Nummular eczema is an itchy chronic dermatitis, which is a type of microbial eczema. Clinically manifested by a rash of rounded bright red coin-shaped plaques with clear borders, towering over healthy skin, bounded by a marginal border of epithelial cells – remnants of opened vesicles. The process is accompanied by itching, combs appear, a secondary infection joins, crusts form. Nummular eczema is diagnosed clinically, if an infectious component is suspected, a microbiological examination of epidermal smears is carried out. Treatment is desensitizing, anti-inflammatory.
Nummular eczema is a type of microbial eczema of unclear etiology, characterized by generalized rounded itchy foci. The disease is widespread in dermatology, accounting for about 10% of the total number of dermatoses. In patients with a weakened immune system, the proportion of pathology increases. Perhaps this is due to the fact that nummular eczema is polyethological, but always has an infectious component that has a negative impact on the state of the immune system. In addition, patients with nummular eczema have a predisposition to disorders of immune regulation and concomitant diseases of the gastrointestinal tract, in which about 80% of immune cells are located.
Dermatitis is equally common in men and women. It can be diagnosed at any age, the peak incidence falls on the period of 30-50 years. Racial predisposition and endemicity are not detected. Nummular eczema develops at any time of the year, worsens during acute respiratory infections and acute respiratory infections. The disease is a type of eczema and is included in the group of microbial eczema. The pathology got its name because of small rounded foci, shaped like coins. Modern dermatologists believe that with this form of eczema, the cellular and humoral link of immunity is disrupted, which causes sensitized skin to respond to the action of any antigen with local immune inflammation in the form of coin-shaped foci.
Any form of eczema is heterogeneous. Factors contributing to the development of nummular eczema are tonsillitis, caries, hyperhidrosis, tuberculosis, incorrectly taken medications, somatic diseases and stress, which, against the background of hereditary predisposition, reduce the body’s immunity and cause the development of a pathological process. However, there is no complete clarity in the etiology of the disease. Since nummular eczema is a type of microbial eczema, the cause of skin damage is considered to be bacteria to which the body is sensitized.
The skin with nummular eczema is constantly in a state of readiness for active interaction with a foreign antigen. The peculiarity of such allergization is the gradual transition from monovalence to polyvalence. Initially, the skin reacts to one antigen, and over time begins to react to many stimuli. This is probably due to a hereditary predisposition. Genetics defines multifactorial inheritance with pronounced expressiveness and penetrance of genes. If one of the parents is sick, the probability of developing eczema in a child is 40%, if both – 60%. An important role in the occurrence of nummular eczema is played by the failure of the digestive tract with fermentopathies, dyskinesia and broken membrane barriers, leading to direct ingestion of foreign antigens in the form of non-split, not fully digested proteins.
The immune mechanism of the development of the eczematous process consists in the occurrence of an allergic antigen-antibody reaction at the level of the epidermis and dermis. Epithelial cells – keratinocytes – are present in the epidermis. Lymphocytes and mast cells predominate in the dermis. The lymphoid population, consisting of T-helpers and T-killers, begins the process of sensitization of hereditarily allergic skin. Keratinocytes, acting as immunoregulators, immediately express class II MHC, which provide interaction between T-lymphocytes and macrophages during the immune response. An excess of antibodies destroys the skin, immune reactions become autoimmune.
Involvement in the process of the epidermis leads to a violation of its protective function, facilitates the penetration of the infectious origin into the dermis, which additionally sensitizes the skin, causes inflammation, damages the cells of the epidermis and dermis. Dermal and epithelial cells begin to produce cytokines and mediators that aggravate inflammation and sensitization of hypersensitive skin. The stage of exudation begins to prevail. The epidermis and dermis swell, the vessels of the dermis expand compensatorily. Clinically, this is manifested by erythema erythema, on the surface of which a polymorphic rash occurs.
Nummular eczema symptoms
A typical clinic of nummular eczema is characterized by the appearance of pink erythema on the background of unchanged skin. The element has an oval shape, resembles a nickel with a diameter of up to 3 cm with clear outlines, rises above the level of healthy skin. The appearance of the spot is accompanied by unbearable itching. The typical location of erythema is the skin of the extremities.
