Urticaria is a common allergic disease in dermatology, commonly known as rash lumps, wind clumps, wind bumps, etc. It is a restrictive edematous reaction due to the dilation and increased permeability of small blood vessels in the skin and mucous membranes. Fifteen to 20 percent of people have at least one episode of urticaria in their lifetime. It is caused by a variety of factors that rapidly cause temporary, congestive, exudative, and puffy lesions and plaques on the skin and mucous membranes, accompanied by intense itching. The lesions can occur or fade rapidly, leaving no trace of skin. In mild cases, the lesions may be accompanied by itchiness and itching, but in severe cases, they may be accompanied by fever, abdominal pain, diarrhea, laryngeal edema, respiratory distress, hypotension, shock, and other systemic symptoms. Such symptoms should be disposed of promptly at a hospital.
The causes of urticaria are quite complex, and we can only treat urticaria better if we find the cause and remove it. About 3/4 of patients cannot find the cause, especially chronic urticaria.
1, drugs Many drugs are often prone to cause this disease, especially penicillin. The reaction is usually caused by the production of IgE antibodies to the drug first, or the formation of an antigen-antibody complex. However, some drugs are themselves histamine releasing agents, such as morphine, codeine, dulcolax, cylindrical arrow toxin, polymyxin, vitamin B1, etc.
2, food and food additives Mainly animal protein foods, such as fish, shrimp, crab, meat, eggs (or have been spoiled); plant foods such as eggplant, bamboo shoots, spinach, apples and plums and other vegetables and fruits. Adding food pigments, condiments, preservatives, natural or synthetic substances in food including yeast, salicylic acid, citric acid, azo-like tetrazolium and benzoic acid derivatives can also cause the disease.
3, inhalants such as pollen, animal dander, feathers, fungal spores, dust, formaldehyde, acrolein, castor powder, cosmetics, pyrethrum, gas and other inhalation can occur urticaria, and these patients are often accompanied by respiratory symptoms.
4.Infection Various infection factors can cause this disease, including: ① bacterial infection, such as acute tonsillitis, pharyngitis, impetigo, boils, cholecystitis, appendicitis, pancreatitis, paranasal sinusitis, etc. (ii) viruses, such as the prodromal phase or jaundice phase of viral hepatitis is common. Coxsackie virus infection and infectious mononucleosis are directly related to the occurrence of urticaria. Parasites, such as Plasmodium, Ascaris, hookworms, pinworms, ameba, trichinella, Giardia lamblia and other intestinal parasites, as well as schistosomes, filarial worms and trichinella.
5, insect bites Bees, wasps and other insect bites caused by metabolic reactions, wind mass is a prominent symptom. Caterpillars, beetles, bag spiders and moths and other hair scales into the skin can also occur.
6, physical factors such as mechanical stimulation, cold, heat, sunlight, etc.
7, mental factors and endocrine changes such as mental tension, emotional impulses, etc. Menstruation, menopause, pregnancy, etc. can also be affected by this disease.
8. Internal diseases 7-9% of patients with SLE have urticaria. In addition, lymphoma, carcinoma, hyperthyroidism, rheumatism and rheumatoid arthritis, hyperlipidemia, and chronic lesions such as oral, dental, and gum diseases, gastritis, enteritis (allergic colitis, ulcerative colitis), cholecystitis, nephritis, liver disease, ulcerative disease, and diabetes.
9, genetic factors Urticaria related to genetics are hereditary familial urticaria syndrome, familial cold urticaria, delayed familial restrictive heat urticaria, erythropoietic protoporphyria.
