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Urticaria and angioedema are also called rubella and angioedema, and they can occur separately or simultaneously; they appear as non-finger skin edema and sometimes involve the upper respiratory or gastrointestinal mucosa. Urticaria only damages the surface layer of the skin, manifested as a rash of red masses at the edges and pale in the center, sometimes fused into giant wind masses. Vascular edema affects the deep layers of the skin (including subcutaneous tissue), and localized edema is easily identified. These manifestations can appear and disappear quickly.

Basic Information

nickname
Rubella mass and angioedema
Visiting department
dermatology
Common locations
skin
Common symptoms
Itchy skin often appears first, followed by wind masses, bright red or pale

Causes of urticaria and angioedema

Urticaria
The cause of urticaria is very complex, and about three-quarters of patients cannot find the cause, especially chronic urticaria. Common causes are: food and food additives; inhalants; infections; drugs; physical factors such as mechanical stimuli, cold and heat, sunlight; insect bites; mental and endocrine changes; genetic factors.
Angioedema
The cause of angioedema is similar to urticaria. Common causes are: food and food additives; inhalants; infections; drugs; physical factors such as mechanical stimuli, cold and heat, sunlight; . Hereditary angioedema is caused by decreased and inactive levels of C1 esterase inhibitors in the blood and tissues.

Clinical manifestations of urticaria and angioedema

Urticaria
The basic damage is the appearance of wind masses on the skin. Skin itching often occurs first, followed by wind masses, bright red or pale, skin color, and a few patients have edema erythema. Wind masses vary in size and shape, and the onset time is uncertain. The wind mass gradually spread and merged into a piece. Due to the edema of the dermal papilla, the epidermal hair follicle mouth was seen to sag downward. The wind mass lasts for several minutes to several hours, and a few can be extended to a few days to fade without leaving traces. The rash occurs repeatedly in batches and is more common in the evening. Wind masses are common and limited. Angioedema is sometimes combined, and occasionally bullae are formed on the surface of the wind mass.
Some patients may be accompanied by nausea, vomiting, headache, bloating, abdominal pain, diarrhea, and severe patients may also have systemic symptoms such as chest tightness, discomfort, pale skin, accelerated heart rate, weak pulse, decreased blood pressure, and shortness of breath.
Those who have cured the disease in a short time are called acute urticaria. Chronic urticaria is called repeated episodes of at least twice a week for more than 6 consecutive weeks. In addition to the common urticaria mentioned above, there are the following special types of urticaria.
(1) Skin scratches: Urticaria / artificial urticaria patients have weaker mechanical stimuli that cause physiological responses to increase and produce wind masses on the skin. After the patient scratched, or a tight wind or garter appeared on the tight wind, itching.
(2) Delayed skin scratches. Skin scratches show wind masses and erythema 6 to 8 hours after stimulation, and wind masses last for 24 to 48 hours. There are more than one delayed skin lesions, which form small sections or spots along the scratch, the damage is deeper or wider, and even spreads to the sides. Local fever and tenderness.
(3) Delayed stress urticaria rash occurs 4 to 6 hours after local skin compression, and usually lasts 8 to 12 hours. It is manifested as local deep painful swelling, which may be accompanied by chills, fever, headache, joint pain, general malaise, and mild increase in white blood cell count. Large-scale local swelling is similar to angioedema, which easily occurs in palmar plantar and buttocks with a 24-hour incubation period.
(4) The cholinergic urticaria rash is characterized by the occurrence of generalized small wind masses of 1 to 3 mm other than palms and palms, which are obvious around them. Satellite-shaped wind masses are sometimes seen, and only redness or smallness without redness is visible. Sparse wind mass. Sometimes the only symptom is itching without wind. The damage lasts for 30 to 90 minutes, or for hours. Most occur during or shortly after exercise, accompanied by itching, tingling, burning, heat or skin irritation, and can also be induced by heat or emotional stress.
(5) Cold urticaria can be divided into familial and acquired. The former is relatively rare and is autosomal dominant. A delayed reaction occurs half an hour to four hours after being cold. The rash is a non-itchy wind mass with a bluish-purple center surrounded by pale halo. The rash lasts for 24 to 48 hours with a burning sensation and accompanied by fever, Systemic symptoms such as joint pain and increased white blood cell count. The latter is more common. Patients often occur when the temperature drops sharply or after contact with cold water. Within a few minutes, itchy edema and wind masses occur locally, which are more common on the face and hands, but can also be affected in other severe parts. Headaches, flushing of the skin, hypotension, and even fainting can occur.
(6) After a few minutes of solar urticaria exposure to the skin, itching, erythema, and wind masses appear locally. The wind mass subsided after about 1 to several hours. A rash can be accompanied by chills, fatigue, syncope, and intestinal cramps. These symptoms disappear within hours.
(7) Contact urticaria is characterized by wind masses and erythema when the skin contacts certain allergens. Can be divided into two types of immune mechanisms and non-immune mechanisms. Non-immunity is caused by primary stimulants directly acting on mast cells to release histamine and other substances. Almost all contacts are sick and do not require substance sensitization. The immunity is a type I allergy, which can detect specific IgE antibodies.
In addition, there are less common types of urticaria such as hot urticaria, sports urticaria, tremor urticaria, waterborne urticaria, adrenergic urticaria, and current urticaria.
Angioedema
It is an acute localized edema, which mostly occurs in loose tissues, such as eyelids, lips, foreskin and extremities, scalp, ears, and oral mucosa, tongue, and throat. The skin is tense and shiny at the skin, the state is not obvious, it is light red or pale, the texture is soft, and it is non-concave edema. The patient was consciously not itchy or mild, or had numbness. The swelling subsided after 2 to 3 days, or lasted longer, leaving no trace after subsiding. Single or repeated in the same area, often with urticaria. When vascular edema occurs in the laryngeal mucosa, there may be tightness, discomfort in the throat, hoarseness, difficulty breathing, and even suffocation. Generally no systemic symptoms.

