Eczema is an inflammatory skin lesions, characterized by erythematous-vezikuleznaya itchy rash; occurs acutely, then takes chronic prone to relapse.
Eczema is not a single etiology and is a skin reaction, which may be caused by exposure of the skin to a variety of external factors; developing only in the presence of change of reactivity of skin. However, the mechanism of development up to the present time is not installed. Some foreign and domestic dermatologists treat eczema how allergic reaction; others put forward the theory of neurogenic pathogenesis, according to which eczema should be considered as a neurosis of the skin, characterized by sensitive and trophic disorders. Changes prior to the development of skin eczema process, there reflex result in disorders of the Central nervous system, possibly under the influence of a serious mental experiences. In other cases, the cause functional changes in the skin are diseases of internal organs (cholecystitis, cholangitis, perioodina, stones of kidneys and other). In some patients, the development of eczema can be associated with dysfunction of endocrine glands. Sometimes eczema can occur as a consequence of damage to the peripheral nerves.
There are the following main forms of eczema: ordinary (vulgar), contact, microbial.
eczema photo

Fig. 1. Impetiginosa eczema. Fig. 2. Microbial eczema. Fig. 3. Acute weeping eczema.

In the acute period of ordinary eczema is characterized vsapaniem on erythematous, slightly swollen background tiny bubbles (the so-called microvesicles). Quickly skrivas, bubbles form large number of small point abrasions with drops of serous exudate like dew (acute weeping eczema; Fig. 3). As subacute process, the number of newly formed vials decreases, and on the surface of the affected area along with bubbles revealed a small pityriasis peeling. Part of bubbles, not skrivas, dries up, forming a crust. Because of eczema develops Tacloban, all of these elements - the bubbles, scratches, brown and peeling is usually seen on the affected area at the same time, causing one of the most typical symptoms of eczema is polymorphism.
The transition of eczema in the chronic form is gradual and is expressed in emerging seal skin of the affected area and strengthening of skin picture (lichenification). Color of skin is becoming more pronounced congestive shade. On the surface of the affected area prevails peeling, but along with this there, although much less than in acute and subacute forms, the eruption of vesicles, education small point bruises and scabs. In chronic period may be acute, characterized by coming again active hyperemia, skin rash microvesicles and weeping. Subjectively eczema is always celebrated itching, worse during periods of exacerbation. Foci of eczema are of different size, the contours of them for the most part without sharp boundaries, less often sharply defined. Relatively rare eczema is limited to one hearth. The process usually apply to other, first of all symmetric plots, sometimes the whole body. The most common initial localization of eczema is a skin on the backs of the hands and face.
The so-called disgestrotical eczema is localized on the skin of the palms and soles. The characteristic feature of it is the following: on the background of mild inflammatory infiltration appear dense, the size of a small pea multi bubbles, reminding cooked sagas of grain, which consistently or rupture, education abrasions, or dry up, forming a plate, brown scales and crusts. Lesions are severely limited; gradually increasing in size, they can go to the back of the hand or the foot, where the inflammatory process takes typical of conventional eczema clinical picture.
Eczema is often complicated by a purulent infection that education is expressed on the surface of the hearth loose honey-yellow or green crusts,develops the so-called impetiginosa eczema (Fig. 1).
In addition to the primary, may develop secondary eczema, i.e. transition in eczema and other skin diseases, such as allergic dermatitis (see), long-standing impetigo (see), a chronic diffuse streptoderma (see Piodermia).
The reason for contact eczema often increased sensitivity to different, especially chemical stimuli. The process is mostly localized in the skin of the back of the hands, forearms, face, where at first appear erythematous-edematous, often weeping lesions resembling the chronic course of ordinary eczema.

Eczema (gr. ekzema - skin rash, eczema), a kind of skin reaction in the form eritematos-vezikuleznaya itching epidermofitia due serous inflammation mainly papillary layer of derma and alopecia spongiosum subulate layer of the epidermis with the formation of small cavities, the so-called microvesicles.