Clinical manifestations
The skin is often pruritic, followed by the appearance of a wind vesicle, which is bright red or pale, skin-colored, or in rare cases, only an edematous erythema. The size and shape of the phyllodes vary, and the duration of the attack is variable. The puffs spread gradually and may fuse with each other to form patches, and the epidermal follicle opening may be depressed due to dermal papillae edema. The rash lasts from a few minutes to a few hours, and in a few cases it may last for several days and then fade away without leaving a trace. The rash occurs repeatedly or in batches, mostly in the evening. Very few patients do not itch because the severe itching can affect sleep. The rash is often widespread or may be limited. They are sometimes combined with angioedema. Occasionally, large blisters are formed on the surface of the cluster, called herpetic urticaria, with blisters as large as a pea or a fingernail, with a tense wall and clear content, secondary to a long-standing cluster, where the dermal papillae have been edematous for a long time, resulting in a gap and the formation of blisters, and the entire epidermis is lifted up to become the top of the blisters. There is also hemorrhagic urticaria. In some patients, after scratching the skin with a blunt instrument, a localized wind mass consistent with the scratch appears, i.e. a positive skin scratch test. Some patients may have nausea, vomiting, headache, head distension, abdominal pain, diarrhea, and some may also have systemic symptoms such as chest tightness, discomfort, pallor, accelerated heart rate, weak pulse, decreased blood pressure, and shortness of breath. Urticaria caused by acute infection and other factors may be accompanied by high fever and increased white blood cells.
If the disease heals within a short period of time, it is called acute urticaria. If the disease recurs for several months or more, it is called chronic urticaria. According to Champion’s statistical report of 554 cases, the average duration of urticaria alone is 6 months, the duration of angioedema alone is about 1 year, and the duration of urticaria combined with angioedema is about 5 years. There are also several special clinical types of urticaria as follows.
(a) Peptone urticaria (peptone urticaria) When overeating (over-eating pork and seafood) and mental excitement and drinking a lot of alcohol, the peptone in the food is absorbed into the blood through the mucous membrane of the gastrointestinal tract without being digested, and causes skin redness and wind masses, accompanied by weakness and headache. The duration of this type of urticaria is very short, lasting only 1 to 2 d.
(B) Serum sickness urticaria is caused by a foreign body serum, vaccine or drug. Patients have fever, arthralgia, swollen lymph nodes, and lesions are most commonly seen as wind clusters, especially polycyclic wind clusters. Sometimes there is proteinuria and tubuluria with renal damage. Blood sedimentation is usually normal. Total complement is decreased. Plasma cells are increased in the peripheral blood.
(C) contact urticaria (contact urticaria) Skin contact with certain allergens after the occurrence of wind and redness, known as contact urticaria. It can be divided into three types: immune, non-immune and unknown mechanism. Non-immune contact urticaria, caused by primary urticogenic substances, does not require sensitization and can cause disease in almost all exposed individuals. Histamine, slow-reacting substances, and bradykinin are responsible for the reaction due to direct stimulation of mast cells by the contact substance, and it is also possible that the contact substance acts directly on the blood vessel wall. The substances that are the cause are dimethyl sulfoxide, Trafuril, cobalt chloride solution, benzocaine, certain food preservatives and flavorings (such as benzoic acid, sorbic acid, cinnamic acid, Peruvian balm, acetic acid, ethanol, etc.). Urticaria produced by arthropods, seaweeds, caterpillars and poisonous moths are caused by the injection of toxic sap into the skin through stings or bites, so they are not true contact urticaria, but some people classify them as such.
Immune contact urticaria is a type I allergic reaction, and in some cases antigen-specific IgE can be demonstrated. its clinical manifestations can be divided into four categories: ① urticaria limited without distant damage and without systemic symptoms; ② urticaria with angioedema; ③ urticaria and asthma, rhinitis, conjunctivitis, gastrointestinal or oropharyngeal dysfunction coexist; ④ urticaria and rapid onset allergy. There are many causative substances listed in literature reports, including certain foods, textiles, animal dander, saliva, hair, drugs, cosmetics, industrial chemicals, etc. There are also reports of contact urticaria from exposure to semen, bovine placenta, and topical nitrogen mustard.
