1. acute urticaria accounts for about 1/3 of all urticaria.
(1) The onset is urgent, and the skin lesions are often sudden. It is a localized red air mass with different sizes, clear boundaries and different shapes, which can be round, quasi-round or irregular. At first, it is isolated and dispersed, and can gradually increase with scraping, and merge into a non-plastic, ground figure or ring. For example, the serum in the microvessels oozes out quickly, pressing the wall of the tube, and the wind mass can be pale, red around, and the skin is uneven and orange peel-like.
(2) Most skin lesions disappear naturally from half an hour to several hours, leaving no trace after disappearance, but new wind masses appear one after another, which can appear repeatedly within 1 day.
(3) Consciously severe itching and burning sensation.
(4) the location is uncertain, which can be spread all over the body or limited to a certain part. Sometimes mucosa can also be involved, such as gastrointestinal tract involvement, causing mucosal edema, nausea, vomiting, abdominal pain, diarrhea and other symptoms. When the laryngeal mucosa is invaded, chest tightness, asthma and dyspnea occur, which can cause laryngeal edema and suffocation in severe cases, which is life-threatening. If accompanied by high fever, chills, rapid pulse and other systemic symptoms, we should pay special attention to the possibility of serious infection such as sepsis.
(5) Skin scratches can be positive.
(6) Eosinophils increased in blood routine. If there is severe staphylococcus aureus infection, the total number of white blood cells increases or the cell count is normal, the percentage of neutrophils increases, or there are neutrophils at the same time.
2. Chronic urticaria accounts for 2/3 of urticaria. Wind masses occur repeatedly, sometimes for a long time, often lasting more than 2 months. There are light and heavy passes, such as aggravation in the morning or before going to bed. Some have no certain regularity, and the general symptoms are generally mild. Most patients can't find the cause.
In addition, there are some special types of urticaria in clinic:
(1) Factual urticaria: also known as dermatoglyphics: ① The patient's skin is very sensitive to external mechanical stimuli, and there is usually no wheal on the skin. If the skin is scratched by nails or blunt objects, there will be a strip-shaped bulge consistent with the scratch (Figure 1 2), which will soon disappear with itching; ② It can occur at any age without obvious reasons. Infection focus, diabetes, thyroid dysfunction, menopause, etc. They are all related to the onset, and can also be caused by drugs such as penicillin, and some people think that it is related to the abnormal function of skin mast cells. ③ The course of disease is uncertain, which can last for several months or exist for a long time; ④ In a few cases, wheal reaction reappeared in situ after 0.5 ~ 6 hours and lasted for 48 hours, which was called delayed dermatoglyphics.
(2) Peptone urticaria (acute protein allergic urticaria): caused by proteolytic peptone in food. Under normal circumstances, peptone is not absorbed into the blood and is easy to digest, but when overeating and mental excitement or drinking at the same time, peptone can be absorbed into the blood through intestinal mucosa and cause disease. Skin congestion, redness, wheal, headache and fatigue. Generally, the course of the disease is short, and it can subside in1~ 4 hours, sometimes lasting several hours or 1 ~ 2 days. Antigen antibody reaction.
(3) Cold urticaria: There are two kinds: acquired urticaria and familial urticaria.
① Familial cold urticaria: autosomal dominant inheritance. It is rare, and it begins to develop soon after birth and can last for life. The pathogenesis and medium are not clear, and it is more common in women, and the symptoms can be alleviated with age. Generally, after contacting with cold air or cold water for 0.5 ~ 4 hours, it develops into a red maculopapular rash with a diameter less than 2 cm, which is unreal, itchy and burning, often accompanied by systemic symptoms such as chills, fever, headache, joint pain and leukocytosis. The ice cube test is positive, that is, putting ice cubes on the patient's forearm skin can cause typical blisters in this part after 2 minutes, while the passive transfer test is negative.
