allergens that cause exacerbations, possible complications, respiratory allergies, the need to prevent exacerbations and much more. In general, these events are carried out in the form of special educational programs (trainings).
The content of the article
Dermatitis- inflammatory skin lesion that develops at the site of physical exposure. or chem. factors.The domestic dermatological school identifies the concept of “dermatitis” with the concept of “contact dermatitis” and considers it incorrect to call dermatitis a skin lesion due to non-contact exposure to the body. For example, changes in the skin that occur as a result of oral or parenteral administration of medications should be called toxicermia. At the same time, the term “dermatitis” is still used to designate some skin diseases with different mechanisms of development: Dühring’s disease, progressive pigmentary dermatitis, atonic dermatitis and are.
The term “dermatitis” is traditionally used in two cases: to characterize any changes that occur as a result of contact of a substance with the skin, simple dermatitis (artificial, toxic) and as a synonym for allergic contact dermatitis.
Allergic mechanisms do not take part in the occurrence of simple dermatitis. It is caused by so-called obligate irritants, i.e. those that cause an inflammatory reaction in any person. This is a chemical. substances (acids, alkalis), mechanical (scuffs) and physical. factors (temperature, X-rays and ultraviolet rays), plants (caustic buttercup, ash, lumbago, poisonous star anise, spurge, nettle, parsnip, etc.). The cause of allergic contact dermatitis is facultative irritants, which cause an inflammatory reaction of the skin only in individuals with a genetic predisposition to the development of this disease and altered immunity. These include metal ions, rubber, synthetic polymers, cosmetics, medicines, and some plants. Simple dermatitis can occur after a single contact with a strong irritant or after repeated contact with a moderate one. Unlike allergic contact dermatitis, simple dermatitis does not require an incubation period to occur. Some chem. substances, eg. cement, have the properties of obligate irritants and allergens.
Allergic contact dermatitis
Allergic contact dermatitis allergic dermatitis, eczematous dermatitis, allergic contact eczema - an inflammatory allergic skin lesion that develops at the site of direct contact with a substance to which the body has been sensitized as a result of previous exposure.Etiology and pathogenesis of allergic contact dermatitis
The number of substances with potential contact allergen properties is very large, as well as the endless possibilities in which they can come into contact with the skin. However, only certain chemicals. substances are responsible for the occurrence of allergic contact dermatitis. These substances, called haptens, have a low mol. mass (500-1000 daltons), easily penetrate the skin and are able to bind covalently to chemicals. elements of body proteins. In some cases, it is not the substances themselves that act as haptens, but rather the products of their metabolism. Delayed-type contact hypersensitivity is most easily induced by substances that dissolve skin fats or products that can penetrate the stratum corneum of the epidermis and have affinity for epidermal cells. The ability of a particular agent to cause allergic contact dermatitis depends on its ability to bind to proteins. Allergic contact dermatitis can be caused by various chemicals. substances, medicines, plants. Unlike simple dermatitis, allergic contact dermatitis occurs only in certain individuals exposed to the substance and only upon repeated exposure. Allergic contact dermatitis can be the result of systemic use of a drug in persons previously sensitized by this drug or chemical. a substance that has similar antigenic determinants. Allergization occurs 7-10 days after the first contact with a potential allergen; more often, the development of contact allergy requires repeated and prolonged exposure to a sensitizing agent, even years in the case of professional allergization.One of the most powerful contact allergens is the sap of plants from the sumac family, of which there are 100-150 varieties. About 70% of people exposed to sumac poison suffer from allergic contact dermatitis. The allergic genesis of allergic contact dermatitis is confirmed by the fact that people who have never had contact with this plant (residents of Europe) do not develop allergic contact dermatitis.
For allergic contact dermatitis to occur, the hapten must penetrate the skin, bind to the protein, and form an antigen. Of great importance in this process is Langerhans cells, which are found in the epidermis, thymus and lymph nodes. Langerhans cells have a specific affinity for substances with low mol. mass (haptens). It is therefore proposed that these cells absorb the hapten as it passes through the epidermis, conjugate it to proteins, and convert it into a complete antigen. Then the antigen, using the same cells, is transferred to regional The lymph nodes, in which the number of T lymphocytes increases. Sensitized T lymphocytes from the lymph nodes migrate into the skin and blood. This process lasts almost 10 days - the incubation period. If chem. the agent again comes into contact with the patient's skin, allergic contact dermatitis develops after 12-48 hours. This time (reaction time) is shorter than the incubation period, since the skin contains T lymphocytes sensitized to this substance. The interaction of T lymphocytes with antigen leads to the production of lymphokines, the entry of neutrophils, basophils, lymphocytes, eosinophils into the site of inflammation, and damage to skin cells, which is manifested by symptoms of allergic contact dermatitis. This contact hypersensitivity is a classic example of delayed-type hypersensitivity, as evidenced by the following facts: the inflammatory process of allergic contact dermatitis. associated with the accumulation of mononuclear cells of the lymphoid series; contact sensitivity can be passively transferred using a suspension of lymphoid cells (but not serum) taken from a sensitized animal; contact sensitivity is accompanied by changes in the draining lymph nodes (proliferation of T lymphocytes), which is typical for allergic reactions of the cellular type; when cultivating lymphocytes from patients with allergic contact dermatitis. RBTL is observed with hapten-protein conjugates, which also indicates sensitization of T lymphocytes. The role of the T-immune system in the pathogenesis of the disease is confirmed by the functional deficiency of T lymphocytes in patients with allergic contact dermatitis.
