S'orticària, connota comunemente comente a pedde, est una cunditzione de sa pedde caraterizada dae s'aparitzione de pedde ruja, arta e infèrchida (pedde).
Sa fisiopatologia de s'orticària interessat su lìberu de istamina e àteros mediadores inflamatòrios dae sos mastocitos, chi sunt tzèllulas immunitàrias agatadas in sa pedde e àteros tessidos.
In s'orticària aguda, su lìberu de istamina e àteros mediadores est ativadu dae una reatzione allèrgica a un'allergèniu ispetzìficu, comente a màndigu, meighinas o puntura de babbautzu.
Custu faghet chi sos mastocitos si degranulant, liberende istamina e àteros mediadores chi faghent pèrdere sos vasos sanguignos, batende a sa formatzione de rodas.
In s'orticària crònica, sa càusa est a s'ispissu disconnota, ma si pensat chi siat acapiada a unu mecanismu autoimmune.
In custu casu, su corpus produet autoanticorpos chi pigant a bersàgliu su retzidore IgE de arta afinidade (FcεRI) in sos mastocitos, batende a s'ativatzione issoro e a sa liberatzione de istamina e àteros mediadores.
In ambos casos, s'istamina e àteros mèdiadores s'emitent e custu batit a sos sìntomos caraterìsticos de pruritu, rossu e inframentu.
Su tratamentu de sòlitu ìmplicat s'impreu de antiistaminos pro blocare sos efetos de s'istamina e minimare sos sìntomos.
In casos graes, àteros meighinas comente sos corticosteroides o s'omalizumab podent èssere impreados pro controllare sa cunditzione.
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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