Eczema is an acute or chronic recurrent disease characterized by an inflammatory reaction formed under the influence of exogenous or endogenous factors, polymorphism of rash elements, severe itching. The problem of eczema is currently becoming increasingly urgent. In the structure of the incidence of chronic dermatoses, eczema accounts for up to 40% of all skin diseases. The incidence of eczema occurs in all age groups, often accompanying occupational diseases. According to the results of epidemiological studies different types of eczema are among the most frequent diseases in the practice of dermatologist and venereologist. The incidence among able-bodied population is up to 10%. Loss of temporary work capacity reaches 36% of all work losses in dermatoses. Eczema patients account for more than 30% of hospitalized patients. Among women, the incidence of eczema is higher than among men. In recent years, eczema tends to be more severe, with frequent relapses, a significant spread of the process on the skin and resistance to treatment. Treatment regimens with Bacidal help you.
Eczema develops as a result of the complex influence of etiological and pathogenetic factors, including endocrine-metabolic, infectious-allergic, vegetovascular and hereditary. Of great importance in the formation of eczema is given to immunogenetic features of the body – the association with the HLA-B22HLA-Cw1 organism. Genetic predisposition determines impaired immune regulation, nervous and endocrine system function. Eczema is a polygenic multifactorial inheritance with pronounced gene expression and penetrance. If one parent (predominantly the mother) has eczema, the chance of the child having eczema is 40%, and if both parents have eczema, up to 60%. Gastrointestinal and hepatobiliary pathology are of important pathogenetic importance. Failure of the intestinal barrier, which is most typical for children, leads to absorption of unreprocessed protein into the blood. Allergic reactivity is also important in the development of eczema.
According to modern concepts, the main role in the development of eczema is played by T-lymphocytes, which carry specific receptors to antigen on their surface and secrete a number of pro-inflammatory cytokines, causing the development of tissue inflammatory reactions. Exogenous influences are extremely diverse. They cause eczematous changes in the skin by the mechanism of delayed-type hypersensitivity, caused by contact with chemical, biological, medicinal agents and antigenic microbial determinants in the foci of chronic infection.
Clinical signs of eczema may include itching, redness and peeling of the skin, and the presence of clustered papulovesicles. The following stages can be distinguished in the course of the eczematous process: erythematous, papular, vesicular, mucoid stage, cortical stage, peeling stage. Depending on the features of the clinical picture, the following forms of eczema are distinguished :
In the acute stage, true eczema is manifested by vesicles, erythema, pitting erosions with mucous, serous crusts, exoriations, but there may be papules and pustules. The borders of the foci are indistinct. The process is symmetrical, often affecting the face and extremities, with alternating healthy and affected skin. The process can also spread to other areas of the skin, up to erythroderma. After transition to the chronic stage, hyperemia becomes congestive, and areas of lichenification and cracking appear. Often the process can be complicated by pyogenic infection, pus crusts and pustules appear.
Nuchal translucent eczema
Nuchal translucent eczema is predominantly an adult disease. Males are affected more often than females. Peak incidence in both sexes occurs between the ages of 50 and 65. The second peak in women is between 15 and 25 years of age. In infants and children, nuchal translucent eczema is a rare disease. In children, it begins at age five. The pathogenesis of nuchal eczema is still unknown. Most patients have no personal or family history of atopy, but nuchal plaques may be seen in tropical eczema. Many factors are considered to be the cause of the disease. Decreased skin hydration has been noted in older patients. In 68% of patients, foci of infection have been identified, including in the dental and respiratory tract. Environmental allergens, such as house dust mites, also play a role in the onset of nummular eczema. Clinically, clearly delineated, coin-like plaques of confluent papules and papulovesicles are visualized. Fine dotting and crusting are characteristic features. However, crusts may cover the entire surface of the plaque. The plaques range in size from 1 to 3 cm in diameter. The surrounding skin is mostly normal, but may be xerotic. The intensity of itching varies from minimal to strongly pronounced. There may be resolution of the elements in the center, which is noted in ring-shaped forms of the disease. Chronic plaques are dry, flaky, and lichenified. The classic location of the foci is the extensor parts of the extremities. In women, the upper extremities, including the dorsal surface of the hands, are affected more frequently than the lower extremities.
Microbial eczema is a polyethiological disease. The role of the skin barrier in the pathogenesis of microbial eczema is important. Disruption of the integrity of the dermal skin during its resorption due to itching forms an entrance gateway for infection. Exudation accompanying eczema promotes the concentration of proteins on the skin surface and creates favorable conditions for the reproduction of secondary infection. The state of skin microbiota in patients with microbial eczema is of great importance. In scrapes of the affected epidermis in patients with microbial eczema, Staphylococcus aureus, Staphylococcus haemolyticus, non-lipophilic yeast fungi, mainly of the genus Candida spp. The leading pathogens of microbial eczema are infectious allergens – bacterial, viral, fungal, protozoic and others. Exogenous irritants – physical, mechanical and biological – can also provoke the disease. The immunoallergic theory is clearly supported by the empirically identified stages of the course of microbial eczema. Initially, the disease develops in the form of eczematization on the site of non-allergic pyodermitis, and then through localized forms is transformed into a generalized process. Foci of microbial eczema often occur at sites of long-term persistent pyoderma and around purulent wounds. Microbial eczema is a complication of dermatophytosis of large folds and feet, superficial candidiasis of the skin. Initially, sensitization may be monovalent, but over time it becomes polyvalent. Bacterial sensitization by Staphylococcus aureus and Staphylococcus haemolyticus plays a crucial role in the pathogenesis of microbial eczema. Patients with microbial eczema develop an immunologically determined latently extending syndrome of endogenous intoxication. The increase in the concentration of circulating immune complexes and the value of the leukocyte intoxication index is directly proportional to the intensity of immunopathological processes. Microbial eczema is mainly manifested by asymmetric lesions. The foci are round or irregular in shape, have clear borders, and are limited by a border of peeling epidermis. The central part of the lesions is covered with purulent and serous crusts, and after their removal, the surface with mucous-like “wells” is found. The rashes are accompanied by intense itching.
