荨麻疹 · 风团为什么来得快走得也快

参考文献 · 6

1. Zuberbier, T., Ansari, Z. A., Abdul Latiff, A. H., Abuzakouk, M. M., Agcaoili-De Jesus, M. S., et al. (2026). The international guideline for the definition, classification, diagnosis and management of urticaria. Allergy, 81(8), 2582-2632. GA2LEN-led GRADE guideline, consensus conference 6 December 2024. Urticaria is a frequent, mast cell-driven disease defined by a rapid appearance of wheals, angioedema or both; the lifetime prevalence of acute urticaria is estimated to be approximately 20%. A wheal: a sharply circumscribed superficial central swelling almost invariably surrounded by reflex erythema, an itching or sometimes burning sensation, and a fleeting nature, the skin returning to normal usually within 30 min to 24 h. Angioedema: a sudden deep swelling in the lower dermis and subcutis or mucous membranes, with tingling, burning, tightness and sometimes pain rather than itch, resolving more slowly (can take up to 72 h). Acute urticaria lasts 6 weeks or less, chronic more than 6 weeks; spontaneous (no definite eliciting factor) or inducible (a definite subtype-specific trigger such as cold); in most inducible urticarias symptoms appear within 10 min of exposure and resolve within 1-3 h after it stops; CSU episodes may recur after months or years of full remission. Mast cell activation releases mediators such as histamine and platelet-activating factor, responsible for sensory nerve stimulation (pruritus), vasodilatation (erythema) and inflammatory cell chemoattraction; wheals show degranulated mast cells with oedema of the upper and mid dermis and dilated, more permeable postcapillary venules; in angioedema similar changes occur primarily in the lower dermis. Besides the histamine receptor, other mast cell receptors such as MRGPRX2 are involved. In more than 50% of CSU patients the pathophysiology is driven by two autoimmune mechanisms: type I (autoallergy, IgE autoantibodies against autoallergens) and type IIb (mast cell-activating IgG autoantibodies); some patients have both. Acute urticaria frequently follows upper airway infections, including COVID-19, and some cases evolve into CSU. Acute urticaria, being self-limiting, needs no workup beyond a history (recommendation against routine diagnostic measures), except suspected food allergy or drug hypersensitivity, especially to NSAIDs. Drugs cause urticarial reactions via IgE (e.g., penicillin) or non-IgE mechanisms (e.g., NSAIDs); NSAIDs aggravate pre-existing CSU in up to one-fourth of patients, with paracetamol and COX-2 inhibitors considered safer options. Food allergy is rarely a trigger of CSU; diagnostic pseudoallergen- or histamine-low diets may be considered only in selected patients, usually for 2-3 weeks, and should not delay effective treatment; overdiagnosis of histamine intolerance should be avoided. Some CSU patients experience trigger-induced augmentation of wheals or angioedema, among others by stress and infections; up to one-third of CSU patients perceive stress as an aggravating factor. Because severity fluctuates and spontaneous remission may occur at any time, the need for continued drug treatment should be re-evaluated every three to 6 months. Trigger avoidance should be balanced with quality of life (not, for example, stopping all exercise). Strong recommendation: a standard-dosed modern second-generation H1-antihistamine as first-line treatment for all types of urticaria, taken daily rather than on demand in chronic urticaria; H1-antihistamines act as inverse agonists that stabilise the inactive state of the H1 receptor; modern second-generation H1-antihistamines are minimally or nonsedating; recommends against first-generation H1-antihistamines as first-line (sedation, impaired driving, lethal overdoses reported); updosing is off-label. Topical corticosteroids, frequently and successfully used in many allergic diseases, are not useful in urticaria; strongly recommends against prolonged systemic corticosteroids, while a short course of up to 10 days may help in acute urticaria or exacerbations. Anaphylaxis, urticarial vasculitis and bradykinin-mediated angioedema (e.g., with ACE inhibitors, hereditary angioedema) must be distinguished from urticaria (full text PMC13466004; PMID 41649409). 10.1111/all.70210
2. Kanani, A., Betschel, S. D., & Warrington, R. (2018). Urticaria and angioedema. Allergy, Asthma & Clinical Immunology, 14(Suppl 2), 59. Urticaria occurs in 15-25% of people at some point in life; lesions are often transient, resolving within about 24 h without scarring, though some last up to 48 h; about 40% of patients with urticaria also have angioedema. Mast cells, widely distributed in the skin and mucosa, carry high-affinity IgE receptors; their degranulation rapidly releases histamine, leukotrienes and prostaglandins, which cause vasodilation and leakage of plasma in and below the skin, followed by a delayed (4-8 h) secretion of inflammatory cytokines that potentially leads to further inflammation and longer-lasting lesions. Chronic urticaria prevalence is estimated at 0.5-5%, peak onset at 20-40 years, more common in women; in CSU an external trigger usually cannot be identified; in about 45% IgG autoantibodies recognise IgE or the alpha subunit of the high-affinity IgE receptor on mast cells and basophils; antithyroid antibodies in about 27%. The most common causes of acute urticaria are medications, foods, viral infections, stress, parasitic infections, insect venom and contact allergens; the predominant foods are milk, eggs, peanuts, tree nuts, fish and shellfish; in about 50% of acute urticaria the cause is unknown (acute spontaneous urticaria), and up to 36% of these progress to CSU. Dermatographism is the most common physical urticaria (stroking or scratching; tight waistbands and sock elastic); cholinergic urticaria follows a rise in body temperature with exertion or heat. In CSU, NSAIDs, alcohol and opiates should be avoided as they can significantly exacerbate it; food avoidance with elimination diets is not helpful for CSU. Second-generation non-sedating H1-antihistamines are the mainstay of therapy; first-generation antihistamines should be avoided (sedation, cognitive impairment). Hereditary and acquired angioedema present as angioedema without urticaria or itch, and ACE inhibitor angioedema should be suspected in anyone on an ACE inhibitor who develops angioedema without urticaria; bradykinin-mediated angioedema with laryngeal involvement can lead to fatal asphyxiation; up to one-third of ACE inhibitor angioedema occurs months to years after starting the drug (full text PMC6157046; PMID 30263036). 10.1186/s13223-018-0288-z
