L- urtikarja, magħrufa b' mod komuni bħala l- ħruq, hija kundizzjoni tal- ġilda kkaratterizzata mill- dehra ta ' ħruq, imqajma, ħomor (ħruq) fuq il- ġilda.
Il- patofiżjoloġija ta ' l- urtikarja tinvolvi r- rilaxx ta ' l- istamina u medjaturi infjammatorji oħra minn ċelloli mast, li huma ċelloli immuni li jinstabu fil- ġilda u tessuti oħra.
Fl- urtikarja akuta, ir- rilaxx taʼ l- istamina u taʼ medjaturi oħra jiġi kkawżat minn reazzjoni allerġika għal allerġenu speċifiku, bħal ikel, mediċina, jew biċċiet taʼ insetti.
Dan jikkawża li ċ- ċelloli masti jitneħħew mill- granuli, u joħorġu l- istamina u medjaturi oħra li jikkawżaw li l- vini tad- demm isiru li jnixxfu, u dan iwassal għall- formazzjoni ta ' wheels.
Fl- urtikarja kronika, il- kawża spiss ma tkunx magħrufa, imma huwa maħsub li hija relatata maʼ mekkaniżmu autoimmuni.
F' dan il- każ, il- ġisem jipproduċi autoantikorpi li jimmiraw lejn ir- riċettur IgE ta ' affinità għolja (FcεRI) fuq iċ- ċelloli mast, li jwassal għall- attivazzjoni tagħhom u r- rilaxx ta ' histamina u medjaturi oħra.
Kemm fl- urtikarja akuta kif ukoll fil- urtikarja kronika, ir- rilaxx ta ' l- istamina u medjaturi oħra jwassal għas- sintomi karatteristiċi ta ' ħakk, ħmura, u nefħa.
It- trattament tipikament jinvolvi l- użu ta ' antiistaminiċi biex jimblokkaw l- effetti ta ' l- istamina u jnaqqsu s- sintomi.
F' każijiet severi, jistgħu jintużaw mediċini oħra bħal kortikosterojdi jew omalizumab biex jikkontrollaw il- kundizzjoni.
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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