Urticaria, leyi tivekaka tanihi swirhumbana, i xiyimo xa nhlonge lexi vonakaka hi ku huma ka swirhumbana swo tshwuka leswi nga ni swirhumbana, leswi nga ni swirhumbana enhlongeni.
Pathophysiology ya urticaria yi katsa ku humesiwa ka histamine ni swilo swin'wana leswi vangaka ku pfimba hi tisele ta mast, leti nga tisele ta nsawutiso leti kumekaka enhlongeni ni le ka tinyama tin'wana.
Eka vuvabyi lebyi, histamine ni swin'wana leswi endlaka leswaku miri wu humesa ti-histamine swi humesiwa hi ku va munhu a vabya loko a dya swakudya swo karhi, a nwa mirhi kumbe loko a lumiwe hi switsotswana.
Leswi swi endla leswaku tisele leti ti nga ha vi na tisele, ti humesa histamine ni swin'wana leswi endlaka leswaku misiha ya ngati yi nga ha koti ku famba kahle, leswi endlaka leswaku ku va ni swirhumbana.
Eka vuvabyi lebyi nga tshungulekiki bya swirhumbana, hakanyingi xivangelo xa kona a xi tiviwi, kambe ku anakanyiwa leswaku byi vangiwa hi mavabyi lama tlulelaka miri.
Eka xiyimo lexi, miri wu humesa ti autoantibodies leti kongomisiwaka eka high-affinity IgE receptor (FcεRI) eka tisele ta mast, leswi endlaka leswaku ti tirha kutani ti humesa histamine na swihlanganisi swin'wana.
Eka vuvabyi lebyi bya xihatla ni lebyi nga tshungulekiki, ku humesiwa ka histamine ni swin'wana leswi endlaka leswaku miri wu tshukatshuka swi vanga ku tshwukiselana ka marhambu, ku tshwuka ni ku pfimba.
Vutshunguri bya kona byi katsa ku tirhisa mirhi leyi lwaka ni switsongwatsongwana leswaku yi sivela ku tirha ka histamine ni ku hunguta swikombiso swa kona.
Eka mavabyi lama nga ni khombo swinene, ku nga ha tirhisiwa mirhi yin'wana yo tanihi ti-corticosteroid kumbe omalizumab leswaku yi lawula vuvabyi lebyi.
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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['Loko u nga nghenisi vuxokoxoko hinkwabyo lebyi nga laha henhla swi nga endla leswaku ku tirhana ni xivilelo xa wena swi hlwela.']
['Ku Tihlanganisa']
['Hi kombela u hi rhumela imeyili hi xivutiso/xiringanyeto xihi na xihi.']
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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