The development of allergic contact dermatitis is associated with a hereditary predisposition. Children of parents sensitive to DNCB are more easily sensitized than children of parents not sensitive to DNCB. A similar genetic predisposition was identified in twins and in animal experiments.
The role of antibodies in the development of allergic contact dermatitis is debated. Around the vessels, in the dermis and vesicles of patients with allergic contact dermatitis, lymphoid cells with membrane immunoglobulins, mainly immunoglobulin E and immunoglobulin D, are detected. These cells are found in the skin even in the absence of clinical symptoms of allergic contact dermatitis. It has been suggested that they are memory cells that carry a predisposition to the disease. In patients experimentally sensitized with DNCB, lymphocytes bearing immunoglobulin D appear, and in patients with allergic contact dermatitis, the number of circulating lymphocytes with surface immunoglobulin D increases.
Pathomorphology of allergic contact dermatitis
Histological changes in the skin in allergic contact dermatitis are not specific. Before clinical signs of the disease appear in the skin of a sensitized person, vasodilation and perivascular infiltration of mononuclear cells occur 3 hours after contact with the allergen; after 6 hours, skin infiltration with mononuclear cells and intracellular edema (spongiosis) occur in the deep layers of the epidermis. In the next 12-24 hours, spongiosis intensifies and intraepidermal vesicles are formed; infiltration of mononuclear cells covers the entire epidermis. Thickening (acanthosis) of the epidermal layer becomes visible to the naked eye. After two days, spongiosis disappears and vesicular changes dominate, as well as acanthosis, and parakeratosis occurs. Spongiosis, vesiculation, acanthosis, parakeratosis, and exocytosis are characteristic of acute allergic contact dermatitis. Microscopic changes in the disease tend to vary in different parts of the affected epidermis (spotty histological picture). Skin biopsy for allergic contact dermatitis can only help in cases where it is necessary to distinguish this condition from dermatological disorders with a characteristic histological picture. Simple dermatitis differs from allergic contact dermatitis by more pronounced destruction of the epidermis and the presence of polymorphonuclear cells in the infiltrates.Allergic Contact Dermatitis Clinic
Allergic contact dermatitis is characterized by papulovesicular and urticarial elements, erythema, swelling, blisters, fissures, which causes weeping dermatitis. In the later stages, crusts and peeling appear. Upon recovery, no scars remain unless there is a secondary infection; pigmentation is rarely present (with the exception of phytophotocontact dermatitis from meadow grass). Depending on the etiological cause, the localization, prevalence, outline and clinical picture of the disease have features.Phytodermatitis is characterized by linear damage to the dorsal surfaces of the hands, interdigital spaces, ankles, sometimes in the form of leaves of the plant that caused allergic contact dermatitis. Such allergic contact dermatitis can be combined with damage to other organs (conjunctivitis, allergic rhinitis, bronchitis) and symptoms general defeat(fatigue, fever, headache).
Occupational allergic contact dermatitis is characterized by skin thickening, peeling, lichenification, cracking and pigmentation. In some cases, the skin itself and, to a lesser extent, the epidermis are involved in the process, which is clinically expressed by erythema and edema, for example. for allergic contact dermatitis to nickel. Occupational allergic contact dermatitis is more characterized by hand involvement and eczematization of the process. In allergic contact dermatitis caused by artificial resins, erythematous rashes are observed, often with swelling. With sensitization associated with ursol and turpentine, mainly erythematous-bullous elements appear. In many cases of occupational eczema, for example. with “cement eczema”, sensitization to chromium ions or “nickel scabies” with an allergy to nickel, the clinical picture is dominated by symptoms such as microvesiculation, weeping, and skin itching.
Depending on the clinical picture and severity inflammatory process has acute, subacute and chronic forms. The acute form of the disease is characterized by erythema, the formation of small vesicular elements, which subsequently dry out into thin, easily torn off crusts. Swelling, urticaria, and blisters may occur. The clinical picture of subacute dermatitis is the same, but inflammatory changes are less pronounced. Chronic form The disease develops with prolonged constant contact with an allergenic substance, for example. by type of activity. This is the so-called occupational allergic contact dermatitis, or occupational eczema. The clinical picture in this condition is polymorphic; the clarity of the boundaries of the pathological process is lost, lesions begin to appear on other areas of the skin that are not in contact with the allergen.