② Acquired cold urticaria: It may be an autoimmune allergic reaction. Most of the cold allergies are idiopathic, and about 1/3 has a history of genetic allergy. It often begins with children. When the temperature drops suddenly, after children are exposed to cold air, cold water or cold objects, wheal or patchy edema appears at the exposed or contacted parts, which can last for 0.5 ~ 4 hours and then disappear. In severe cases, hand numbness, lip numbness, chest tightness, palpitation, abdominal pain, diarrhea, syncope and even shock may occur. If it happens while swimming, it will lead to cold shock and even drowning. According to statistics, about 25% patients will cause swelling of mouth and throat when eating cold food, and in severe cases, they will suffocate and die. The antibody is IgE. It is believed that cold can make a normal metabolite in the body become an antigen, thus causing antibody production. It may also be that the three-dimensional structure of skin protein is changed due to cold factors, so that antibodies cannot recognize their own tissue proteins. The formation of wheal is due to the accumulation of IgM macromolecular globulin after cold skin. The main mediators are histamine and kinin. The pathogenesis belongs to IgE-mediated immediate allergic reaction. If the ice test is positive, you can also use ice water to soak the test. You can immerse your arm in cold water at 5 ~ 10℃ for 5 minutes, and if it causes blisters and erythema, it is positive. Passive metastasis test was positive. In rare cases, cold urticaria can occur in globulinemia (myeloma, macroglobulinemia, leukemia, liver disease and systemic lupus erythematosus), paroxysmal cold hemoglobinuria (syphilis), cold fibrinogen and cold hemolysis, especially in patients with mononucleosis.
(4) Cholinergic urticaria: also known as papular urticaria or systemic urticaria. More common in young people aged 23 ~ 28. Exercise, heat, emotional tension, eating hot drinks or alcoholic drinks and other inducing factors stimulate the central nervous system. The nerve junction of sweat gland is stimulated by cholinergic afferent nerve, which causes acetylcholine to release and act on mast cells, or occurs due to cholinesterase deficiency. About 5% ~ 7% of urticaria. The skin lesions are small air masses with a diameter of 1 ~ 3 mm, which are red, scattered and unconformity. The rash usually appears 2 ~ 10 min after the stimulation of the above factors, lasts for 30 ~ 50 min, rarely exceeds 3 hours, the rash completely disappears, and the palms and soles rarely appear, and itching is felt consciously. Sometimes there is a refractory period of 8 ~ 8 ~ 24h after each attack. During this period, even if you encounter the above stimulation again, there will be no rash. About13 patients may be accompanied by headache, edema around the mouth, tears, eye swelling pain, salivation, nausea, vomiting, abdominal pain and other symptoms, and a few have dizziness, hypotension and asthma attacks. The course of the disease gradually improved after several years. If 1∶5000 methacholine skin test or scratch test is positive, wheal can appear at the injection site and satellite wheal around it (rare in normal people). However, repeated testing by mild patients or the same patient often leads to inconsistent results.
(5) Solar urticaria: After the skin is irradiated by sunlight or artificial light for several seconds to several minutes, itching, erythema, wheal and occasional vascular edema appear locally. In severe cases, the rash may be accompanied by chills, fatigue, syncope, spasmodic abdominal pain and bronchospasm. Often idiopathic, sometimes accompanied by systemic lupus erythematosus, erythropoietic protoporphyria and so on. According to its possible pathogenesis and light response to different wavelengths, it can be divided into 2 categories and 6 subtypes. The first category is generally considered to be related to IgE allergy, but no related pathogenic antigen has been found yet. This class is further divided into three subtypes, namely type I, type IV and type VI. Type ⅰ is mainly allergic to short-wave ultraviolet at 280 ~ 320 nm. After irradiation, obvious histamine release, mast cell degranulation, neutrophil and eosinophil chemokines were observed in local skin. Type ⅳ is allergic to 400 ~ 500 nm visible light. At present, it has been proved that this type is a hereditary metabolic disease, which may be a skin manifestation of delayed dermatoporphyria, and its photosensitive source is protoporphyrin VII. However, unlike other porphyria, its urinary porphyrin excretion is normal, and erythrocyte protoporphyrin, fecal porphyrin and fecal porphyrin increase. This kind of patients can activate the complement system in serum after illumination and produce a series of inflammatory reactions. Type ⅵ is caused by 400 ~ 500 nm light, and the difference with Type ⅵ is caused by β carotene. The other category also includes three subtypes. Type Ⅱ is caused by 300 ~ 400 nm long-wave ultraviolet, type Ⅲ is 400 ~ 500 nm visible light, and type ⅴ is 280 ~ 500 nm broad-spectrum light. It is generally believed that these patients have nothing to do with immune response, and most of them can't find the reason. But a few patients belong to the early or late stage of SLE. It may also be caused by drugs, such as ibuprofen, sulfanilamide and chlorpromazine.
