Toxicoderma is an acute toxic—allergic inflammatory lesion of the skin that occurs when exposed to an allergen that penetrates the skin hematogenically. Toxicoderma is characterized by a variety of morphological elements of the rash (papules, vesicles, spots, pustules, blisters) and may be accompanied by damage to the mucous membranes. The diagnosis of toxicoderma is based on its clinical picture, patient interview, laboratory tests and back-seeding, examination of the state of internal organs. Treatment of toxicoderma must necessarily include eliminating the effects of the factor that caused it, as well as carrying out detoxification and desensitizing measures. Antihistamines, glucocorticoids, local and symptomatic agents are prescribed.
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Most cases of toxicoderma (toxidermia) occur by the mechanism of an allergic reaction of an immediate type after acquired sensitization of the body or in connection with idiosyncrasy (congenital intolerance). At the same time, unlike allergic contact dermatitis, the causal factor of toxicoderma does not come into contact with the patient’s skin. Getting into the body in various ways, it is absorbed into the blood and reaches the skin through the blood vessels. Thus, with toxicoderma, the allergen’s effect on the skin occurs as if “from within” the body.
The most severe forms of toxicoderma include Stevens-Johnson syndrome and Lyell syndrome. The severity of clinical manifestations in toxicoderma depends on the antigenic activity and the amount of allergen, the frequency of its exposure, the predisposition of the body to allergic reactions: urticaria, atopic dermatitis, occupational eczema, solar dermatitis, allergic rhinitis, bronchial asthma, etc.
A chemical that is a causal factor in the development can enter the body in various ways: by inhalation (inhalation), with food (alimentary), by drug injections or by absorption after application to the skin.
Due to the occurrence of modern dermatology, there are 4 etiological groups of toxicoderma: medicinal, alimentary, occupational and autotoxic. Drug-induced toxicoderma develops as a result of taking medications and occurs in the vast majority of cases. It can be caused by sulfonamides (sulfadimesin, norsulfazole), antibiotics (biomycin, penicillin, neomycin, streptomycin), barbiturates, B vitamins, serums, etc.
Alimentary toxicoderma can be associated both with the use of the food product itself and with various additives included in its composition (dyes, baking powder, preservatives). In terms of prevalence, it is in second place after drug-induced toxicoderma. Occupational toxicoderma is caused by activities related to various chemical compounds. The most active antigens are substances containing a benzene ring with an amino group or chlorine.
Autotoxic toxicoderma occurs when exposed to allergens and toxins formed in the body as a result of metabolic disorders. This can be observed in chronic diseases of the gastrointestinal tract (gastritis, gastric ulcer, hepatitis, pancreatitis, peptic ulcer) and kidneys (pyelonephritis, glomerulonephritis, hydronephrosis, chronic renal failure), malignant processes (lung cancer, kidney adenocarcinoma, colon cancer), etc. Autotoxic toxicoderma can take a chronic course.
The clinical picture is characterized by a large variety of forms. Skin rashes can be papular, vesicular, erythematous, urticary and papullo-vesicular in nature. The lesion of the oral mucosa and lips can have a vesicoerosive, catarrhal or hemorrhagic character. In some cases, toxicoderma affects not only the mucous membrane of the mouth, but also the mucous membrane of the genitals, urethra, anal rectum. Rashes on the skin and mucous membranes with toxicoderma are usually accompanied by various subjective sensations of the patient: tension, burning, soreness, itching of the skin in the lesions.
For the same provoking substance, different people can develop different morphological variants of toxicoderma. On the other hand, a number of substances cause the development of toxicoderma with a clinic characteristic of them. For example, toxicoderma associated with the intake of iodine salts is manifested by so-called “iodine acne” – soft juicy plaques rising above the surrounding skin and covered with crusts, under which the surface with purulent discharge is exposed.
Toxicoderma may be accompanied by the development of general symptoms: malaise, fever, periodic arthralgia. Pronounced discomfort and itching in the area of rashes can cause disorders in the nervous system with the appearance of increased irritability, emotional lability, sleep disorders. It is possible to add symptoms indicating toxic-allergic damage to the kidneys and / or liver. Vascular wall damage is manifested by hemorrhagic syndrome.
Depending on the prevalence of clinical manifestations, a fixed and widespread form of toxicoderma is distinguished. The fixed form of toxicoderma in most cases is manifested by the appearance on the skin of several erythematous spots of a rounded shape with a diameter of 2-3 cm. Over time, the spots can acquire a brownish color, bubbles form in the middle of some of them. With the elimination of further allergen entry into the body, fixed toxicoderma takes place within 10 days. Repeated exposure to the provoking factor leads to the appearance of rashes in the same places and on new areas of the skin.
Common toxicoderma is characterized by a multiple nature of rashes, often accompanied by damage to the mucous membranes and internal organs with the development of myocarditis, hepatitis, kidney failure. It is characterized by chills, fever, diarrhea and vomiting, severe condition of patients.
The basis for the diagnosis is its characteristic clinical picture. The collection of anamnesis is aimed at identifying the causal factor of the disease. With toxicoderma, setting skin allergic tests often does not give results. The use of provocative samples with a suspected allergen is associated with the risk of developing a severe form of toxicoderma. Therefore, only in vitro tests can be carried out to determine the provoking substance: the reaction of basophil degranulation, blast transformation of lymphocytes, agglomeration of leukocytes, etc.
To exclude the infectious nature of the rashes, the discharge is seeded, skin scraping for pathogenic fungi, smear microscopy for pale treponema, and an RPR test for syphilis. With a common form of toxicoderma, a coagulogram and a study of the main biochemical parameters in the analysis of blood and urine are carried out. If internal organs are affected, consultation with a cardiologist, gastroenterologist, nephrologist may be required; ECG, Echo-EG, ultrasound of the abdominal cavity and liver, ultrasound or CT of the kidneys.
The differential diagnosis of toxicoderma is carried out with infectious diseases accompanied by a rash (scarlet fever, rubella, measles), pink Zhiber’s lichen, secondary syphilis, lichen planus, urticaria, systemic lupus erythematosus, multiform exudative erythema, allergic vasculitis.
Of paramount importance in the treatment is the prevention of further exposure to the substance that caused it. For this purpose, with alimentary and autotoxic variants of toxicoderma, laxatives and diuretics, cleansing enemas, intravenous desensitizing solutions of sodium thiosulfate and calcium chloride, antihistamines (loratadine, etc.) are used. With toxicoderma caused by the use of sulfonamide preparations, the introduction of sodium thiosulfate is contraindicated! Patients with severe form of toxicoderma are shown extracorporeal methods of blood purification: hemosorption, membrane plasmophoresis, cascade plasma filtration, cryoaferesis, etc. Their treatment is carried out only in a hospital and consists in the appointment of glucocorticosteroids, intravenous infusions of saline or dextran, plasma or blood albumin, preventive antibiotic therapy, maintenance of kidney and liver function.
Local therapy of skin lesions depends on the morphological features of toxicoderma. Powders or water-shaken suspensions with zinc oxide, glucocorticosteroid ointments, anti-inflammatory and antipruritic drugs for topical use are used. The wet areas are treated with aniline dyes, astringents and disinfectants.