Contact urticaria of unknown mechanism is a reaction type with both immune and non-immune manifestations, such as those caused by peroxynivalenol.
Diagnosis of contact urticaria can be determined by applying an open spot of the allergenic substance to normal skin, and after 15 to 30 min, if a wind cluster occurs.
(d) Dermographism is a physiological reaction to a weak external mechanical stimulus, resulting in skin lesions. It can occur at any age. Patients complain of localized itching of dermographism after scratching or on tight belts and garters, and more dermographism is produced due to scratching. The disease can coexist with other types of urticaria.
Kalz et al. found 80 positive tests in 100 patients treated with penicillin for syphilis, 10 of which remained positive long after penicillin was discontinued.
Newcomb et al. (1973) found that certain patients with skin scrapie occurred due to the involvement of IgE antibodies. Recently it has been suggested that skin scratching is associated with the presence of some functional abnormality in the skin mast cells without an increase in the number of mast cells.
(E) Delayed dermographism The lesions appear about 6 to 8 h after the skin is scratched and last 24 to 48 h. Some patients also have immediate dermographism. Late lesions are not just one strip, but often form small segments or dots along the scratch, with deep or wide damage, or even spreading to both sides to form a mass. Baughman et al. found that most patients were associated with fungal products, such as tinea pedis, antibiotics, etc.
(vi) Delayed pressure urticaria The rash occurs 4-6 h after the skin is pressurized. it manifests as localized deep in painful swelling. The rash may occur on the palms, metatarsals or buttocks and usually lasts 8-12 h. It may be accompanied by chills, fever, headache, arthralgia, general malaise and mild leukocytosis. It is thought that it may be caused by abnormal changes in kinin activity. It has been studied that there is no significant relationship between this disease and immunological aspects. However, Saurat et al. (1975) have reported one case of a severe patient with reduced serum complement values. Warin (1976) reported that both father and son suffered from stress urticaria, which seems to have a genetic factor.
(VII) Cold urticaria
1, acquired cold urticaria (acquired cold urticaria) the main mediator is histamine, and there are kinins. The antibody is lgE, and its serum level is more than five times higher than normal. Passive transfer is positive. The antigen may be a normal skin protein or a denatured skin protein released after cold stimulation of the skin; in other patients, the formation of wind clumps is the result of the action of IgM macromolecular globulin aggregation after cold exposure. Positive ice test.
(1) Primary Occurs suddenly at any age. Commonly occurs within minutes of immersion in cold water or exposure to cold, with localized itchy edema and puffiness. Most often seen on the face and hands, but in severe cases other parts of the body can also be involved. When these patients swim in cold water or are exposed to cold rain, systemic symptoms similar to histamine shock may occur, such as headache, skin flushing, hypotension, and even fainting. The allergy to cold may disappear on its own after several months or years.
(2) Secondary Cold urticaria can occur in patients with certain underlying diseases such as cryoglobulinemia, cryofibrinogenemia, cryolysis, macroglobulinemia, syphilis, connective tissue disease, and bone marrow malignancy.
(3) Transient Urticaria is associated with certain factors such as drugs (oral ashwagandha) or infections (infectious mononucleosis) in a transient presentation.
(4) Delayed cold allergy Ice test is positive at 24 h or 48 h.
2. Familial cold urticaria is inherited in an autosomal dominant manner. It begins in infancy and often lasts throughout life. A delayed reaction occurs 0.5h to 4h after exposure to cold, and the rash is a non-itchy wind mass with a burning sensation, accompanied by systemic symptoms such as fever, arthralgia, and leukocytosis. Passive transfer test was negative. The ice test was negative. However, Sofer et al. (1977) found a positive delayed skin reaction to cold in patients with this disease. That is, local erythema and deep swelling occurred 9 to 18 h after the ice test.