Almost immediately, the primary elements of the rash appear on the surface of the hyperemic spot: serous bulls, papules and nodules, reflecting the picture of true eczematous polymorphism. Itching causes patients to comb the inflamed surface, resulting in excoriation, covered with hemorrhagic crusts. At the same time, existing vesicles are opened, exposing erosive surfaces, a secondary infection joins. The remaining and newly added vesicles transform into pustules and also open up, forming erosions with purulent “fatty” crusts. Papules merge with each other, form plaques, along the perimeter of which a scalloped border of the remains of epithelial cells is clearly visible.
Rashes can spread to the trunk and buttock area. At the same time, the spilled bulls are opened, leaving open erosive surfaces oozing with serous fluid. The process of getting wet begins. Large erosions combine with each other, new deposits do not appear, the severity of the process gradually decreases. “Serous wells” dry up, thick yellow crusts form on their surface. If a staphylococcal infection interferes with the process, pus is released from under such crusts when pressed.
Unlike papules, plaques do not merge, but Staphylococcus can seed their perimeter with pustules. When such an element is traumatized, the process of “screening out” allergids consisting of secondary bullae, erythemas and nodules spreads. Secondary allergids combine to form wet erosions. With the further spread of the process and the aggravation of the severity of the inflammatory component, a deterioration in the general condition of the patient is observed. When the inflammatory phenomena subside, the skin dries up, cracks may appear on it. With frequent alternation of remissions and exacerbations, the transformation of nummular eczema into idiopathic eczema is possible.
Diagnosis of nummular eczema does not cause difficulties. The diagnosis is made by a dermatologist based on the clinical picture and anamnesis data. Taking into account the concomitant pathology, a standard laboratory examination is necessarily prescribed: UAC, OAM, biochemistry. Patients are consulted by a gastroenterologist, neurologist, allergist, endocrinologist.
Histopathology is atypical, morphological examination is carried out only for differential diagnosis. Complicated forms require enzyme immunoassay and allergological examination of blood serum for antibodies (specific IgE/IgG, general IgE). If infection is suspected, microbiological studies of epidermal smears are prescribed. In case of secondary infection, a culture study is carried out in order to identify the pathogen and determine its sensitivity to antibiotics. Differentiate nummular eczema with dermatitis, psoriasis, scabies and dermatomycosis.
Nummular eczema treatment
Nummular eczema is one of the most resistant to dermatitis therapy. The goal of treatment is to achieve stable remission. First of all, it is necessary to sanitize the foci of chronic infection, correct somatic pathology, normalize the work of the nervous, endocrine and digestive systems.
Sedatives are used to relieve stress (preferably based on natural components), tranquilizers, antidepressants, neuroleptics, herbal teas and herbal infusions are used. Desensitization of the body is carried out by intravenous injections of sodium and calcium salts. Desensitizing drugs are prescribed. In complicated cases, topical steroids (according to individual schemes in short courses), antibacterial drugs, detoxification and plasma substitutes are indicated. To prevent exacerbation, a course of histaglobulin is prescribed. Additionally, it is possible to use vitamin therapy, purified sulfur preparations and enzymes that improve the functioning of the digestive tract. For the prevention of dysbiosis, bifid-containing and lactose-containing agents are indicated.
The tactics of external treatment depends on the severity of the process. With pronounced wetness, hormonal aerosols, wet-drying dressings, anti-inflammatory lotions, antibacterial and zinc-based astringents give a good result. When the process subsides, ointments with topical steroids, antibacterial and antiseptic agents are used. Topical steroids are also effective for itching. Pyodermic layers are treated with antibacterial therapy internally and externally, depending on the prevalence of skin lesions. A good effect is given by UFO, PUVA therapy, photophoresis, ultraphonophoresis, UHF therapy, magneto-, ozone-, oxygen therapy, acupuncture, therapeutic mud, paraffin applications. In severe cases, hemosorption and plasmapheresis are connected.
Prevention consists in observing the diet with the exception of potential allergens. It is necessary to limit contacts with cosmetics and household chemicals, wear underwear made of natural fabrics, and be regularly monitored by a dermatologist. The prognosis depends on the severity of the pathology and is generally regarded as relatively favorable, taking into account the violation of the quality of life.