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Toxicoderma
Last reviewed: 23.04.2024
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Toxicoderma - toxic and allergic skin diseases that occur as a result of exposure to chemicals that enter the body.
The causes and pathogenesis of toxicoderma
Toxicodermia occurs due to various causes:
- medicines, food products, industrial and domestic chemical
- substances that have allergenic or toxic properties. These substances enter the body mainly through the digestive and respiratory tract. Medicinal products can cause toxicodermy for intravenous, intramuscular, subcutaneous, vaginal, urethral administration, and also as a result of suction through the skin during external application.
In the practice of a dermatologist, the most common drug toxicoderm. Any medicine can cause toxicoderm. But most often the cause of toxicodermia are antibiotics, sulfonamides, analgesics, barbiturates: they account for 50-60% of all medicinal toxicoderms. Toxicoderma can be caused by vitamin preparations, especially PP, C, B group.
Particular attention should be paid to toxiccodermia caused by corticosteroid and antihistamine drugs, which are registered in 7% of patients among medicinal toxicoderms. On the second place there are food toxic cermets, which constitute 10-12% of all toxicoderm. The cause of food toxicodermia is the food itself or a substance formed during long-term storage, cooking. Strict specificity of sensitization to this or that food product, for example, to eggs from the same chicken, almonds from one tree is marked.
Toxicodermia can be caused not by the food substance itself, but by various impurities: preservatives, dyes, etc.
Toxicodermia can also be caused by various metals (dentures and metal structures used in orthopedics and traumatology), since they contain chromium, nickel, cobalt, molybdenum, which enter the bloodstream and sensitize the body.
All of the above substances are incomplete antigens (haptens) and when they enter the body they combine with proteins and turn into conjugates that have the property of a full-fledged antigen. Develop allergic reactions of various types through T- and B-cell immunity.
Histopathology
Histopathological changes in toxicogerminal pathognomonic features do not have and are similar to changes in eczema. Histologically, lymphocytic vasculitis of the small vessels of the upper dermis is typical.
Symptoms of toxicoderma
The disease begins acutely or after a few hours, more often 2-3 days after exposure to the causative agent. The clinical picture of toxicoderma is distinguished by a large morphological diversity. For toxicoderma, the appearance of multiple symmetrically located rashes, consisting of spotty, papular, nodular, vesicular, urtic, bullous, pustular and papular-pustular elements, accompanied by pruritus is characteristic. At the same time there is a combination of different types of rash. In the pathological process, mucous membranes may be involved. In varying degrees of severity, there is a violation of the general condition of the patient.
Spotted toxicosis in most cases occurs favorably and often manifests itself in the form of erythematous spots, much less often - hemorrhagic (purpura) and pigmented. Erythematous spots can be point, roseous, ring-shaped. Spotted rash with toxicodermia is often edematous, flakes all over the surface, can be limited or merge into extensive erythema, up to universal erythroderma. With peeling of the center of the toxicodermic spot, it clinically resembles a spot of pink lichen. With the defeat of the palms and soles, a complete rejection of the stratum corneum is observed.
For papular toxicoroderma, the appearance of acute-inflammatory hemispherical papules, which are of limited or disseminated nature, is characteristic. The size of papules often varies from miliary to lenticular. Sometimes with the use of anti-tuberculosis (PASC, streptomycin), antidiabetic and vitamin preparations, there is a rash in the form of flat polygonal papules reminiscent of red flat lichen. In some cases, papules merge into plaques. Subjective patients are concerned about the itching of the skin. Spotted and papular eruptions observed by the author of the patient appeared after repeated administration of the analgesic - citramone.
Knotty toxicosis often occurs as a result of the action of sulfonamides, preparations of iodine, bromine, vaccines, grisofulvin, cyclophosphamide, methotrexate. It manifests itself in the form of painful inflammatory knots, slightly elevated above the level of the skin and having vague outlines.
