L'orticaria, comunemente conosùa come orticaria, xe na condision deła pełe caraterixada dała comparsa de brufoli rossi, alti e pruriginosi (orticaria) suła pełe.
Ła patofisiologia de l'orticaria ła coinvolge el rilascio de istamina e altri mediatori infiammatori dai mastociti, che xe cellule immunitarie che se cata neła pele e altri tessudi.
Ne l'orticaria acuta, el rilascio de istamina e altri mediatori xe provocà da na reazion ałergica a un ałergene specifico, come cibo, medexina o puntura de inseto.
Questo fa sì che i mastociti se degranuli, e i łibera istamina e altri mediatori che fa sì che i vasi sanguigni i se slarga, portando ała formasion de roture.
Ne l'orticaria cronica, ła causa xe spesso sconosùa, ma se pensa che ła sia ligà a un mecanismo autoimune.
In sto caso, el corpo produxe autoanticorpi che i mira al recetor IgE de alta affinità (FcεRI) sui mastociti, portando ała so ativasion e al rilascio de istamina e altri mediatori.
Ne l'orticaria acuta e cronica, el rilascio de istamina e altri mediatori porta ai sintomi carateristici de prurito, rosso e gonfiore.
El tratamento el coinvolge tipicamente l'uso de antiistaminici pa blocar i efeti de l'istamina e ridur i sintomi.
Nei casi gravi, altri medeghi come corticosteroidi o omalizumab pol essar usà pa controlar a condission.
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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