What is pathophysiology of Urticaria?

['Pirengang kaca puniki']

Napi patofisiologi urtikaria punika?

Urtikaria, ketah kauningin pinaka gatal-gatal, inggih punika kahanan kulit sané kacihnayang antuk kawéntenan gatal, munggah, benjol barak (wheals) ring kulit.

Pathophysiologi urtikaria ngeranayang pelepasan histamin miwah mediator inflamasi tiosan saking sel mast, inggih punika sel imun sané wénten ring kulit miwah jaringan tiosan.

Ring urtikaria akut, pelepasan histamin miwah mediator tiosan kapicu olih reaksi alergi ring alergen spesifik, sekadi ajeng-ajengan, ubad, utawi sengatan serangga.

Puniki ngawinang sel mast degranulate, ngeculake histamin miwah mediator tiosan sané ngawinang pembuluh darah dados bocor, sané ngawinang kawentuk roda.

Ring urtikaria kronis, panyebabnyané sering nénten kauningin, sakéwanten kasengguh mapaiketan sareng mekanisme autoimun.

Ring kasus puniki, angga ngasilang autoantibodi sané nargetang reseptor IgE sané madué afinitas tegeh (FcεRI) ring sel mast, sané ngawinang aktivasi miwah pelepasan histamin miwah mediator tiosan.

Ring urtikaria akut miwah kronis, pelepasan histamin miwah mediator tiosan ngawinang gejala karakteristik ngilu, kemerahan, miwah bengkak.

Perawatan ketahnyané ngawigunayang antihistamin anggén nambakin efek histamin miwah ngirangin gejala.

Ring kasus sané abot, tamba tiosan sekadi kortikosteroid utawi omalizumab prasida kawigunayang anggen ngendaliang kawentenannyané.

['Rujukan']

PubMed/Medline https://www.nlm.nih.gov/databases/download/pubmed_medline.html

RefinedWeb https://arxiv.org/abs/2306.01116

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.

Marrouche N, Grattan C: Childhood urticaria. Curr Opin Allergy Clin Immunol. 2012, 12 (5): 485-90.

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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