(6) Urticaria compression: 4 ~ 8 hours after skin compression, local skin appears red edema patches, often deep edema, involving dermis and subcutaneous tissue, similar to vascular edema, burning pain or pain, which lasts for about 8 ~ 12 hours and subsides. About half of the patients may have fever, sweating, dizziness, headache, nausea, fatigue, weakness, shortness of breath, irritability and other systemic symptoms, and a few have mental depression. Common in the soles of feet, buttocks and other oppressed parts after walking. The white blood cell count can be slightly increased. The pathogenesis may be related to kinin. Statistics show that about 94% of these patients are accompanied by chronic urticaria, 43% are positive for aspirin provocation test and 63% are accompanied by scratches, but they have nothing to do with genetic allergy. Most stress urticaria is delayed, but very few are immediate, and skin lesions appear after 20 minutes of local compression. The diagnosis method is as follows: hang a 2 ~ 10 kg weight under the shoulder with broadband, or ask the patient to take a seat, hang the broadband in the middle of the thigh 10 ~ 30 min, take off the broadband and observe it immediately, and then observe it continuously for 4, 6, 8 to 20 hours respectively, while scratching his back to confirm that there are scratches at the same time. If the scratch is positive, if the scratch is positive,
(7) Serum urticaria: It is caused by the application of allogeneic serum, including various antiviral sera, vaccines, gamma globulin or albumin, blood transfusion, and all sera and their products and blood provided by human beings or animals. Erythema, itching and wheal appear at the injection site or all over the body, as well as annular erythema and nodular erythema. In addition, about 2.7% of patients can also have fever, lymph node enlargement, myalgia, joint pain, purpura, low exercise ability and other systemic symptoms, which are called serum sickness, and its symptoms are self-limited and gradually disappear. However, a few people with severe symptoms occasionally lead to death. About 65438 0% ~ 3% of recipients developed systemic urticaria after blood transfusion. At present, it is believed that the formation of immune complex causes the changes of blood vessels and smooth muscles, and it can also indirectly lead to the release of mediators by mast cells through allergic toxins. It was found that 0/5% ~ 20% of/kloc-recipients had IgG antibodies against IgA, which could combine with IgA in donor blood to form immune complex, activate complement, and cause urticaria and vascular edema. However, some of them have no antibodies, and urticaria will also occur after gamma globulin injection. The reason is that after gamma globulin injection, the concentration of immunoglobulin G in blood increases, which leads to mutual coagulation and fixation of complement.
(8) Contact urticaria: wheal and erythema appear after skin contact with some allergens, which can be divided into three types: immune, non-immune and unknown mechanism. Non-immune contact urticaria is caused by primary urticaria allergens, and almost all contact can occur without sensitization. Its pathogenesis is that contact substances directly stimulate mast cells to release histamine, slow-acting substances and bradykinin. The more common substances are animals or plants such as jellyfish, nettles, caterpillars and butterflies. A variety of chemicals may also cause it. According to the survey, about 88% of adults are positive for 5% benzoic acid, 85% for 5% phenylacrylic acid and 58% for 25% sorbic acid. Most of them reacted after 45 minutes of contact with the above substances and subsided within 2 hours. These substances can be caused not only by non-immune reaction, but also by immune reaction. The rash can be confined to the contact site or spread to the whole body. To determine the contact substance, the most common method is to do patch test. Most cases of immune contact urticaria belong to IgE-mediated immediate allergic reaction, and the common contact substances are fish, shrimp, vegetables, animal hair, dander, eggs, drugs and chemicals. The difference from the above non-immunization is that:
① Generally, the first contact will not produce wheal, but repeated contact will happen;
2 people with allergies, such as asthma, hay fever (hay fever) and eczema, are more likely to occur;
(3) Once the disease occurs, in addition to itching, redness and wheal at the contact site, there will be systemic symptoms such as rhinitis, conjunctivitis, asthma, diarrhea, abdominal pain, nausea and vomiting;
(4) In addition to the contact parts such as hands, inhalation and oral contact can also cause reactions;
⑤ Most of the reactions are caused by protein, drugs or chemicals. In addition to itching, burning sensation, erythema, wheal and even blisters within a few minutes to 1 ~ 2 hours after contact, there are also systemic reactions such as runny nose, tears, asthma, abdominal pain, diarrhea, vomiting and even asphyxia shock, also known as allergic contact urticaria syndrome. A reaction with both immune and non-immune manifestations in people with unknown mechanism, such as the reaction caused by ammonium sulfate.