(H) Cholinergic urticaria is caused by the release of acetylcholine from cholinergic nerves due to exercise, intake of hot food or drinks, sweating and emotional excitement, which then increases the level of cyclic guanosine monophosphate (c GMP) in basophils and mast cells, resulting in the release of histamine. A mild form of cholinergic urticaria can occur in more than 15% of normal adolescents. This type of rash is characterized by the occurrence of small, generalized 1 to 3 mm bumps in addition to the palms and plantars, or tiny, sparse bumps with or without a red halo. Sometimes the only symptom is a severe itch without a cluster. The damage lasts 30 to 90 minutes or up to several hours. A small number of patients have systemic symptoms such as nausea, vomiting, abdominal pain, diarrhea, sweating, birth, headache, dizziness, and weakness. Intradermal injection of 1:5,000 acetylcholine produces a typical wind cluster in normal subjects, but patients have small satellite like wind clusters around the wind cluster, which can be used for differential diagnosis. After skin scratching, small wind masses appear at the scratch. Recently, it has been found that the acetylcholine or nicotinic acid tartrate skin test is positive only in severe cases, and repeated skin tests are not always positive in the same patient. Exercise or hot water baths are more effective and simple tests. The disease can recur for months or years, but may resolve spontaneously. This type of urticaria has a negative passive transfer test.
(ix) Heat urticaria
1.Localized heat urticaria Localized heat urticaria can appear within a few minutes after the skin is heated and occurs repeatedly. Histamine release is demonstrated locally. Acetylcholine test is negative. It is thought that this non-allergic mechanism may be due to the membrane rupture of skin mast cells caused by the action of heat and some tissue factor or plasma factor.
2. Familial localized heat urticaria of delayed type occurs 2h after heat, with sharp edges, most pronounced at 4-6h, and lasts for 12h. Onset begins in early childhood. Passive transfer test is negative.
Treatment.
The first step in the treatment of urticaria is to look for the above-mentioned possible triggers, which requires meticulousness, patience, and the ability to recall for yourself what you have been exposed to. You can also visit a dermatologist to do tests for inhalant allergens, food allergens, patch tests or food intolerances according to your condition. Once identified, avoid and remove them. During the rash period, you should also take antihistamines or use other anti-allergy treatments.
Next is anti-allergy treatment: antihistamines are often preferred. There are many types of antihistamines, some of which have a drowsy effect, some of which are not or are mild, and they are chosen according to each person’s condition, work and life situation. For drivers and people who work at height, use those without drowsiness, and for heavy itching and poor sleep, use those with sedative effects. For acute urticaria light can be injected benadryl or promethazine, while oral loratadine, cetirizine, cycloheximide, uazine, paracetamol, etc. can be maintained. If there is laryngeal edema and respiratory distress, immediately administer oxygen and prepare for tracheotomy. With a history of anaphylaxis, immediately inject 0.1% noradrenaline and intravenous hydrocortisone, along with antihistamines. Do not stop the medication immediately after the rash subsides, but also take more medication for a few days, and gradually reduce the dosage to prevent recurrence.
Chronic urticaria should focus on finding the cause, identifying the cause and treating it symptomatically, as well as the key to avoiding recurrence. The treatment routine is oral antihistamines, one drug can not be controlled, two or three can be used in combination, and even corticosteroids can be combined. There is a triple therapy of antihistamines + reserpine + anorectic blood, and satisfactory results are obtained.
Allergen desensitization is performed for those who test positive for allergens.
For some chronic urticaria where no cause can be found, non-specific treatment can also be used: e.g. self-blood therapy, closure therapy, acupuncture therapy, oxygen therapy, etc.
Traditional Chinese medicine also has a more therapeutic effect on urticaria, although it has to be treated on a dialectical basis according to the specific situation of each individual.
Topical medications are used to soothe and relieve itchiness and treat the symptoms. For example, dermatoprene, Eudragitol, Halometasone, Eloson, Furfuryl lotion, compound menthol lotion, ice pack compresses, etc.
All treatments should be carried out under the guidance of a physician and it is not recommended to purchase your own medication for treatment.