Toxicoderma

Toxicodermia is a toxic-allergic skin disease that occurs as a result of exposure to chemicals entering the body.

Causes and pathogenesis of toxicoderma

Toxicodermia occurs under the influence of various reasons:

• medicines, food products, industrial and household chemicals
• substances that have allergenic or toxic properties. These substances enter the body primarily through the digestive and respiratory tracts. Medicines can cause toxicoderma when administered intravenously, intramuscularly, subcutaneously, vaginally, or urethrally, as well as as a result of absorption through the skin when applied externally.

In the practice of a dermatologist, drug toxicoderma is most often encountered. Any drug can cause toxicoderma. But the most common cause of toxicoderma are antibiotics, sulfonamides, analgesics, barbiturates: they account for 50-60% of all drug toxicoderma. Toxicoderma can be caused by vitamin preparations, especially PP, C, group B.

Special attention should be paid to toxicoderma caused by corticosteroid and antihistamine drugs, which are registered in 7% of patients among drug toxicoderma. In second place are food toxicoderma, which constitutes 10-12% of all toxicoderma. The cause of food toxicoderma is the food product itself or a substance formed during long-term storage, culinary processing. Strict specificity of sensitization to a particular food product is noted, for example, to eggs from the same chicken, almonds from the same tree.

Toxicoderma 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), as they contain chromium, nickel, cobalt, molybdenum, which enter the blood and sensitize the body.

All of the above substances are incomplete antigens (haptens) and when entering the body they combine with proteins and turn into conjugates that have the properties of a complete antigen. Allergic reactions of various types develop through T- and B-cell immunity.

Histopathology

Histopathological changes in toxicoderma do not have pathognomonic features and are similar to changes in eczema. Histologically, lymphocytic vasculitis of small vessels of the upper part of the dermis is quite characteristic.

Symptoms of toxicoderma

The disease begins acutely or after several hours, more often on the 2-3 day after exposure to the causative agent. The clinical picture of toxicoderma is characterized by a large morphological diversity. Toxicoderma is characterized by the appearance of multiple symmetrically located rashes consisting of spotted, papular, nodular, vesicular, urticarial, bullous, pustular and papulopustular elements, accompanied by itching. At the same time, a combination of different types of rash is observed. Mucous membranes may be involved in the pathological process. A violation of the general condition of the patient is noted to varying degrees of severity.

Spotted toxicoderma in most cases proceeds favorably and often manifests itself in the form of erythematous spots, much less often - hemorrhagic (purpura) and pigmented. Erythematous spots can be punctate, roseolous, ring-shaped. Spotted rashes in toxicoderma are often edematous, peeling over the entire surface, can be limited or merge into extensive erythema up to universal erythroderma. When the center of the toxicoderma spot peels, it clinically resembles a spot of pink lichen. When the palms and soles are affected, complete rejection of the stratum corneum is observed.

Papular toxicoderma is characterized by the appearance of acute inflammatory hemispherical papules, which are limited or disseminated. The size of the papules often ranges from miliary to lenticular. Sometimes, when using anti-tuberculosis (PAS, streptomycin), antidiabetic and vitamin drugs, a rash in the form of flat polygonal papules resembling lichen planus is noted. In some cases, the papules merge into plaques. Subjectively, patients are bothered by itching of the skin. In a patient observed by the author, spotted and papular rashes appeared after repeated use of the analgesic citramone.

Nodular toxicoderma often occurs as a result of the action of sulfonamides, iodine, bromine, vaccines, grizsofulvin, cyclophosphamide, methotrexate. It manifests itself as the formation of painful acute inflammatory nodes, slightly elevated above the skin level and having fuzzy outlines.

Vesicular toxicoderma is characterized by the appearance of disseminated vesicles, which are surrounded by an erythematous rim. Rarely, vesicular toxicoderma is limited to damage only to the palms and soles and in these cases is manifested by dyshidrosis. In severe cases of toxicoderma, vesicular edematous erythroderma may develop: universal edematous erythema, blisters, abundant weeping, swelling of the face, extremities, large-plate peeling, impetiginous crusts. Secondary coccal flora often joins and pustules are formed.

Pustular toxicoderma in most cases develops after taking halogenated drugs: iodine, bromine, chlorine, fluorine. However, other drugs can also cause pustular toxicoderma. The morphological element is a pustule, which is sometimes located in the center of acute inflammatory hemispherical papules. The rash is often localized in areas of the skin 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 a hyperemic border (pemphigoid toxicoderma) or a localized rash in a limited area (fixed toxicoderma) are observed. Bullous rashes usually occur in severe toxicoderma and, as a rule, manifest as erythema multiforme exudative. Blisters of various sizes, often large, have rapid spherical growth, are prone to suppuration and have hemorrhagic contents. When the wall of the blisters is damaged, erosions are exposed, resembling elements of pemphigus vulgaris. In most cases, mucous membranes (mouth, eyes, genitals) are affected.

The general condition of most patients remains severe. Patients complain of general weakness, malaise, headache, dizziness; increased body temperature, increased ESR, leukocytosis, eosinophilia, moderate anemia, and severe pathology from the internal organs are noted. The most severe, widespread variants proceed according to the type of Stevens-Johnson syndrome or universal erythroderma, against the background of which large-plate peeling develops, and large blisters appear on certain areas of the skin, more often in the folds of the skin. Palmar-plantar keratoderma, alopecia, allergic vasculitis are symptoms of a severe form of toxicoderma.

In the practice of a dermatovenerologist, the most common form of toxicoderma is fixed toxicoderma, which often occurs after taking analgin, sulfonamides (biseptol), antibiotics, barbiturates and other drugs.

The disease manifests itself as one or more rounded bright red large spots 2-5 cm in diameter, which soon acquire a bluish tint, especially in the central part, and after the disappearance of the inflammatory phenomena, persistent pigmentation of a peculiar slate-brown color remains. Against the background of edematous spots, blisters and bubbles of various sizes may appear. With each repeated intake of the corresponding drug, the rash reappears in the same places, increasingly intensifying the pigmentation and gradually spreading to other areas of the skin. The favorite localization of fixed toxicoderma rashes is the mucous membrane of the mouth, genitals.

Toxicoderma usually occurs acutely. As the allergen is eliminated from the body, the rash resolves. Sometimes toxicoderma lasts for a long time even after the etiologic factor has ceased to act.

Differential diagnosis

Spotted toxicoderma should be distinguished from syphilis, pink lichen, spotted psoriasis; papular toxicoderma - from psoriasis, papular syphilis, lichen planus; bullous toxicoderma - from pemphigus, Lever's pemphigoid, etc.

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Treatment of toxicoderma

Treatment depends on the form of toxicoderma, the severity of the general condition and the prevalence of the process. First, it is necessary to eliminate the etiological factor that caused toxicoderma.

For the spotted form, it is sufficient to use antihistamines (tavegil, fenistil, analergin, diazolin, suprastin, etc.), hyposensitizing (calcium chloride or calcium gluconate, sodium thiosulfate) agents and external corticosteroid ointments.

In the case of papulopustular form, mucous membrane lesions and severe course, corticosteroids are prescribed orally or parenterally. The dose of hormones is determined depending on the severity of the process. In moderate cases, 40-50 mg of prednisolone per day is recommended, and in severe cases - 0.5-1 mg per kg of the patient's weight. In addition, diuretics and laxatives are prescribed. Detoxification therapy is carried out (rheopolyglucin, hemodez), according to indications - plasmapheresis, hemosorption.

Disinfectant solutions, aniline dyes, corticosteroid ointments, and aerosols are used externally.