(9) Water-borne urticaria and water-borne pruritus: water contact at any temperature can cause itching, and a few people can have urticaria, and the wind mass is small. Typical skin lesions will appear within 30 minutes after wet application of tap water to the back. There are reports of similar patients in the family. Itching without urticaria is often idiopathic, and it is also seen in the elderly with dry skin, and also in patients with polycythemia vera, Hodgkin's disease, spinal dysplasia syndrome, eosinophilia syndrome and so on. Water-borne itching can also occur in patients with acute hematological diseases. The experiment proved that the histamine level in the blood of patients with idiopathic water-borne pruritus and urticaria increased, the mast cells in the diseased tissues degranulated, and the passive transfer test was negative. Oral administration of H 1 receptor antagonist 1h before bathing can reduce the formation of wheal.
(10) autoimmune urticaria: circulating autoantibodies were found in the sera of some patients with chronic idiopathic urticaria, hence the name. According to statistics, autoantibodies have been found in at least 30% patients with chronic idiopathic urticaria. Intradermal injection of autologous serum can cause wheal and erythema reaction. There are IgG autoantibodies against IgE or high affinity IgE receptor (FcεRla). Both autoantibodies release histamine and stimulate eosinophils in the blood. The condition of urticaria is directly related to the amount of autoantibody FcεRIa in serum.
(1 1) Adrenal urticaria: small itchy wind mass with white halo around it, which can be caused by emotional excitement and coffee intake. Intradermal injection of norepinephrine can cause wheal, which is caused by sensitivity to norepinephrine secreted by sympathetic nerve endings and should be differentiated from cholinergic urticaria. Beta blockers and antihistamines are commonly used in clinical treatment, and adrenaline is avoided.
(12) Urticaria vasculitis: It is characterized by urticaria and necrotizing vasculitis. From 65438 to 0973, it was reported by Mike Du Fei. Histologically, leukocyte vasculitis was fragmented. Because some cases have persistent and severe low-completion vasculitis, they are named low-completion vasculitis. In the future, many scholars have successively diagnosed necrotizing phlebitis, urticaria, low complement vasculitis, urticaria syndrome and so on. Now, urticaria vasculitis is more appropriate. Patients have recurrent chronic urticaria damage, which often lasts for more than 24 hours, and a few have laryngeal edema. Accompanied by irregular fever, arthritis, joint pain, lymphadenopathy, abdominal pain, and accelerated erythrocyte sedimentation rate, some patients had kidney damage, and 32% patients had low completion rate. After the skin injury subsides, it will leave purpura, scales and pigmentation. Consciously mild itching and pain. It is found that there is immune complex deposition (type ⅱ allergic reaction) in venules behind capillaries, which may be the reason.
The disease can be divided into two subtypes: hypocompletremia type and normal complement type. The systemic damage of the former is greater than that of the latter. The disease is effectively treated with prednisone, indomethacin (indomethacin), colchicine and dapsone.
