Urticaria ngu ai gaw, hpyi shan hta hkyeng ai, pung pung rai nna, hpyi hta hkyawk ai lam byin ai.
Urticaria a pathophysiology hta, hpyi hte kaga hkum hkrang hta mu lu ai immune cell ni rai nga ai mast cell ni kaw nna histamine hte kaga inflammatory mediators ni hpe shalawt dat ai lam lawm ai.
Dai hta n-ga, ana htang maja ai lam byin wa yang, ana htang maja ai lam byin wa ai.
Dai majaw, mast cell ni gaw histamine hte kaga tsi ni hpe shapraw nna sai lam ni hta hka shang wa ai majaw, sai lam ni hta sai lam ni byin wa ai.
Hkum shan hta ana byin ai lam gaw n chye lu tim, hkum hkrang a ninghkap ai lam (autoimmune mechanism) hte seng ai ngu sawn la ma ai.
Dai shaloi, hkum hkrang gaw mast cell ni hta high-affinity IgE receptor (FcεRI) hpe madung tawn ai autoantibodies ni hpe shapraw nna, dai ni hpe shamu shamawt ya ai hte histamine hte kaga mediator ni hpe shalawt ya ai.
Dai hta n-ga, ana htang maja ai lam, hkyeng ai lam hte pu ba ai lam ni byin wa ai.
Dai ana hpe tsi lajang ai shaloi, antihistamine tsi ni hpe lang nna, ana a kumla ni hpe shayawm ya ai.
Grau sawng ai shaloi, corticosteroid (sh) omalizumab zawn re ai kaga tsi ni hpe mung, dai ana hpe hkang lu na matu lang mai ai.
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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