Types of allergic skin diseases and principles of treatment
The common clinical allergic skin diseases are zoonoses, contact dermatitis, eczema, drug rash, atopic dermatitis, auto-sensitivity dermatitis, papular zoonoses and so on. The clinical characteristics and treatment principles of these diseases are described as follows.
1. Urticaria
1.1, clinical features.
Urticaria is a limited edema reaction due to reactive dilation and increased permeability of small blood vessels in the skin and mucous membranes, mainly manifested as red or pale spasmodic itchy wind masses with clear edges. The etiology of measles is complex, and most patients cannot find the exact allergen. The most common allergens are food, including fish, shrimp, crab, eggs, fruits (strawberries, peaches, grapes and cherries, etc.), meat, garlic, alcohol, etc. Other factors include drugs (such as penicillin, serum products, various vaccines, sulfonamides), infectious factors (including viruses, bacteria, fungi, parasites, etc.), physical factors, animal and plant factors, psychological factors, visceral and systemic diseases, etc. can be pathogenic factors. In terms of pathogenesis, type I allergic reactions predominate, with very few type II and III allergic reactions or non-allergic mechanisms.
Urticaria is the most common clinical allergic skin disease, occurring at least once in the lifetime of 15-20% of the population. According to the course of the disease, it is divided into two categories: acute urticaria usually heals within days or even hours after treatment, while chronic urticaria is recurrent for more than 3 months or even decades. The typical lesion is a red or pale white bruise of varying size, round, oval or irregular in shape, isolated, scattered or fused into patches, usually lasting no more than 24 hours, but new bruises occur one after another, with intense itching of the lesions. Acute urticaria can be accompanied by panic, irritability, nausea, vomiting, and even lower blood _ pressure and other allergic body gram-like symptoms, part of the gastrointestinal mucous membrane edema abdominal pain, when severe, rather like acute abdomen, and can appear diarrhea, if the involvement of the trachea, larynx mucosa, respiratory distress, or even asphyxia. Chronic urticaria is generally lighter in systemic symptoms, with more and less wind clusters, and recurrent attacks, often for months or years. There may be regularity, such as aggravation in the morning or before bedtime or seasonal attacks. Most patients cannot find the cause themselves.
In addition, there are several special types of zoonotic rash: 1, skin scratching: also known as artificial urticaria. It is caused by scratching or scratching the skin with a hard object for 5-15 minutes, and then there are striated elevations along the scratch, accompanied by itching, which will soon subside. 2. Cold urticaria: There are two types of urticaria, familial and acquired, the latter being more common. After contact with cold wind, cold water or cold objects, the exposed or contacted area produces wind or patchy edema. 3, cholinergic urticaria: mostly seen in young people. Due to exercise, heat, emotional stress, eating hot drinks or ethanol drinks to make the deep body temperature rise, prompting the action of acetylcholine on mast cells and occur. It is a rare case of solar urticaria, caused by medium-wave and long-wave ultraviolet light or visible light, which occurs on exposed skin with itching and stinging sensation. 6, angioedema: is a kind of limited edema occurring in the more lax parts of the subcutaneous tissue and mucous membranes, divided into hereditary and acquired, the latter is common, often accompanied by other genetic allergic diseases. It occurs mainly on the eyelids, lips, mouth, external genitalia, and hands and feet. The lesions are sudden, limited swelling with indistinct borders, normal or light red skin color, and shiny surface, which can gradually subside in 1-3 days. If it occurs in the laryngeal mucosa, it may cause respiratory difficulty and even death by asphyxiation.