Drug-induced allergic contact dermatitis is induced by various drugs upon skin contact; the development of anaphylaxis due to contact with the drug is extremely rare. The causative factors are medications usually used in ointments for the local treatment of skin diseases: antibiotics, especially neomycin and streptomycin, etc. antibacterial drugs, anesthetics, novocaine, glucocorticosteroid drugs. Identification of the sensitizer medicinal product difficult, since in dermatology ointments with a complex composition are often used, for example. antibiotics and glucocorticosteroid drugs, antibiotics and anesthetic drugs. Of particular importance is the background against which these drugs are prescribed, since, on the one hand, a violation of the integrity of the epithelium when the skin is damaged creates conditions for rapid penetration of the drug, and on the other hand, it indicates the existing inferiority of the immunocompetent function of the skin, which contributes to the formation of drug allergic contact dermatitis. The disease can also develop in healthy individuals on unaltered skin when using various creams in which substances such as para-aminobenzoic acid and ethylenediamine are added in small quantities as stabilizers. Hormonal creams can also cause disease. This process is quickly cured after discontinuation of the cream that caused the disease. Most often, drug-induced allergic contact dermatitis occurs in persons associated with medicinal substances: pharmaceutical industry workers, pharmacists, medical staff. This allergic contact dermatitis is characterized by a chronic course with the transition to occupational eczema. Stopping contact with sensitizing substances does not always lead to recovery, since the disease is often complicated by autoimmune processes.
The course of the disease changes if the sensitizing agent enters the body orally, parenterally, or other routes; in such cases, eczematization of the process occurs, skin itching intensifies, and becomes generalized.
Differential diagnosis carried out with atonic dermatitis, true eczema and microbial and mycotic eczema.
Treatment of allergic contact dermatitis
Treatment must be carried out in two directions: preventing further contact with the agent that caused the disease; treatment of the pathological process. The first direction includes establishing the cause using allergological diagnostic skin patch tests and eliminating the allergen. General measures include the use of protective clothing, automation of production processes, improvement of ventilation, replacement of highly allergenic substances with less allergenic ones (hypoallergenic cosmetics, etc.), use of protective creams, and reduction of injuries. Drug-induced allergic contact dermatitis is often associated with the use of ointments containing sensitizing substances, especially in the topical treatment of skin diseases. Therefore, it is better to use oil creams that do not contain preservatives. It is necessary to carefully prescribe ointments based on lanolin, since it may have sensitizing properties, ointments with complex compositions, since the substances contained in these mixtures in small quantities are often not indicated, namely, they may have allergenic properties.In some cases of illness, it is enough to eliminate the sensitizing agent to cure the patient. However, this is not always possible, since many substances are widely distributed in everyday life, industry, and nature.
Local therapy includes the following therapeutic measures. In the first few minutes after contact with a sensitizing substance, e.g. juice of plants, it is necessary to rinse the skin thoroughly. When treating moderate disease, hormonal ointments are used, preferably fluoride-containing ones. These ointments should be used carefully on the face (risk of acne) and in the area of skin folds (skin atrophy). You can use such ointments six to seven times a day, gently rubbing into the inflamed skin. To improve penetration, occlusive dressings are recommended for 6-10 hours. It is necessary to avoid ointments of other compositions, and do not prescribe ointments with anesthetic substances, as they can increase sensitization and are also sensitizers themselves. Local administration of antihistamines may worsen the course of the disease. When a secondary infection occurs, it is recommended to use systemic antibiotics, and locally - hormonal ointments, but not ointments with a combined composition (antibiotic - glucocorticosteroid drug). In acute cases of severe allergic contact dermatitis, local treatment consists only of indifferent lotions - saline, water or Burov's solution. The use of homomonal ointments at the vesicular and weeping stages is not indicated. If itching is severe, use cold water or ice.
General therapy includes the following treatment measures: systemic glucocorticosteroid drugs are used only in the acute stage of severe allergic contact dermatitis with blisters, swelling and weeping. Domestic dermatologists recommend low doses of hormonal drugs (prednisolone 10-15 mg or another drug in an equivalent dose for 10-12 days with a gradual dose reduction), foreign ones recommend Preference is given to higher doses according to the following regimens: I - the first four days 40 mg of prednisolone or another drug in an equivalent dose, the next four - 20, the last four days 10 mg and cancellation; II - loading dose for the first 24 hours of an acute condition (60-100 mg of prednisolone, preferably in one dose), then reducing the dose over two to three weeks.
Atopic dermatitis
Atopic dermatitis- a chronic recurrent skin disease, the main symptoms of which are skin itching and lichenification.The term “topical dermatitis” was introduced by Schulzberger, Cock and Cook in 1923. Previously, the disease was called neurodermatitis. However, atopic dermatitis is not entirely correct to identify with diffuse neurodermatitis, since this concept is broader and includes those forms of true, especially childhood, eczema and diffuse neurodermatitis, which occur most often in childhood, in persons with an allergic predisposition and impaired immunity. Atopic dermatitis makes up 2-5% of skin diseases, combined or alternating with other atopic diseases - bronchial asthma, hay fever, allergic rhinitis.
Etiology of atopic dermatitis
In most cases, especially in childhood, food allergens - eggs, flour, milk, etc. - are assumed to be the etiological factors of atopic dermatitis. This is confirmed by the following: the connection between eating certain foods and exacerbation of the disease; improvement after elimination of suspected foods in childhood; the first appearance of symptoms of atopic dermatitis after the introduction of complementary foods into the diet - vegetables, fruits, eggs, meat; positive allergy diagnostic skin tests for one or more allergens in the majority of patients with atopic dermatitis; detection of antibodies related to immunoglobulin E against various allergens. At older ages and in adults, a connection with allergies to household allergens, microbial, epidermal and mite allergens is assumed. However, a clear correlation between contact with an allergen and the development of atopic dermatitis is not always revealed: elimination of the suspected food allergen, in particular milk, does not always lead to remission of the disease; the intensity of skin tests with suspected allergens and the content of antibodies related to immunoglobulin E in serum do not correlate with the prevalence and severity of the process.A hereditary predisposition to the development of atopic dermatitis is assumed - an autosomal dominant type of inheritance. There is a connection between the incidence of the disease and the presence of histocompatibility antigens HLA-A9, HLA-A3.
