Urticaria, e e itsegeng thata jaaka motlhwa, ke bolwetse jwa letlalo jo bo lemogiwang ka go nna le matshwao a a magwata, a a tlhatlogileng, a mahibidu mo letlalong.
Pathophysiology ya urticaria e akaretsa go ntshiwa ga histamine le dilo tse dingwe tse di bakang go ruruga mo diseleng tsa mast, tse e leng disele tsa mmele tse di mo letlalong le mo dithishung tse dingwe.
Fa motho a na le urticaria e e masisi, histamine le dilo tse dingwe tse di bakang bolwetse jono di ntshiwa ke fa a tshwaediwa ke sengwe se se rileng, jaaka dijo, melemo kgotsa go longwa ke ditshenekegi.
Seno se dira gore disele tse dikgolo di se ka tsa nna le dithoro, di bo di ntsha histamine le dilo tse dingwe tse di dirang gore ditshika tsa madi di dutle, mme seo se dira gore go nne le makgwafo.
Mo go urticaria e e sa foleng, gantsi ga go itsiwe gore e bakwa ke eng, mme go akanngwa gore e bakwa ke thulaganyo ya mmele ya go lwantsha malwetse.
Mo lebakeng le, mmele o tlhagisa di-autoantibody tse di lebisitsweng kwa go tse di nang le kamano e e kwa godimo le IgE receptor (FcεRI) mo diseleng tsa mast, mme seo se dira gore di bereke le go ntsha histamine le di-mediator tse dingwe.
Mo go urticaria e e masisi le e e sa foleng, go ntshiwa ga histamine le dilo tse dingwe tse di e bakang go dira gore motho a nne le matshwao a a jaaka go nna le go baba, go nna le mmala o mohibidu le go ruruga.
Gantsi kalafi e akaretsa go dirisa di-antihistamine go thibela ditlamorago tsa histamine le go fokotsa matshwao.
Mo mabakeng a a masisi, go ka dirisiwa melemo e mengwe e e jaaka di-corticosteroid kgotsa omalizumab go laola bolwetse jono.
Wahlgren CF: Pathophysiology of itching in urticaria and atopic dermatitis. Allergy. 1992, 47 (2 Pt 1): 65-75.
Raap U, Liekenbröcker T, Wieczorek D, Kapp A, Wedi B: [New therapeutic strategies for the different subtypes of urticaria]. Hautarzt. 2004, 55 (4): 361-6.
[Recommendations for the diagnosis and treatment of urticaria in children]. Arch Argent Pediatr. 2021, 119 (2): S54-S66.
Brzoza Z, Grzeszczak W, Rogala B, Trautsolt W, Moczulski D: Possible contribution of chemokine receptor CCR2 and CCR5 polymorphisms in the pathogenesis of chronic spontaneous autoreactive urticaria. Allergol Immunopathol (Madr). , 42 (4): 302-6.
Sweeney TM, Dexter WW: Cholinergic urticaria in a jogger: ruling out exercise-induced anaphylaxis. Phys Sportsmed. 2003, 31 (6): 32-6.
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What is pathophysiology of urticaria?
Urticaria, commonly known as hives, is a skin condition characterized by the appearance of itchy, raised, red welts (wheals) on the skin.
The pathophysiology of urticaria involves the release of histamine and other inflammatory mediators from mast cells, which are immune cells found in the skin and other tissues.
In acute urticaria, the release of histamine and other mediators is triggered by an allergic reaction to a specific allergen, such as food, medication, or insect sting.
This causes the mast cells to degranulate, releasing histamine and other mediators that cause blood vessels to become leaky, leading to the formation of wheals.
In chronic urticaria, the cause is often unknown, but it is thought to be related to an autoimmune mechanism.
In this case, the body produces autoantibodies that target the high-affinity IgE receptor (FcεRI) on mast cells, leading to their activation and the release of histamine and other mediators.
In both acute and chronic urticaria, the release of histamine and other mediators leads to the characteristic symptoms of itching, redness, and swelling.
Treatment typically involves the use of antihistamines to block the effects of histamine and reduce symptoms.
In severe cases, other medications such as corticosteroids or omalizumab may be used to control the condition.
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