Urticaria, nke a na-akpọkarị hives, bụ ọrịa akpụkpọ ahụ nke a na-ahụkarị site n'ọdịdị nke ọnya, nke dị elu, nke na-acha ọbara ọbara (wheals) na akpụkpọ ahụ.
Pathophysiology nke urticaria na-agụnye ntọhapụ nke histamine na ndị ọzọ na-akpata mbufụt site na mkpụrụ ndụ mast, nke bụ mkpụrụ ndụ na-eguzogide ọrịa a na-ahụ na akpụkpọ ahụ na akwara ndị ọzọ.
N'ọrịa urticaria siri ike, a na-ewepụta histamine na ihe ndị ọzọ na-eme ka ọ na-arụ ọrụ site na mmeghachi omume na-adịghị mma nye ihe na-eme ka ọ na-arụ ọrụ, dị ka nri, ọgwụ, ma ọ bụ ahụhụ.
Nke a na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ ndị na- eme ka mkpụrụ ndụ.
N'ọrịa urticaria na-adịgide adịgide, a na-amaghị ihe na-akpata ya, ma a na-eche na o nwere ihe jikọrọ ya na ọrịa autoimmune.
N'ọnọdụ a, ahụ na-emepụta autoantibodies nke na-elekwasị anya na high-affinity IgE receptor (FcεRI) na mkpụrụ ndụ mast, na-eduga na mmegharị ha na ntọhapụ nke histamine na ndị ọzọ na-elekọta.
Ma n'ọrịa urticaria siri ike ma n'ọrịa urticaria na-adịghị ala ala, ntọhapụ nke histamine na ndị ọzọ na-eme ihe na-eduga n'ihe mgbaàmà ndị a na-ahụkarị nke ọnya, ọbara ọbara, na mbufụt.
Ọgwụgwọ na-agụnyekarị iji ọgwụ ndị na-egbochi histamine egbochi mmetụta nke histamine ma belata mgbaàmà.
N'ọnọdụ ndị siri ike, a pụrụ iji ọgwụ ndị ọzọ dị ka corticosteroids ma ọ bụ omalizumab chịkwaa ọnọdụ ahụ.
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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