1.2.Treatment principles
Acute urticaria can be treated with various antihistamines such as paracetamol, ketotifen, cetirizine, clostebol, etc. Usually 2-3 antihistamines are used in combination, and 25% glucose 40m1 + 10% calcium gluconate l0ml can also be considered for slow intravenous infusion. With abdominal pain, anticholinergics can be given. Such as pramipexine, atropine, 654- 2, etc.; serious condition or with body grams or laryngeal edema and respiratory distress, should be immediately subcutaneous injection of 0. 1 % “epinephrine 0. 5m1. at the same time oxygenation. And give dexamethasone 5-10 mg into 5%-10% glucose solution 250~500m1 intravenously. If necessary, repeat epinephrine 0.5m1 after 15 minutes. To prevent recurrence, a good foundation should be laid.
Chronic urticaria should first be identified as a suspected allergen and avoidance measures should be taken. Such as eliminating suspected allergic foods from the diet. Eliminate allergens from the environment. The dose of antihistamines can be adjusted according to the attack. Short-term antihistamines can be combined with two or three drugs. For long-term use, multiple antihistamines can be used alternately. For intractable urticaria. It can also be combined with H1 receptor antagonists such as nitisin. Special types of urticaria often use drugs that have both anti-5-hydroxytryptamine and anticholinergic effects. For example, hydroxyzine, dechlorothiazide has a better effect on physical urticaria, and cycloheximide has a more prominent effect on cold urticaria. Cholinergic urticaria can be used atropine or 654- 2, etc. Topical medication can be used in summer to relieve itching, such as stovepipe lotion. In winter, the choice of emulsion with anti-itch effect. Such as Benadryl cream, etc.
2. contact dermatitis
2. 1. Clinical features.
Contact dermatitis is an acute or chronic inflammatory reaction that occurs in the skin and mucous membrane contact areas due to contact with a substance. The causative factors can be divided into two major categories: animal, plant and chemical. Such as animal fur, caterpillars, toxins of cryptomeria, lacquer tree, pyrethrum, metal products, chemical materials, certain topical drugs, cosmetics, pesticides, rubber, plastics, etc.. If the exposure is allergenic in nature, the disease usually develops after 4 days of initial exposure and within 48 hours if re-exposed. If it is a primary irritant. The onset is usually within minutes to hours. The lesions occur at the site of contact. They appear as well-defined erythema, papules, or papules. In severe cases, the redness and swelling are obvious and blisters and blisters appear. Even erosion and ulceration. However, the edema is obvious in loose tissues such as eyelids and foreskin, and the boundaries are not clear. If the exposure is to gas or dust, the lesions are diffuse and without clear boundaries. The affected area is often itchy and painful, and a few severe patients may have systemic reactions. Contact dermatitis can be cured within 1-2 weeks after removal of the irritant and active treatment. After healing, a patch test can be performed to detect the allergenic substance. Clinically, it needs to be differentiated from eczema. The latter often has no clear history of exposure, and the lesions are polymorphic and often occur symmetrically. The borders are diffuse and tend to be chronic. It is prone to recurrence. The cause is often difficult to find.
2. 2. Treatment principles
Find the cause of the disease, get rid of the contact, and actively treat the symptoms. Local drug treatment depends on the affected lesions. In the acute stage, the redness and swelling are obvious with the use of topical Furfurylite lotion, and when there is much exudation, cold wet compresses with 3% boric acid solution. In the subacute stage, a small amount of exudation is treated with wet dressing or glucocorticoid paste, zinc oxide oil, and glucocorticoid cream when there is no exudation. Antibiotics can be added when there is infection. Systemic treatment should be selected according to the severity of the disease oral antihistamines, glucocorticoids can be added if necessary.
3, eczema
3.1, clinical features.
Eczema is caused by a variety of internal and external factors of superficial dermis and epidermal allergic inflammation. The etiology is complex, and it is generally believed that a variety of internal and external factors interact to cause eczema-like lesions. Internal factors such as chronic infectious lesions, endocrine metabolic changes, blood circulation disorders, psychological factors, genetic factors, etc. External factors such as certain allergenic foods, inhalants, sunlight, hot and dry environments, and chemicals. The susceptibility and tolerance of patients to various exogenous factors are often related to genetic factors and can change with age and environment.
