Urtikaria, konosí komo urtikaria, ta un kondishon di kueru ku ta karakterisá pa e aparensia di rasgonan kòrá, ku ta pone kueru kria.
E fisiopatologia di urtikaria ta envolvi e liberacion di histamina y otro mediadornan di inflamacion di mast cell, cual ta celnan inmunologico haya den cuero y otro tehido.
Den urtikaria agudo, e liberacion di histamina y otro mediadornan ta wordo causa pa un reaccion alergico na un alergeno specifico, manera cuminda, medicamento of un picadura di insecto.
Esaki ta pone e mast cellnan desgranula, liberando histamine y otro mediadornan cu ta causa e sanger di e vasonan pa ta leak, loke ta conduci na e formacion di wheals.
Den urtikaria króniko, e kousa hopi bia no ta konosí, pero ta kere ku e ta relashoná ku un mekanismo autoimunológiko.
Den e kaso aki, e kurpa ta produsí autoanticuerpo ku ta dirigí riba e receptor IgE di afinidat haltu (FcεRI) riba e mast cellnan, loke ta kondusí na nan aktivashon i liberashon di histamina i otro mediadornan.
Den urtikaria tantu agudo komo króniko, e liberashon di histamina i otro mediadornan ta kondusí na e síntomanan karakterístiko di keintura, kemadura i hinchamentu.
E tratamentu ta enserá usualmente e uso di antihistamin pa blòkia e efektonan di histamina i redusí e síntomanan.
Den kasonan grave, por usa otro remedi manera kortikosteroide òf omalizumab pa kontrolá e kondishon.
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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