It is commonly known as “rubella mass”. It is a restrictive edema reaction due to the dilation and increased permeability of small blood vessels in the skin and mucous membranes. Fifteen to twenty percent of people have had at least one episode of urticaria in their lifetime.
[Etiology and pathogenesis]
(I) Etiology The cause of urticaria is complex and cannot be found in about 3/4 of patients, especially in chronic urticaria.
1, drugs Many drugs often predispose to this disease, especially penicillin. Usually the reaction is caused by the production of IgE antibodies to the drug first, or the formation of antigen-antibody complexes. However, some drugs are themselves histamine releasing agents, such as morphine, codeine, dulcolax, cylindrical arrow poisoning base, 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 infectious factors can cause this disease, including.
①Bacterial infections, such as acute tonsillitis, pharyngitis, impetigo, boils, cholecystitis, appendicitis, pancreatitis, paranasal sinusitis, etc.
② Viruses, such as the prodromal phase or jaundice phase of viral hepatitis are 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 wind clumps, which are bright red or pale, skin-colored, or in rare cases, only edematous erythema. The size and shape of the puffs 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 When overeating (over-eating pork and seafood) and mental excitement and drinking a lot of alcohol, the peptone in food is absorbed into the blood through the mucous membrane of the gastrointestinal tract without being digested, and causes skin redness and wind mass, accompanied by weakness and headache. The duration of this type of urticaria is very short, lasting only 1 to 2 d.
(B) Serum urticaria is caused by allogeneic serum, vaccines or drugs. Patients have fever, arthralgia, swollen lymph nodes, and lesions are most common with 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.
(iii) Contact urticaria The occurrence of skin lesions and redness after contact with certain allergens is called contact urticaria. It can be divided into immune, non-immune and unknown mechanisms. 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.
(i) urticaria limited, without distant damage and without systemic symptoms.
② urticaria with angioedema.
(iii) coexistence of urticaria and asthma, rhinitis, conjunctivitis, gastrointestinal or oropharyngeal dysfunction.
(iv) 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.
The 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) Skin Scratching Patients with external weak mechanical stimuli cause an increased physiological response, resulting in skin lesions. It can occur at any age. Patients complain of localized itching of the vesicles after scratching or on tightly bound belts, garters, etc., and more vesicles are produced as a result of 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.
(v) Delayed cutaneous scratching The lesions appear about 6 to 8 h after the cutaneous scratching, with erythema lasting 24 to 48 h. Some patients also have immediate cutaneous scratching. 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 to 6 h after skin pressure. manifests as localized deep in painful swelling. The rash may occur on the palms, metatarsals or buttocks and usually lasts for 8 to 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 for life. The rash is a non-itchy wind mass with a burning sensation and is 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 drink, sweating and emotional excitement, which then increases the level of guanosine cyclophosphate (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) Fever urticaria
1. localized febrile urticaria Localized skin heat can be followed by a wind cluster within a few minutes and recurrent. Localized histamine release is demonstrated. Acetylcholine test is negative. It is thought that this non-allergic mechanism may be due to the rupture of the membrane of skin mast cells caused by the action of heat and some tissue factor or plasma factor.
2. Delayed familial restrictive heat urticaria occurs 2h after heat, with sharp edges, most pronounced at 4-6h, and lasts for 12h. Onset begins at an early age. Passive transfer test is negative.