The etiology and pathogenesis. Eczema is a condition that has no single etiology and due to various exogenous and endogenous factors. To explain the pathogenesis of eczema are available in mainly two theories: neurogenic and allergic.
Neurogenic theory based eczematous reactions believes functional changes of the skin and, in particular, its nervous system. Patients with eczema not only amazed but apparently healthy skin sites discovered prior to the development of eczema of the skin changes, electrobios and tactile sensitivity.
Installed and other functional changes from the unaffected skin of patients with eczema. These changes include significant lengthening sensitive chronaki skin and cut realizy, inertia thermal regulation reflex, lowering resistance to an electric current, as well as increased sensitivity of the skin to various chemical stimuli. The last in patients with eczema is not the specific nature and is identified as a rule, polyvalent on different chemical substances, including such that they have the skin of patients not touching. All these functional changes precede appearance of eczema, attaches to it and with the improvement of the disease weakened. However, full restoration of normal function is achieved not always that causes the occurrence of relapse.
Functional changes of the skin there reflex because functional changes from the Central nervous system, as evidenced by the data of the study of higher nervous activity in patients with eczema expressed in the cortico dynamics. The causes of these violations can be different. In some cases, they arise under the influence of emotional factors, severe psychic experiences, in other cause can be a variety of pathological changes in the internal organs, particularly abdominal organs (like viscero-kochannogo reflex), and disorder of the functions of the endocrine glands. Convincing evidence about the role of the nervous system in the pathogenesis of eczema, is the possibility of its occurrence due to the damage of peripheral nerves.
An example is the so-called post-traumatic eczema arising after injuries that result in a constant irritation of the separate branches of the cutaneous nerves (education navrom, and damage to the nerve in the rumen), leading to the development of functional changes of the skin distal to the location of the scar. The removal of these stimuli neurosurgical intervention may lead to the normalization of functions of the skin and cure eczema. Indirectly confirm neurogenic the nature of the pathogenesis of eczema positive results, often notice when using hypnotherapy, electrosleep, sedatives. Detected in patients with eczema functional disorders of the skin are not, apparently, the immediate cause of the development of eczema, and stipulate only the predisposition to it [Adamson (J. Jadassohn)], against which a variety of external factors contribute to the development of eczematous process. According to some authors (O. N. Podvysotsky, P. C. Kozhevnikov, P. M. Leonenko), long-term effects on the skin of exogenous factors can itself cause functional changes in the Central nervous system and thus lead to eczematous reactions (skin-skin reflex). From this point of view can be explained by the process of secondary ackzematosnye, i.e. appearance of eczema on the background of other skin diseases (dermatitis, pyococcal epidermoidnyi and others).
Allergic theory received among dermatologists wide recognition. According to this theory eczema occurs as a result of skin sensitization to various exogenous, and possibly endogenous stimuli. Sensitization, as a rule, strictly specific, monovalency, but can be and group to substances similar in chemical structure. Despite the impact of the stimulus is only for a limited part of skin sensitization covers all the skin that is determined by the method episotomy tests. Sensitization sometimes persists for many years.
Allergic theory recognized in relation to the so-called contact eczema, or eczematous dermatitis, but is controversial in relation to the true eczema, different from the contact eczema ability to occur and propagate out of touch with any specific stimulus (see Dermatitis). Unclear is the question about the mechanism of the process of sensitization. Many authors consider sensitisation as immunobiological process, in response to the antigen-antibody. A number of dermatologists put forth the theory of neural mechanism sensitization. So, Sharpie (J. Charpy) in experiments on Guinea found that the application of the stimulus (dinitrochlorobenzene and others) directly to the spinal nodes, rear roots or posterior horn of the spinal cord causes in 24-48 hours sensitization of all skin cover with typical for eczema histological changes of the skin at the site overlay tests. S. I. Pavlov in experiments on Guinea pigs have shown the inability to raise awareness of animals through denervated flap. These facts bring allergic sensibilisation theory to neurogenic.