Pathogenesis of atopic dermatitis
There are two theories of the pathogenesis of atopic dermatitis. The first associates the disease with a violation of immunological mechanisms and sensitization to various allergens. The second involves a vegetative imbalance in the structures of the skin (blockade of adrenergic B receptors). The immunological theory is based on numerous facts of changes in cellular and humoral immunity in atopic dermatitis. The features of humoral immunity in atopic dermatitis are as follows: an increase in the level of immunoglobulin E parallel to the severity of the disease and a decrease after a long remission (at least a year); identification of antibodies related to immunoglobulins E against various allergens; correlation between an increase in nonspecific immunoglobulin E and antibodies related to immunoglobulin E; an increase in the number of B lymphocytes carrying immunoglobulin E on the surface; detection of mast cells with immunoglobulin E fixed on them in the skin of patients with atopic dermatitis; an increase in the serum level of nonspecific immunoglobulin G and fast-acting anaphylaxis antibodies related to immunoglobulins G4; decreased serum immunoglobulin A levels in 7% of children suffering from atopic dermatitis; transient deficiency of immunoglobulin A in most sick children in the first three to six months of life.Features of cellular immunity in atopic dermatitis are as follows: reduction in the number and functional activity of G lymphocytes; increased tendency to develop infectious diseases, disseminated vaccinia, herpes simplex, warts, molluscum contagiosum and chronic fungal infections, i.e. clinical signs disorders of cellular immunity; negative tests for tuberculin and candida antigen; deficiency of circulating T-suppressor cells induced by Con-A and thymosin. In severe atopic dermatitis with signs of secondary infection, a decrease in neutrophil phagocytosis and chemotaxis is often observed. The immunological theory is based on these facts and suggests that the pathogenesis of atopic dermatitis is associated with dysfunction of regulatory cells, in particular with a deficiency of T-suppressors, as a result of which, firstly, autocytotoxic cells (T lymphocytes, macrophages) appear that can damage epidermal cells, secondly, an increased amount of antibodies related to immunoglobulins E is synthesized, which can react with the antigen on target cells - basophils, mast cells, monocytes, macrophages. In addition, the possibility of participation in the pathogenesis of atopic dermatitis by late reactions dependent on immunoglobulin E cannot be excluded. The question of the significance of autoimmune processes in atopic dermatitis has not been resolved.
The theory of autonomic imbalance is based on the following: patients experience white dermographism, vasoconstriction in response to acetylcholine and cold, decreased response to histamine, and a disturbance in the cyclic nucleotide system. Facts accumulated in recent years about the regulation of immunological homeostasis, in particular the synthesis of immunoglobulin E, through the system of cyclic nucleotides and the role of autonomic regulation in this process, allow us to connect the immunological and autonomic theories of the development of atopic dermatitis.
Pathomorphology of atopic dermatitis
The shock tissue in atopic dermatitis is the vessels of the epidermis. With atopic dermatitis, they expand, increase vascular permeability, release of cellular elements into the surrounding tissues, and edema, resulting in spongiosis, erythema, papules and vesicles. Acute atopic dermatitis is manifested by spongiosis (intracellular swelling) and intraepidermal vesicles containing lymphocytes, eosinophils and neutrophils; parakeratosis is observed (incomplete keratinization with the presence of nuclei in the stratum corneum of the epidermis); in the upper layer of the dermis, swelling, vasodilation, and perivascular infiltration of leukocytes are noted. Subacute form characterized by intraepidermal vesicles, acanthosis (thickening of the Malpighian layer), parakeratosis and less pronounced spongiosis; with this form, inflammatory infiltration of the dermis by lymphocytes is observed. In chronic atopic dermatitis, acanthosis forms, dilation of capillaries with thickening of their walls in the upper part of the dermis, perivascular infiltration with lymphocytes, eosinophils, and histiocytes are detected. In areas of lichenification, hyperplasia of the epidermis occurs with slight edema, pronounced thickening of the dermal papillae, and an increase in the number of monocytes, macrophages and mast cells.Clinic of atopic dermatitis
Atopic dermatitis occurs mainly in childhood and lasts until 25-40 years. Features of the clinical picture, course and outcome of the disease depend on age. In all phases of atopic dermatitis, intense skin itching is noted, especially pronounced in infancy and childhood. As a result of itching, excoriation appears and, most often, lichenification, which is a pronounced increase in the visible normal pattern of the skin, especially on the neck, in the popliteal fossae, and elbow bends, associated with constant itching and thickening of the epidermis. Children are often involved in the process thumbs legs, dorsal and ventral surfaces, especially in winter. Atopic dermatitis is characterized by an increased skin pattern on the palms - “atopic palms”, varnished nails, Denis line (a characteristic fold along the edge of the lower eyelid), dark coloring of the eyelids, a transverse fold between the upper lip and nose (with a combination of atopic dermatitis and allergic rhinitis), it is assumed autosomal dominant inheritance