(13) Vascular edema: Vascular edema, also known as angioneurotic edema, Quincke edema or huge urticaria, is a localized edema that occurs in subcutaneous tissue or mucosal loose parts, and can be divided into acquired edema and hereditary edema. The latter is rare. Acquired angioedema is often accompanied by other allergic diseases, and its etiology and pathogenesis are similar to urticaria. IgE-mediated type I allergic reaction can cause acute hair. Contrast agents and some drugs such as non-steroidal anti-inflammatory drugs (aspirin, indomethacin), codeine and angiotensin converting enzyme inhibitors can also be caused by non-immune mechanisms. For foods such as fruits and fish, the inhalants are mainly feathers and animal dander, and the slow growth of hair is often caused by cold and sunlight. In addition to hereditary angioedema, angioedema is often accompanied by urticaria. About 15% ~ 20% of the general population suffers from urticaria, angioedema or both, but the incidence of chronic urticaria or angioedema is low. Vascular edema often occurs in 30 ~ 40 years old, and the incidence rate is the highest in women aged 40 ~ 50 years old. About 50% of patients get sick after 5 years old, and 10% ~ 20% of patients get sick intermittently after 20 years old.
① Hereditary angioedema: Hereditary angioedema is an autosomal dominant genetic disease. It was first reported by Robest Grave in 1843, and then by Quincke in 1882, two cases occurred in the same family. Later, scholars gradually realized its heredity, so they named it hereditary angioedema. Pathogenesis is closely related to complement, coagulation, fibrinolysis and kinin formation. The patient has biochemical abnormalities, and it is observed that intradermal injection of kallikrein (a protein hydrolase) usually does not respond. It is also proved that there is a lack of CIINH protein in serum, and this inhibitor can also resist angiotensin. It is considered that 85% of patients are due to the decrease of the level of CI cholinesterase inhibitor (CIEI) in blood, and 15% patients have dysfunction besides the decrease of CIEI, which leads to the over-activation of CI, thus activating C4 and C2 to release kinins. With the participation of plasmin, kinin increases vascular permeability, and mast cells release histamine, which leads to angioedema. Both C4 and C2 dropped during the attack, and C4 also dropped during the rest. Most cases occur in late childhood or adolescence. Most of them have family history, often involving several generations, but about 20% have no positive family history. The clinical manifestations are recurrent, localized, non-concave subcutaneous edema, no erythema and itching, and pain due to expansion of skin and subcutaneous tissue. The onset of the disease is spontaneous, and about half of the patients are related to minor injuries, such as collision, squeezing, lifting heavy objects, sex life and riding horses. Generally, swelling occurs 4 ~ 12h after trauma. The onset of some patients is related to emotional excitement, infection and sudden temperature change. Before and after menstruation, contraceptives based on kimono and estrogen often appear. During the attack, the edema gradually increased within a few hours and subsided to normal within 24 ~ 72 hours. Limbs (96%), face (85%), intestinal mucosa (88%) and oropharynx are most commonly involved, and the damage can reach several centimeters in diameter or occupy a limb. Swelling of the face and lips will develop and involve the upper respiratory tract. All patients with skin lesions have different degrees of gastrointestinal symptoms. Recurrent abdominal pain can be the only manifestation of the disease in most family members, and abdominal cramps similar to acute abdomen can occur. Acute laryngeal edema is the most serious and life-threatening manifestation, and 26% untreated patients can die of laryngeal edema.
② Acquired angioedema: The skin lesion is acute localized swelling, involving subcutaneous tissue, with unclear boundary, normal or reddish skin color, bright surface and elastic touch. It often occurs in loose tissues such as eyelids, lips, earlobes, vulva (foreskin is the most common part), or in the mouth and tongue. If it occurs in laryngeal mucosa, it can cause dyspnea and even suffocation, leading to death. Often accompanied by urticaria, the damage is often single, which lasts for 2 ~ 3 days and often occurs repeatedly in the same part. This disease often occurs at night and is discovered only when you wake up. Often there is no itching, even if there is, it is very mild, or there is only a slight burning and discomfort. About 1/4 cases have a history of recurrent erythema, which can occur before or at the same time as edema, or has nothing to do with edema attack. The disease can involve visceral mucosa, and when it affects gastrointestinal tract, acute intestinal obstruction such as abdominal cramps, fullness, nausea, vomiting and inability to exhaust gas may occur. In severe cases, dehydration and blood pressure drop may occur, and barium meal radiography may cause mucosal edema.