Numerous studies do not reveal patients with eczema any natural disorders of metabolism. Correct to assume that observed in patients with eczema metabolic disorders, as well as some functional changes of internal organs (for example, secretory function of the stomach), are not the cause of eczema, as a consequence of the same functional changes in the Central nervous system, which cause and note patients with eczema functional changes of the skin.
Although nominated by Annoy (P. Unna) parasitic theory etiology of eczema was rejected, but now generally recognized that the microbes and, in particular, peacocke and pathogenic fungi can cause eczema. Unlike conventional forms of pyodermia (or mycosis), microbial eczema is believed to be the result of skin sensitization to bacteria or their degradation products. Microbial (or mycotic) eczema usually develops secondarily on the background of long-standing pyococcal skin infections (impetigo, chronic pyococcal epidermolytic), whence comes sensitization. Assume also that the sensitisation may be due and focal lesions of infection in other organs.
Histopathology. Microscopic changes with eczema are marked as in the epidermis and the dermis. In the acute period in the dermis find a sharp dilation of blood vessels, in particular capillaries papillary layer, and marked swelling. Around vessels moderate infiltration mainly of lymphocytes. In the epidermis in this period focal intercellular edema (sponges), located mainly on papillae. Increasing, it penetrates the entire thickness thorn layer of cells which are detached from one another, resulting cavity formed, the so-called microvesicles. Moving to the Horny layer, cavities are opened, forming defects of the epidermis as "eczematous wells. Along with serous exudate, throughout the extracellular tubules, they migrate individual cellular elements, mostly lymphocytes, which in small quantities fill the cavity of the bubble. In the stratum corneum in individual sectors parakeratosis. Granular layer in these areas is missing. As acute nephritis phenomena and transition in subacute eczema, and later a chronic condition swelling of the skin is reduced, but increased okoloserdecna infiltration, which gradually takes diffuse nature and permeates not only the papillary, but at more or less the depth of reticular layer of derma. In the epidermis - the phenomenon of acanthosis; thorn in the layer, although in smaller numbers than in the acute period, pockets of spongiosa followed by the formation of cavities (microvesicles). In the stratum corneum is parakeratosis; granular layer is missing.

Classification. Uniform, generally accepted classification of eczema does not exist. According to the data on the etiology and pathogenesis of eczema most correct should recognize the following types: 1) true (vulgar, constitutional) eczema; 2) contact (professional, eczematous dermatitis); 3) microbial (mycotic) eczema.
The clinical picture. True eczema is characterized by the variety and diversity, due to a kind of disease. It started badly, eczema proceeds pristupoobrazna prone to frequent exacerbations and relapses often becomes chronic, once again interrupted by the exacerbation of the inflammatory process. Acute eczema is on erythematous rash background microvesicles (printing. table, Fig. 3). After opening formed small dot erosion ("eczematous wells), separating drops serous exudate (acute, weeping eczema). As subacute inflammation number of bubbles decreases, and the affected areas
there are small pityriasis peeling. Part of bubbles dries to form crusts. Because eczema develops pristupoobrazna, all items (bubbles, drip weeping, brown and peeling) are marked on the affected areas at the same time, which is one of the most characteristic symptoms of eczema - evolutionary polymorphism. However, when expressed polymorphism is often observed the prevalence of one of the morphological signs of eczema over the other. This gives grounds to distinguish different forms of eczema: bubble, weeping, squamous and other Transition eczema in the chronic form is characterized by infiltration of the affected area, congestive hyperemia and lichenification - increased skin of the figure. On the surface of the affected area prevails peeling, but celebrated, although in much smaller numbers than in the acute and subacute eczema, skin rash bubbles, education point of bruises and scabs. In chronic period (and this is very typical) may be increasing. Subjectively - itching of various intensity; foci of eczema is a different size, they are without clear boundaries, you are severely limited. Relatively rare eczema is limited to one lesion. More often eczematous process has a tendency to spread; for some patients it affects large areas of the skin.