of this trait. Patients are characterized by white dermographism, severe dry skin, as with ichthyosis, there are changes in the neurological status, which creates a special psychosomatic condition - “atopic personality”. Atopic dermatitis can be complicated by contact allergies to locally applied substances; in such cases, the condition is interpreted as “mixed dermatitis,” i.e., atopic dermatitis and allergic contact dermatitis. Mixed dermatitis is often observed in women - “housewife eczema” - with a characteristic localization on the hands. In the overwhelming majority of such cases, an allergic predisposition in the family is revealed. In severe forms of atopic dermatitis, it is often complicated by infection. The course of the disease is chronic and relapsing. The chronic process is characterized by thickening of the epithelial layer, dryness, lichenification, and pigmentation disorders. Exacerbation often manifests itself as eczematous rashes with weeping. With age, the complete disappearance of atopic dermatitis and the appearance of bronchial asthma, hay fever, and allergic rhinitis are possible.With atopic dermatitis, there is an increased sensitivity to viral infections: the occurrence of eczema vaccinatum and herpeticum, generalized vaccinia, characterized by the development of grouped vesicles and pustules, mainly in places of existing eczematous foci, an increase in temperature to 39 ° C, and intoxication. Progressive vaccination in children with atopic dermatitis is associated with a defect in the Ti (or) B immune systems. Adults with atopic dermatitis more often develop drug contact dermatitis due to neomycin, ethylenediamine, etc. Severe forms of atopic dermatitis are often complicated by skin infectious processes (impetigo, folliculitis, abscesses, “cold skin abscesses”),
In the clinical picture of atopic dermatitis, a number of signs are identified, the combination of which makes it possible to diagnose the disease.
The prognosis is favorable with an earlier onset of atopic dermatitis (up to six months), limited localization of the process, the effect of glucocorticosteroid drugs and antihistamines, less favorable with dissemination of the process in early childhood, discoid form of erythema; Negative emotional factors worsen the course of atopic dermatitis.
Differential diagnosis of atopic dermatitis
In infancy and early childhood, atopic dermatitis is differentiated from seborrheic dermatitis, scabies, immunodeficiency diseases - Wiskott-Aldrich syndrome, ataxia-telangiectasia, hyperimmunoglobulinemia E and hypogammaglobulinemia syndromes, selective deficiency of immunoglobulin M, chronic granulomatosis of children, lichen planus. Atopic dermatitis in adults must be differentiated from scabies, microbial and mycotic eczema, and contact dermatitis.Treatment of atopic dermatitis
Atopic dermatitis is difficult to treat. Diet restriction is not always effective; if a connection with a food allergy is suspected, an elimination diet is necessary. It is recommended to eliminate highly allergenic foods, spices, limit carbohydrates, and in some cases eliminate milk. The diet should be rich in vitamins. Patients should avoid overeating. Local treatment in the acute exudative stage consists of using lotions with Burov's solution (1: 40) and hypertonic, astringent solutions; lotions with chamomile infusion are advisable. Between changing gauze dressings, you can use glucocorticosteroid lotions and creams (1% hydrocortisone or 0.025% triamcinolone). Application of glucocorticosteroid ointments is most effective in the chronic stage. Better resorption is achieved when using an occlusive dressing. The risk of developing complications from the use of glucocorticosteroid drugs should be taken into account, especially when treating the disseminated form of atopic dermatitis in early childhood. In the chronic stage of atopic dermatitis, especially with ichthyosis, the use of emollient creams is indicated. In cases of lichenification and hyperkeratosis, the use of tar-containing ointments should be very careful - in order to avoidphotodermatosis. General therapy consists of the appropriate prescription of antihistamines to reduce itching, swelling, and erythema; oral glucocorticosteroid drugs should be prescribed only in severe cases, in a short course, when other measures are not effective; for severe itching, tranquilizers are indicated. Recently, attempts have been made to treat atopic dermatitis with immunomodulators - transfer factor, decaris, thymosin. The results obtained are not clear-cut. Specific hyposensitization is indicated for the combination of atopic dermatitis with atopic bronchial asthma, hay fever, and allergic rhinitis. For bacterial complications, the use of oral antibiotics is preferable, since antibiotic ointments worsen the condition. For the treatment of eczema vaccinatum and herpeticum, which complicate the course of atopic dermatitis, v-globulin preparations and immunostimulants are used.
For quotation: Butov Yu.S., Podolich O.A. Atopic dermatitis: issues of etiology, pathogenesis, methods of diagnosis, prevention and treatment // Breast cancer. 2002. No. 4. P. 176
General information Atopic dermatitis (AD) is a common, persistent dermatosis, occupying 50-60% of the structure of allergic diseases, and this figure is steadily growing (Balabolkin I.I., Grebenyuk V.N., Williams H.C. et al. 1994) For the first time the term “ “atopic dermatitis” was proposed by Sulzbeger in 1923 for skin lesions accompanied by increased sensitivity to various allergens, manifested by instability of the cell membranes of skin vessels, combination with other atopic diseases (bronchial asthma, hay fever, rhinitis, etc.).