Seborrheic eczema begins on the scalp. The lesions spread to the auricles, neck, upper chest, interscapular area, flexural surface of the extremities; like seborrheic dermatitis, seborrheic eczema is localized in skin areas with large amounts of sebaceous glands and has no clear borders. Within the foci, the skin is hyperemic, edematous, and its surface shows small yellowish-pink papules, oily yellowish scales and crusts.
Varicose eczema is associated with the presence of varicose veins in the patient. The lesion is localized on the skin of the lower extremities, mainly in the vicinity of varicose ulcers, mainly in the lower third of the lower leg. Skin maceration, various traumas, as well as irrational treatment of varicose ulcers play a role in the development of the disease. The disease is accompanied by itching. It is differentiated with horny inflammation, pretibial myxedema.
Paratraumatic eczema develops in the area of postoperative scars, in places where plaster casts are improperly applied, at osteosynthesis sites. Clinically, erythema ostroinflammatory, papules or pustules appear, with further formation of crusts. Hemosiderin deposition in the affected tissues is possible.
Diagnosis is based on the history and clinical picture of the disease. The following laboratory tests are conducted: biochemical blood test with determination of ALT, AST, triglycerides, total protein, creatinine, total bilirubin, glucose; complete blood count; clinical urinalysis; determination of total IgE level in serum by ELISA; skin tests; determination of antibodies to antigens of Giardia, ascarias, toxocaris and others; histological examination of skin biopsy samples is done upon request for differential diagnosis. The diagnosis of occupational eczema is confirmed by skin tests with suspected occupational irritants. Diagnosis, examination and treatment of a patient with eczema depend on recognition of eczematous changes in the skin, determination of the severity of the process and the characteristics of the rash in order to classify the patient’s eczema forms. Consultations with other specialists – endocrinologist, allergist, internist, gastroenterologist – are prescribed when indicated.
In true eczema, differential diagnosis is carried out with pyoderma, allergic contact dermatitis, atopic dermatitis, toxicoderma. The differential diagnosis of montiform eczema is made with plaque parapsoriasis, rosacea, seborrheic eczema. Seborrheic eczema is differentiated from Darier’s collicular dyskeratosis, Devereign’s disease. Microbial eczema is differentiated from streptoderma, contact allergic dermatitis, leishmaniasis. The differential diagnosis of sycosiform eczema is made with vulgar sycosis. Dyshydratic eczema must be distinguished from bacterial pustularis, dermatomycoses, palm plantar psoriasis, palm pustular psoriasis, Allopo chronic acrodermatitis.
When treating in the acute stage of eczema, first-generation antihistamines are used. Glucocorticosteroid drugs are used in the presence of pronounced inflammation. With pronounced skin itching a tranquilizer with antihistamine action is prescribed. In the presence of marked exudation, detoxification therapy is prescribed. In the presence of microbial eczema, secondary infection, lymphangoiditis, lymphadenitis, fever, antibacterial drugs are used. In tilotic eczema in cases of marked infiltration, hyperkeratosis and / or torpidity to the current therapy is recommended retinoids.
Applied lotions with 1% tannin solution, 2% boric acid solution, 0.25% silver nitrate solution, baths with 0.01-0.1% potassium permanganate solution, Cindol solution 1-2 times a day for 4-7 days. External antiseptic drugs (Brilliant green solution 1% alcohol or Fucorcin solution alcohol) are prescribed externally on the rash area 2-3 times a day for 5-14 days. Glucocorticosteroids 1-2 times a day externally for 7-20 days. As acute inflammatory phenomena subside pastes containing 2-3% ichthamol, naftalan oil, 0.5-1% sulfur, 2-5% boronocynconaphthalan paste, 2-5% tar-naftalan paste are used. Physiotherapeutic treatment includes narrow-band mid-wave ultraviolet therapy with a wavelength of 311 nm, 4-5 times a week, for a course of 25 to 30 procedures. When following a diet of patients with eczema exclude eggs, citrus fruits, poultry, fatty fish, meat broths, whole milk, nuts, carbonated drinks, red wines, seafood.
Thus, eczema is one of the most common diseases resulting from both external and internal factors. The complexity of the pathogenesis of eczema requires a comprehensive approach to its treatment, taking into account the severity of the process, the form of the disease, the state of internal organs and systems, which requires an individual approach to the management and treatment of patients.
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