Acute eczema has a rapid onset, initially limited to one area, and quickly develops into symmetry or even generalization. The damage is polymorphic, with clusters of erythema, papules, and blisters in patches with diffuse, indistinct margins. At a certain stage, a certain form of lesion is predominant, and scratching often causes secondary changes such as vesicles, exudate, pus, and nodules. The itching of the lesions is intense and can subside in a few weeks, but often relapses with a tendency to become subacute or chronic.
Subacute eczema is formed during the reduction or remission of acute eczema, or is caused by the aggravation of chronic eczema. The lesions mainly have papules, papules and small vesicular exudate, may have knot infatuation or flaking. Chronic eczema often evolves from acute eczema, and a few develop a chronic process. The lesions have clear borders, significant skin thickening, and some mossy changes. It is often found on the face, behind the ears, scrotum, vulva, anus, calves and dorsum of the feet. Eczema should be distinguished from contact dermatitis, neurodermatitis, etc.
3. 2. Treatment principles
To remove all kinds of suspected causative factors, such as the onset of avoid spicy food and alcohol, strong tea, coffee. Avoid excessive scalding, eliminate chronic lesions in the body and other systemic disorders. Topical treatment is based on the stage of the disease and the morphological characteristics of the lesions, according to the principles of topical drug application to select the appropriate formulations and drugs (see the treatment of contact dermatitis). Internal drug therapy to anti-inflammatory, antipruritic purposes, including the application of various antihistamines, etc., in addition to itching caused by mental irritability patients can take sedatives such as Valium. In the acute stage, calcium, vitamin C and sodium thiosulfate can be used for sedation, and for those with combined infections, antibiotics can be added.
4. Drug rash
4.1, clinical features.
Drug rash, also known as drug dermatitis, is an inflammatory rash on the skin mucosa caused by drugs entering the body through internal administration, injection, inhalation, enema, suppositories or even through broken skin, etc. The pathogenesis of drug rash is mostly related to metabolic reactions. The etiology includes: 1. Individual factors: including genetic factors, allergies, defects in certain enzymes, the influence of the pathological or physiological state of the body. The same body at different times, the sensitivity to drugs also varies. 2, drug factors: clinical susceptibility to drug rash drugs are antibiotics (such as penicillin, sulfonamides, dysentery, streptomycin, tetracycline, etc.), antipyretic and analgesic drugs (such as aspirin, paracetamol, etc.), sedative-hypnotic and anti-seizure drugs (such as phenobarbital, phenytoin sodium, sleeper, etc.), heterologous serum preparations and vaccines (such as tetanus antitoxin, rabies vaccine, etc.). The clinical manifestations of drug rash are varied.
The clinical manifestations of drug rash are varied, and a drug can cause different lesions and symptoms in different patients, or in the same patient at different times; and the same symptoms and lesions can often be induced by different drugs. Drug rash has a certain incubation period, the first drug rash in 4-20 days, repeated use of drugs, the body is in a sensitized state, often within 24 hours. The rash has various forms, including fixed erythema, measles-like erythema, scarlet fever-like erythema, urticaria-like, erythema multiforme-like, pityriasis rosea-like and more serious herpetic epidermolysis bullosa or exfoliative dermatitis type. The lesions are almost always symmetrical and generalized, except for the fixed erythematous and urticaria-like manifestations. Severe drug rashes such as erythema multiforme, herpetic epidermolysis bullosa and exfoliative dermatitis may be associated with mucosal loss in the oral cavity. Some cases are accompanied by systemic symptoms such as fever and other systemic symptoms, such as bronchospasm when the respiratory tract is involved; vomiting and diarrhea when the digestive tract is involved; and urinary tract when the urinary tract is involved, such as urinary urgency, urinary incontinence or urinary retention. The heart, liver, IIX and other organs may also be damaged.