Currently, blood pressure is considered as independent nosological form , clearly different from contact allergic dermatitis, microbial and seborrheic eczema, limited neurodermatitis. AD occurs most often in early childhood against the background of exudative diathesis, eczematous process, often with aggravated heredity due to poor nutrition, intoxication, metabolic disorders, nervous and endocrine systems(hypofunction of the adrenal cortex, gonads, hyperfunction of the thyroid gland), but can also form in adulthood.
Leading signs of atopy are severe itching, chronic recurrent course, white dermographism, increased serum levels blood IgE, a decrease in IgM and IgA, a sharp increase in IgG, indirectly indicating delayed-type hyperreactivity (Samsonov V.A. 1985, Suvorova K.N. 1998, Sanford A.J. 1995). The impact of unfavorable, exogenous (physical, chemical, biological) and endogenous (genetic predisposition, immune disorders) factors aggravate clinical picture diseases. However, the etiology remains unclear, the pathogenesis has not been fully studied, and a clear classification has not been developed.
Pathogenesis Psychosomatic disorders play a certain role in the development of AD. Severe itching, irritability, restless shallow sleep, inappropriate reactions, white dermographism are classic manifestations of psychosomatic pathology. When assessing the psychosomatic status of patients, a high degree of anxiety, the development of reactive depression, and asthenovegetative syndrome were revealed. (Revyakina V.A., Ivanov O.L., Belousova T.A. 2000).
It has been shown that the main substrate in psychoneuroimmune interaction is neuropeptides (substance P, calcitonin gene-like peptide), which ensure the relationship between nerve fibers, mast cells and blood vessels. Under the influence of the “axon reflex,” vasodilation develops, manifested by erythema. Substance P ensures the release of histamine from skin mast cells and has a direct effect on blood vessels, increasing their permeability, which may explain the poor effectiveness, in some cases, of antihistamines. Thus, a direct relationship is visible between the central and autonomic parts of the nervous system. Improvement in psycho-emotional status under the influence of therapy was correlated with the positive dynamics of the skin process. (Ivanov O.L., Belousova T.A. 2000).
Hereditary predisposition in the pathogenesis of atopic dermatitis is confirmed by the high frequency of occurrence of the association of HLA antigens: A3, A9, B7.8, B12, B40. Clinical data also indicate the role of heredity in the transmission of pathological symptoms from parents to children. Thus, from an allergic father, signs of atopy develop in a child in 40 - 50% of cases, from a mother - in 60 - 70%. If both parents are carriers of atopy, then the incidence of the disease in the child reaches 80%. (Mazitov L.P. 2001).
Research by Toropova N.P. the possibility of transplantental transfer of ready-made antibodies from mother to fetus and its hypersensitization is shown, this apparently explains the development of allergic reactions to mother's milk in the first months of life. Such mothers are recommended to follow a strict diet, limiting the consumption of nitrogenous extractives, chlorides, and proteins.
A certain number of children develop latent sensitization, which manifests itself in the form of allergic reactions at the age of 19-20 years. It is not the disease that is inherited, but a set of genetic factors that contribute to the formation of an allergic factor in the body (Fedenko E.S. 2001).
The functional state of the gastrointestinal tract is of great importance in the formation of blood pressure. Dysfunction of the gastrin regulation link was revealed, consisting of imperfect parietal digestion, insufficient activity of enzymes in the processing of chyme, accumulation in the lumen small intestine a huge number of protein allergenic complexes, their free absorption and the creation of prerequisites for sensitization and aggressive course of the skin process. (Toropova N.P., Sinyavskaya O.A. 1993).
The risk of developing food allergies increases due to non-compliance with the diet of a pregnant woman, children in the first months of life who are bottle-fed, as well as the use of food additives containing xenobiotics. Thus, in children of the first year of life, chicken eggs, cow's milk proteins, and cereals are common causes of AD. The course of AD is aggravated by the development of dysbiosis, due to the often uncontrolled use of antibiotics, corticosteroids, the presence of foci of chronic infection, allergic diseases (asthma, rhinitis), dysmetabolic nephropathies, and helminth infections. The waste products of the latter activate immunocompetent cells that carry out the synthesis of IgE and immune complexes.
In the development of exacerbation of blood pressure, inhaled allergens play an important role. The possibility of forming complex associations with bacterial, fungal, viral and drug allergens has been shown, causing the formation of polyvalent sensitization (Maksimova A.E. 1997).
According to Fedenko E.S. (2001) the causally significant allergen in the development of exacerbation of blood pressure are non-steroidal anti-inflammatory drugs, sulfonamides, B vitamins. We also observed the development of allergic reactions such as toxicoderma, urticaria, to B vitamins in patients with diffuse neurodermatitis, true eczema (Zheltakov M.M. ., Skripkin Yu.K., Somov B.A., Butov Yu.S. 1969).