Urticaria and angioedema examination

Increased blood eosinophils can increase IgE. C1 esterase inhibitor-deficient patients with angioedema lacking C1INH or only inactive C1INH can also be accompanied by abnormal complement component (C1, C4, C2) levels in the anterior segment of the complement system.

Diagnosis of urticaria and angioedema

Urticaria
The disease can be diagnosed based on the clinical appearance of wind-like rash. The diagnosis is generally not difficult, but the causes of urticaria are more complicated. It is often difficult to determine the cause of urticaria. Therefore, detailed medical history, detailed physical examination, and related laboratory tests must be used to make the urticaria as clear as possible. the reason.
Angioedema
The diagnosis of neuroedema is considered based on the localized non-concave edema, which is reddish or pale, and the swelling subsides after 2 to 3 days without leaving any traces. After the diagnosis is established, relevant pathogenic factors should be found.

Urticaria and Angioedema Treatment

Urticaria
(1) The general treatment varies due to the causes of urticaria, and the treatment effect is also different. Specific treatment measures are as follows:
1) Remove the cause: Every patient should try to find the cause of the attack and avoid it. If it is caused by infection, the infected lesion should be actively treated. People with drug allergies should stop using allergic drugs; those with food allergies should stop eating this food after finding out allergic foods.
2) Avoid predisposing factors such as cold urticaria should keep warm, acetylcholine urticaria reduces exercise, sweating and mood swings, and contact urticaria reduces the chance of exposure.
(2) Drug treatment
1) Antihistamines H receptor antagonists have strong antihistamine and other inflammatory mediator effects, and have a good effect in treating all types of urticaria. Commonly used H 1 receptor antagonists include diphenhydramine, cyproheptadine, chlorpheniramine, atorvastatin, cetirizine, mizolastine, loratadine, ebastine, azetamine Ting, desloratadine, etc .; when the treatment alone is not effective, two different types of H 1 receptor antagonists can be used in combination or combined with H 2 receptor antagonists. The commonly used H 2 receptor antagonists are cimetidine Titin, ranitidine, famotidine, etc. It is effective for acute, chronic urticaria and cold urticaria. The dose varies from person to person. Doxepin is a tricyclic antidepressant, which has a better effect on chronic urticaria and has less adverse reactions. For patients with urticaria who are not effective with traditional antihistamines, doxepin is a better choice.
2) Drugs that inhibit the degranulation of mast cells and reduce the release of histamine. Metaisoproterenol sulfate is a 2 adrenergic receptor enhancer, which can increase the concentration of cAMP in the body, thereby inhibiting the degranulation of mast cells. Ketotiol inhibits mast cell degranulation by increasing the concentration of cAMP in the body, and prevents the release of inflammatory mediators (such as histamine, slow-acting substances, etc.). Its inhibitory effect is stronger and faster than sodium cromoglycate, and can be taken orally. Sodium cromoglycate can block antigen-antibody binding and inhibit the release of inflammatory mediators. If combined with glucocorticoids, the dosage of the latter can be reduced and the efficacy can be enhanced. Tranilast can reduce the release of histamine by stabilizing the mast cell membrane.
3) Glucocorticoids is a second-line treatment for urticaria. It is generally used when severe acute urticaria, urticaria vasculitis, pressure urticaria is ineffective against antihistamines, or when chronic urticaria is severely stimulated. Oral, should avoid long-term application. The commonly used drugs are as follows: prednisone; triamcinolone; dexamethasone; debao song. In an emergency, hydrocortisone, dexamethasone, or methylprednisolone is used for intravenous drip.
4) Immunosuppressive agents: When patients with chronic urticaria have an autoimmune foundation and the condition is repeated, and the above treatments cannot achieve satisfactory results, immunosuppressive agents can be applied. Cyclosporine has good curative effects, azathioprine, cyclophosphamide, and alpha Both methotrexate and immunoglobulin can be tried. Tripterygium wilfordii also has a certain effect. Due to the high incidence of immunosuppressive side effects, it is generally not recommended for the treatment of urticaria.
In addition, drugs that reduce vascular permeability, such as vitamin C, vitamin P, and calcium, are often used in combination with antihistamines. Caused by infectious factors, you can choose appropriate antibiotic treatment.
Angioedema
Find the cause and remove it first.
Anti-histamine receptor H 1 antagonists are often used for symptomatic treatment, and anti-histamine receptor H 2 antagonists such as cimetidine (methimid) or Lantidin, sometimes satisfactory results can be obtained. Ketone bodies can also be used in combination.
Sympathomimetic drugs are mainly used for acute urticaria and / or neuroedema, especially in patients with laryngeal edema. 0.1% epinephrine is injected subcutaneously, and severe acute allergic reactions can be injected every 20 to 30 minutes. At the same time, glucocorticosteroids were given intravenously and aminophylline was given orally or intravenously. For the edema of the respiratory tract, especially the larynx, a tracheotomy or intubation should be performed if necessary to keep the respiratory tract open.
Attenuated androgenic male hormones such as danazol, stanazol (Stanozolol), oxymetholone (Anadrolone) and other treatments for congenital C1INH deficiency, can correct their biochemical defects and have the effect of preventing seizures, but cannot be used in children and For pregnant women, the latter can only be treated with anti-plasmin drugs such as 6-aminocaproic acid, which can sometimes control spontaneous attacks.

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