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.
['Kunnafoni nafama: kɛnɛya']
['Nin gafe in labɛnna kalan ni kunnafoni dɔrɔn de kama, a tɛ sɔrɔ dɔgɔtɔrɔ ka ladili wala kɛnɛyabaarakɛla ka baara kɛcogo la.']
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['Aw bɛ ladilikan ɲini tuma bɛɛ aw ka dɔgɔtɔrɔ fɛ walima kɛnɛya baarakɛla dɔ wɛrɛ min bɛ se ka aw dɛmɛ ka aw ka bana furakɛ. Aw kana dɔgɔtɔrɔ ka ladilikan bila ka suma walima ka mɛn a ɲini na sabu aw ye fɛn dɔ kalan nin siti kan. Ni aw hakili la ko aw ka bana bɛ se ka juguya joona, aw ye 911 wele walima aw ka taa aw ka dɔgɔtɔrɔso la joona joona. Nin siti tɛ dɔkɔtɔrɔ ni banabagatɔ ka jɛɲɔgɔnya jira. BioMedLib ni a ka baaradenw, walima nin siti dɛmɛbaga si tɛ kuma si jira walima ka jira, nin kunnafoniw wala u labaarali kama.']
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['Ni i dara a la kô i ka site web ni a baara tchogow bè i ka lakananifènw la, i (walima i ka lasigiden) bè se ka i yèrè ka lakananifènw bila ka o site web ni a baara tchogow bila kènèkan.']
['Waajibi don kunnafoniw ci kɛtɔ ka kɛ sɛbɛn ye e-mail fɛ (e-mail de kan ka lajɛ sɛbɛn ɲɛ Kunnafoniw lajɛ yɔrɔ la).']
["DMCA bɛ a ɲini i ka kunnafoni sɛbɛn bɔlɔlɔw kan kojugukɛ sɛbɛn bɛ sɛbɛn min kɔnɔ, o ka kan ka nin kunnafoniw fara a kan: (1) sɛbɛnni kɛtɔ ka sɛbɛnni kɛ min bɛ sɛbɛnni kɛ ni a ma kɛ kojugukɛ sɛbɛn ye; (2) sɛbɛnni kɛtɔ ka fɛn kofɔlen in kofɔ ani kunnafoni minnu bɛ a to an bɛ se ka fɛn kofɔlen in sɔrɔ; (3) i ka ladɛrɛsi, i ka ladɛrɛsi, telefɔni nimɔrɔ ani i ka ladɛrɛsi; (4) i ka kumaɲɔgɔnya sɛbɛn ko i dalen b'a la ko i bɛ a dɔn ko i bɛ ka fɛn kofɔlen in kɛ ni sariya min ye, o ma di sɛbɛnnikɛbaga ma, a ka ladɛrɛsi tigi, walima sariya wɛrɛ; "]
['(5) a ka seereyasɛbɛ sɛbɛntiya, ko seereyasɛbɛ minɛnen bɛ kojugubakɛlaw kama, ko kunnafoni min bɛ o sɛbɛntiya kɔnɔ, ko tiɲɛ don ani ko i yamaruyalen don ka yamaruya di ka kɛwalew kɛ minnu bɛ tiɲɛni kɛ; ']
['ani (6) sɛbɛn dɔ ka boloci walima ɛkitɔrɔniki sɛbɛn sɛbɛn tigi fɛ walima mɔgɔ min yamaruyara ka baara kɛ sɛbɛn tigi tɔgɔla. ']
['Ni kunnafoni fɔlen ninnu bɛɛ ma fara ɲɔgɔn kan, o bɛ se ka kɛ sababu ye ka mɛn baara kɛli la i ka sɛbɛn kɔnɔ.']
['Ɲɔgɔnkunbɛn']
['Sɛbɛn ɲɛ Ɲiningaliw / ladiliw']
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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