3. NHS. (2024). Hives (page last reviewed 26 April 2024). Hives rashes usually get better within a few days; the main symptom is an itchy rash of raised bumps or patches that can sting or burn, and its colour can be harder to see on brown and black skin. A pharmacist can advise on antihistamines; tell them about any long-term condition; this may not suit young children. Ask for an urgent GP appointment or NHS 111 if hives do not improve after 2 days, you are worried about a child's hives, the rash is spreading, hives keep coming back, you also have a high temperature and feel unwell, or there is swelling under the skin (angioedema). Call 999 if the lips, mouth, throat or tongue suddenly swell, breathing is very fast or a struggle, the throat feels tight or swallowing is hard, skin, tongue or lips turn blue, grey or pale, you suddenly become very confused, drowsy or dizzy, someone faints and cannot be woken, or a child is limp or floppy. Hives occur when a trigger causes high levels of histamine and other chemicals to be released in the skin; triggers include certain foods, contact with plants, animals, chemicals or latex, cold, hot sweaty skin from exercise, emotional stress or spicy food, a medicine, insect bite or sting, scratching or pressing on the skin such as itchy or tight clothing, an infection, an immune system problem, and rarely water or sunlight; finding and avoiding your triggers may help prevent episodes. A GP might prescribe menthol cream, antihistamines or steroid tablets. www.nhs.uk/conditions/hives
4. Cardona, V., Ansotegui, I. J., Ebisawa, M., El-Gamal, Y., Fernandez Rivas, M., Fineman, S., Geller, M., Gonzalez-Estrada, A., Greenberger, P. A., Sanchez Borges, M., Senna, G., Sheikh, A., Tanno, L. K., Thong, B. Y., Turner, P. J., & Worm, M. (2020). World Allergy Organization anaphylaxis guidance 2020. World Allergy Organization Journal, 13(10), 100472. Anaphylaxis is a serious systemic hypersensitivity reaction, usually rapid in onset, that may cause death; it results from the sudden release of mediators from mast cells and basophils. It is highly likely when an acute illness (minutes to several hours) involves the skin or mucosa (generalized hives, itch or flushing, swollen lips-tongue-uvula) together with respiratory compromise, reduced blood pressure or end-organ dysfunction, or severe gastrointestinal symptoms (e.g., severe crampy abdominal pain, repetitive vomiting); or with acute hypotension, bronchospasm or laryngeal involvement after exposure to a known allergen even without skin signs. Skin signs are absent in 10-20% of reactions. Cofactors include exercise, infections, alcohol and medications. Most reactions are not life-threatening in themselves, but because progression cannot be predicted all anaphylaxis must be treated with intramuscular adrenaline (epinephrine), the first-line treatment; H1-antihistamines have a limited role and can help only cutaneous symptoms; after anaphylaxis patients should be referred to a specialist to assess the cause and be educated on prevention of recurrences and self-management (full text PMC7607509; PMID 33204386). 10.1016/j.waojou.2020.100472
5. Sánchez-Borges, M., Ansotegui, I. J., Baiardini, I., Bernstein, J., Canonica, G. W., Ebisawa, M., Gomez, M., Gonzalez-Diaz, S. N., Martin, B., Morais-Almeida, M., & Ortega Martell, J. A. (2021). The challenges of chronic urticaria part 1: Epidemiology, immunopathogenesis, comorbidities, quality of life, and management. World Allergy Organization Journal, 14(6), 100533. Point prevalence of chronic urticaria, from health-system coding in different countries, ranges from 0.1 to less than 1% globally; one-third of patients have both hives and angioedema, 30-40% hives alone and around 10% angioedema alone. The natural history varies widely: around half of patients follow a three-month self-limited course and within a year it resolves in almost 80%, but in more than 10% a duration of 5 years or longer is expected. Females are affected at least twice as often as males, and most patients are over 20. Mechanisms include IgG autoantibodies to FcεRI or IgE on mast cells and basophils (autoimmunity type II) and IgE autoantibodies to self-antigens such as thyroid peroxidase, DNA and IL-24 (autoimmunity type I, autoallergy); histamine, PAF, tryptase, leukotrienes and cytokines from activated skin mast cells cause sensory nerve activation, vasodilatation and plasma extravasation (full text PMC8233382; PMID 34221215). 10.1016/j.waojou.2021.100533
6. NHS. (2023). Anaphylaxis (page last reviewed 21 June 2023). A life-threatening allergic reaction that happens very quickly, usually within minutes of contact with something you are allergic to, such as a food, medicine or insect sting. Symptoms include swelling of the throat and tongue, difficulty breathing or breathing very fast, difficulty swallowing, tightness in the throat or a hoarse voice, wheezing, feeling faint, dizzy or fainting, and blue, grey or pale skin, lips or tongue; there may also be a swollen, raised or itchy rash. Call 999. Use an adrenaline auto-injector if you have one; lie down and raise the legs, or sit up slowly if struggling to breathe; use a second auto-injector if symptoms have not improved after 5 minutes; do not stand or walk at any time, even if you feel better. Anaphylaxis needs immediate treatment in hospital, usually a stay of around 2 to 12 hours. www.nhs.uk/conditions/anaphylaxis