Considerable attention has recently been paid to the polygenic type of inheritance, the characteristic features of which are immune disorders at the level of differentiation of the T-lymphocyte subpopulation. It has been established that null T helper cells (Th 0) under the influence of antigens differentiate into T helper cells of the first type (Th 1) or T helper cells of the second type (Th 2), which differ from each other in the secretion of cytokines, PGE. The first type controls apoptosis of mutated cells through a-TNF, and g-IFN inhibits the development of viruses. The second type provides protection against bacterial allergens and activates antibody formation due to IL-4, IL-5 and IL-13.
In AD, lymphocyte differentiation proceeds through Th2, activating b-cells and the synthesis of allergic IgE antibodies. The process of sensitization occurs with the participation of mast cells with the release of histamine, serotonin, kinins and other biologically active substances, which corresponds to the early phase of the hyperergic reaction. This is followed by an IgE-dependent late phase, characterized by infiltration of T-lymphocytes into the skin, determining the chronicity of the allergic process.
It has been shown that the development of the inflammatory process in patients with AD occurs in the presence of dendritic cells, Langerhans cells with a constantly high level of eosinophils, IgE, cytokines and mediators. The ability of eosinophils to live long and produce neurotoxins and enzymes in the tissue ensures a chronic process accompanied by severe itching, damage to keratinocytes and an even greater release of cytokines and inflammatory mediators, creating conditions for a “vicious circle”.
Thus, the analysis shows that exogenous (physical, chemical and biological) and endogenous (the role of the nervous system, gastrointestinal tract, genetic predisposition and immune disorders) factors take part in the development of AD.
Clinical aspects of blood pressure Typical clinical picture of blood pressure
characterized by: itching of the skin, persistent hyperemia or transient erythema, papulovesicular rashes, exudation, dry skin, peeling, excoriation, lichenification, widespread or limited in nature. The disease usually begins in the first months of life, then taking a recurrent course with the possibility of complete or incomplete remission of varying frequency and duration.
Atopic reactions in childhood occur:
- often in the form of acute inflammatory exudative reactions;
- localized on the face, in folds, outer surfaces of the limbs;
- there is a clear relationship with nutritional factors;
- followed by a chronic, wave-like course of inflammation, vegetative dystonia and lichenification.
At subsequent stages, patients develop:
- persistent lechinization;
- less significant reactions to allergenic irritants;
- less clear seasonality.
Possible clinical forms of manifestation:
Erythematous-squamous;
Vesiculocrustic;
Erythematous-squamous with weak or moderate lichenification in the elbow and popliteal folds;
Lichenoid with a large number of lichenoid papules;
Prurigo-like (Suvorova K.N. 1998).
Based on studies conducted in children with AD, Korotky N.G. identified a number of clinical and pathogenetic options for the development and course of the disease:
1. True, allergic variant AD with a predominance of a specific IgE-mediated immune mechanism
2. Mixed version of blood pressure , where both specific and nonspecific mechanisms are expressed.
3. Pseudo-allergic variant with a predominance of nonspecific mechanisms.
In true, allergic and mixed variants of AD, the severity of the process depends not only on skin damage, which may not always be significant, but also on other organ manifestations of atopy, in particular, bronchial asthma and gastrointestinal pathology. In the pseudoallergic variant of AD, the leading place in the development of the pathological process is given to neurovegetative and microcirculatory disorders.
Diet therapy Due to severe dysfunction of the gastrointestinal tract, timely and adequately prescribed diet therapy, in most cases, promotes remission of the disease or even complete recovery. The elimination diet is based on the reliably proven sensitizing role of certain foods in the development of exacerbations of blood pressure and their exclusion.
Products containing nutritional supplements(dyes, preservatives, emulsifiers), as well as strong, meat broths, fried foods, spices, spicy, salted, smoked, canned foods, liver, fish, caviar, eggs, cheeses, coffee, honey, chocolate and citrus fruits.
The diet should include fermented milk products, cereals (oatmeal, buckwheat, pearl barley), boiled vegetables and meat. The developed diets must be optimal in protein and vitamin content and are compiled in close cooperation with an allergist and nutritionist.
Drug therapy When choosing a systemic drug, the patient’s age, period of illness, and the presence of concomitant diseases are taken into account.
In the treatment of blood pressure, to reduce neurotic reactions, it is prescribed with nutritional and psychotropic drugs . Among herbal preparations, it is preferable to use tincture of peony, motherwort and valerian root, novo-passit. Antidepressants are also used in therapy. Amitriptyline 0.025-0.05 g is prescribed orally; nialamide orally 0.025-0.01 g. Of tranquilizers used diazepam 0.005-0.015 g per day, lorazepam 0.001-0.0025 g per day.
Indications for use antihistamines justified by the essential role of histamine in the mechanism skin itching and the development of inflammation in AD. Due to the presence of a sedative effect, 1st generation antihistamines are not advisable to prescribe to children school age. For planned long-term use, it is more rational to choose any 2nd generation antihistamine (loratadine, terfenadine, cetirizine, ebastine). Ebastine (Kestin) does not cause pronounced anticholinergic and sedative effects, is prescribed in daily dose 10 mg, and if symptoms are severe, the dose may be increased to 20 mg. Cetirizine prescribed in tablets of 0.01 g for 7 days, at a rate of 0.25 mg/kg 1-2 times a day. 2nd generation drugs are currently not used in children under 2 years of age.