The most frequent localization of eczema and rear of the hands and face. Localization eczema, as a rule, is not reflected on the morphological picture of the disease. The only exception is eczema of the hands and soles. Here, depending on the structure of the skin eczema process is manifested in the form of so-called disgidroticheskuyu eczema characterized vsapaniem on limited areas of the palms and soles of bubbles, solid to the touch, pea-sized, reminding cooked sagas grains, amid a mild inflammatory reaction. Consistently bubbles or rupture, or dry up with the formation of yellow crusts. Foci disgidroticheskuyu eczema sharply limited and, gradually increasing in size, apply to the back surface of the hand or foot, where the inflammatory process takes typical for eczema clinical picture. Usually as a result of scratches eczema is complicated by secondary infection. Then on the affected skin formed loose, lumpy honey-yellow peel, after the removal of which is revealed typical drip weeping - so-called impetiginosa eczema (printing. table, Fig. 1).
Contact eczema occurs as a result of skin sensitization to chemical irritants, localized primarily on the back of the hands, arms, face and neck, genitals and affects usually limited areas of skin. From the true contact eczema differs less pronounced polymorphism does not relapse and quickly cured when Troubleshooting an appropriate stimulus. With prolonged contact with sensitizing factor contact eczema proceeds subacute or chronic, not morphologically different from the true eczema, but quickly regresses after eliminating contact with sensitizing agent. Diagnosis is based on a positive result epicutaneous test that detects monovalent character sensitization. In the long polyvalent sensitization may go into polyvalent that means making contact eczema true.
When microbial eczema lesions are traits and eczema, and the main pyococcal skin lesions (printing. table, Fig. 2). Morphologically these lesions are characterized by sharp limitation, all or krupnoplastinchatam outlines. On the periphery are often seen collar flaking of the stratum corneum. The affected area is often plate covered with crusts, after removing solid moist surface, which is clearly revealed "eczematous wells"separating drops serous exudate. Microbial eczema is localized on the shins, rear brushes, scalp. After the primary lesion is often the dissemination process. Apparently, the original form of microbial eczema is the so-called numular eczema characterized vsapaniem sharply limited foci of round shape with a diameter of 2-3 cm or more, slightly above the level of healthy skin. On the surface, painted in bluish-red colour, a rich drip weeping. The most frequent localization and rear brush, in some cases, the process is disseminated.
Diagnosis of eczema is no problem. Microbial eczema should be clearly distinguished from the true, nezametdinova weeping pyococcal Epidermophyton. The most important differential-diagnostic feature is the nature soak: solid when epidermolytic and drip with eczema.
Treatment. Naruzhno in the acute period when expressed weeping appoint cold lotions or wet-drying bandages from knitting solutions (lead water, 1% solution of resorcinol and others). In the subacute period shown naphthalan or Ichthyol (2-5%) paste. In chronic cases when expressed infiltration recommend allowing tools (tar, drug DCA and others) in the form of ointments, pastes, or gradually increasing concentration. Have effect as ointments and creams to steroid hormone (prednizolonovuyu ointment and others). In a persistently recurrent cases shows local radiotherapy rays Vucci.
Common treatment is the appointment of a sedative and neurologically funds (bromine, Valerian, chloral hydrate, trioxazin, meprobamate and other). It is also shown nonspecific desencibilizirutuyu therapy intravenous infusion of calcium chloride or sodium bromide, intramuscular injections of calcium gluconate. It is recommended to normalize and lengthen the patient sleep, appointing a small dose of sleeping pills; shows Spa treatment. In patients with eczema diseases of internal organs simultaneously conduct and their treatment. In cases of common or persistently flowing eczema shown corticosteroids in small doses (prednisone, prednisolone, dexamethasone and other).
Prevention of eczema is a very difficult task. It should be based on a thorough hygienic care of skin, elimination of various external stimuli, as well as the timely treatment of various common internal diseases, particularly on the elimination of various factors that impair the normal function of the CNS. A very effective and efficient event is the examination of patients with eczema that gives the doctor an opportunity to carefully examine the patient, to assign the correct mode and rational treatment.