Vesicular toxiccodermia is characterized by the appearance of disseminated vesicles, which are surrounded by the erythematous whisk. Rarely, vesicular toxicosis is limited to the defeat of only the palms and soles and is manifested in these cases by dyshidrosis. In severe toxicodermia, vesicle-borne erythroderma can develop: universal edematous erythema, vesicles, profuse moccasin, edema of the face, limbs, large-scale scaling, impetiginous crusts. Often joins the secondary coccal flora and pustules are formed.
Pustular toxicoderma in most cases develops after taking halogen drugs: iodine, bromine, chlorine, fluorine. However, other medications may be the cause of the development of pustular toxicorodermia. The morphological element is a pustule, which is sometimes located in the center of the inflammatory hemispherical papules. The rash is often localized on skin areas rich in sebaceous glands (face, chest, upper back), since halogenated drugs are excreted from the body with sebum.
Bullous toxicoderma often occurs after taking analgesics, tranquilizers, antibiotics, sulfonamides. In bullous toxicoderma, widespread rashes of blisters surrounded by hyperemic border (pemphigoid toxicodermia) or localized rash (fixed toxicodermia) are noted. Bullous eruptions usually occur in severe form of toxicoderma and, as a rule, manifest themselves in the form of multiform erythema exudative. Bubbles of various sizes, often large, have a rapid growth, are prone to suppuration and have hemorrhagic contents. If the wall of the blisters is damaged, erosions appear resembling elements of vulgar pemphigus. In most cases, there is a lesion of the mucous membranes (mouth, eye, genitals).
The general condition in most patients remains severe. Patients complain of general weakness, malaise, headache, dizziness; there is an increase in body temperature, increased ESR, leukocytosis, eosinophilia, mild anemia, pronounced pagology from the internal organs. The most severe, common variants proceed according to the type of Stephen-Johnson syndrome or universal erythroderma, against which the development of large-scale scaling, and in some areas of the skin, more often in the folds of the skin, large bubbles appear. Palmar-plantar keratoderma, alopecia, allergic vasculitis are symptoms of severe form of toxicoderma.
In the practice of dermatovenereology, the most common form of toxicoderma is fixed toxicodermia, which often occurs after taking analgin, sulfonamides (biseptol), antibiotics, barbiturates and other drugs.
The disease is manifested by one or several round bright red large spots 2-5 cm in diameter, which soon acquire, especially in the central part, a cyanotic shade, and after the disappearance of inflammatory phenomena there remains a persistent pigmentation of a peculiar aspidic-brown color. Against the background of swollen spots, bubbles and blisters of various sizes may appear. At each repeated admission of the appropriate medication the rashes reappear at the same places, increasing the pigmentation more and gradually spreading to other parts of the skin. The preferred localization of eruptions of fixed toxicodermia is the mucous membrane of the mouth, the genital organs.
Toxicodermia usually proceeds acutely. As the allergen is removed from the body, the rash resolves. Sometimes toxicodermia is prolonged for a long time even after the termination of the etiological factor.
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Treatment of toxicoderma
Treatment depends on the form of toxicodermia, the severity of the general condition and the prevalence of the process. First, we must eliminate the etiologic factor that caused toxicoderm.
With spotted form, it is sufficient to use antihistamines (tavegil, fenistil, analegine, diazolin, suprastin, etc.), hyposensitizing (calcium chlorine or calcium gluconate, sodium thiosulfate) agents and external corticosteroid ointments.
With papulo-pustular form, lesions of mucous membranes and severe course, corticosteroids are administered orally or parenterally. The dose of hormones is determined depending on the severity of the process. In moderate cases recommend 40-50 mg of prednisolone per day, and for severe - 0.5-1 mg per kg of weight of the patient. In addition, diuretic, laxatives are prescribed. Carry out detoxication therapy (reopoliglyukin, gemodez), according to indications - plasmapheresis, hemosorption.
External use disinfectant solutions, aniline dyes, corticosteroid ointments, aerosols.