Diazolin, chloropyramine, clemastine It is preferable to use during periods of severe skin itching, for 7-15 days, if not only an antipruritic, but also a sedative effect is required. Cyproheptadine has antiserotonin activity, which expands the scope of its application. Clemastine from 6 to 12 years, 0.5 - 1.0 mg, over 12 years, 1 mg 2 times a day. Chloropyramine is prescribed to children under 1 year old, 6.25 mg (1/4 tablet), from 1 to 6 years old, 8.3 mg. (1/3 tablet), from 6 to 14 years, 12.5 mg. 2-3 times a day. In therapy, it is often necessary to combine the use of 1st and 2nd generation drugs.
Membrane stabilizing agents . From this group, they are used in the treatment of blood pressure. ketotifen And sodium cromoglycate . They stabilize mast cell membranes and antagonize H1 -histamine receptors, inhibit the development of the allergic process and can act as a calcium channel blocker. Therapeutic effect appears after 2-4 weeks. Sodium cromoglycate additionally affects the gastrointestinal mucosa, preventing the development of allergic reactions at this level. The drug is prescribed in the acute and subacute period of blood pressure in combination with antihistamines. Children from 1 year to 3 years at a dose of 100 mg (1 capsule) 3-4 times a day; from 4 to 6 years - 100 mg 4 times a day; from 7 to 14 years - 200 mg 4 times a day. The duration of the course of therapy is on average from 1.5 to 6 months.
Suitable purpose drugs that improve digestion , to correct the breakdown of allergenic food substances (Festal, Mezim-Forte, Hilak-Forte).
Demonstrated effectiveness enzyme preparations , taking into account violations of the enzyme systems of the gastrointestinal tract in patients. (Korotky N.G. 2000). Dysbacteriosis is an indication for the full use of probiotics, which normalize the microbial landscape of the intestine.
Increasing the effectiveness of treatment is facilitated by prescribing vitamin preparations . Of the B vitamins, preference is given to calcium pantothenate (B 15), which is prescribed at 0.05-0.1 g 2 times a day for a month, and pyridoxal phosphate (B 6), which is prescribed at 0.1-0.2 g per day. It is advisable to administer b-carotene; it increases the resistance of lysosome and mitochondrial membranes to the action of metabolic toxins, stimulates the immune system and regulates lipid peroxidation.
Immunomodulatory therapy is carried out in cases where blood pressure occurs in combination with clinical signs of immunological deficiency and the presence of defects in the immunogram. In the form of a decrease in the B-cell level, phagocytic cells, an increase in IgE, an imbalance of Th 1 -Th 2 cells. Clinical signs include: the presence of foci of pyogenic infection; frequent exacerbations of the skin process; frequent acute respiratory viral infections with low-grade fever and lymphadenopathy; lack of clinical effect from adequate standard therapy for blood pressure.
Application systemic antibiotics appropriate when low-grade fever and lymphadenitis. With preliminary determination of microflora sensitivity to antibiotics. In empirical therapy, preference is given to the use of macrolides and 2-3rd generation cephalosporins.
Systemic glucocorticosteroids (GCS) are most often prescribed in particularly severe, persistent cases of blood pressure, used in a hospital setting and in short courses under the cover of antacid drugs (Almagel) and calcium supplements (calcium gluconate, calcium glycerophosphate). Prednisolone and dexamethasone 20-25 mg per day are used; adults are prescribed betamethasone injections. The mechanism of the anti-inflammatory activity of GCS is to block the activity of phospholipase A, inhibit the synthesis of leukotrienes and prostaglandins, reduce the activity of hyaluronidase and lysosomal enzymes, and activate the synthesis of histaminase (Grebenyuk V.N., Balabolkin I.I. 1998).
External therapy is an integral part of the complex treatment of blood pressure, occupying a leading place in it. By using local treatment a number of effects are achieved: suppression of signs of skin inflammation; eliminating dryness; restoration of damaged epithelium; improving skin barrier functions.
The choice of drug is determined by the stage of the disease, the phase of inflammation and the severity of skin manifestations. In order to achieve success, it is necessary to follow a certain sequence in the administration of local treatment. For acute weeping processes, lotions and dermatological pastes are used. As the inflammation subsides, non-fluorinated corticosteroids are prescribed in the form of a cream or ointment. Ointments have a more pronounced anti-inflammatory effect and are prescribed for the treatment of subacute and chronic skin lesions. Creams are the form of choice for acute processes.
In cases of pyoderma, erythromycin, lincomycin, geoxyzone ointments, and aniline dyes are prescribed. Among other anti-inflammatory drugs that have long been used in the treatment of blood pressure, one should mention products containing tar, naphthalan, and sulfur.
Forecast The course of blood pressure and the quality of life of the patient and his family largely depend on the reliable knowledge he has received about the causes of the development of skin rashes, itching, and on the careful implementation of all doctor’s recommendations and prevention.
Main directions prevention - this is compliance with the diet, especially for pregnant and nursing mothers, breast-feeding children. Particular attention should be paid to limiting exposure to inhalant allergens, reducing exposure to household chemicals, preventing colds and infectious diseases, and prescribing antibiotics accordingly.
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