4. 2. Treatment principles
1, remove the cause: stop all suspicious drugs, take measures to accelerate the excretion of drugs, if necessary, give laxatives and diuretics.
2, topical drugs: lesions can be used furnace twenty stone lotion and glucocorticoid cream. For red and swollen lesions with exudation, use 3% boric acid solution or saline wet dressing, for severe drug rashes such as herpetic epidermolysis bullosa, its vesicles and alternate with exposed dry and traumatic wet dressing. The company’s main business is to provide a wide range of products and services to its customers. In severe drug rash, glucocorticosteroids should be used in sufficient quantity at an early stage, and dexamethasone 10-20mg/day should be given as an IV, and the disease should be controlled within 3-5 days, otherwise the glucocorticosteroid dosage should be increased by 1/3-1/2 on the basis of the original dosage, and the dosage can be gradually reduced after the rash turns lighter in color, no new rash occurs, and the symptoms are relieved. In addition, for severe drug rash, attention should be paid to the prevention and treatment of infection and complications, strengthening supportive therapy and enhancing care.
5, atopic dermatitis
5.1. Clinical features.
Atopic dermatitis, also known as “atopic dermatitis” and “hereditary atopic dermatitis”, is a skin disease associated with hereditary allergic qualities. The pathogenesis is not well understood, but may be due to the interaction of genetic factors, immune factors and environmental factors. It is characterized clinically by itchy skin spasms, a polymorphic rash with a tendency to ooze, varying in performance at different ages, and patients often have asthma, allergic rhinitis, and increased serum IgE.
Clinical classification into two phases: 1. Infantile phase: previously also known as infantile eczema, the onset is often 1-6 months after birth. The lesions are papules, blisters, pustules, vesicles, slurries or pus, crusts and even bleeding, but the vesicular type is more frequent, sometimes mild and sometimes severe, with pronounced itching. The skin lesions are often aggravated when inoculated or teething, and generally gradually improve and heal within 2 years of age. 2, childhood: mostly in infants and children eczema remission after 1 or 2 years, since about 4 years of age began to recur, a few since infancy continue to occur, lesions involving the extensor or flexor side of the limbs, often limited to the N fossa, elbow fossa, etc., followed by the eyelids, face, lesions flushed, exudation phenomenon is lighter than in infancy, papules dark red, accompanied by scratching and other skin The lesions are flushed, less exudative than in infancy, with dark red papules, accompanied by scratching and other skin damage, and over time the rash is thickened and mossy, and itching is still intense during this period. 3. Adult phase: Disseminated neurodermatitis, with rashes in the elbow fossa, N fossa, extremities, neck and eyelids, and can spread throughout the body. Dry and rough, with significant mossy changes, still itchy.
2 .Treatment principles.
Early detection of allergens and prevention can avoid the development of the disease, so should try to avoid suspicious food, inhalants and contacts, breastfeeding infants mothers should avoid spicy, seafood, etc.. The treatment should be a combination of systemic and topical medication, and the principles of treatment are the same as those for acute, subacute and chronic eczema. Local cleaning should be done with cool warm water or saline, avoid using hot water, and attention should be paid to prevent secondary infection.
6, papular urticaria
6. 1. Clinical features.
It is a common papular skin disease of children and adolescents, may be certain insects such as bedbugs, fleas, mosquitoes, mites bite with allergic body and the onset of the disease, may also be related to intestinal parasites, eating certain foods. The lesions are fusiform or round red papules, 1-2 cm in size, often with central papules, blisters or blisters, variable in number, occurring in batches, distributed in strips or clusters. The rash usually fades after 1 week, but can recur if the cause is not removed. Often secondary infections occur due to repeated scratching.
6. 2. Treatment principles.
The cause should be actively sought and removed, in general, a variety of antihistamines, etc., can be used topically with glyburide lotion, with vesicles, exudate with 3% boric acid solution wet compress, secondary infection can be added antibiotics.