Chronic Idiopathic Urticaria: Systemic Complaints and Their Relationship with Disease and Immune Measures

Doong, Judy; Chichester, Kris; Oliver, E; Schwartz, Lawrence B.; Saini, Sarbjit S.

doi:10.1016/j.jaip.2016.11.037

Cited by 56 publications

(36 citation statements)

References 17 publications

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“…A recent study reported a high frequency of systemic signs and symptoms such as joint pain or swelling (55.3%), headache/fatigue (47.6%), flushing (42.7%), wheezing or breathlessness (30.1%), gastrointestinal complaints (26.2%), and palpitations (9.7%) in two thirds of adult patients with CSU that are probably under-recognized in daily practice [6]. Interestingly, the number of organs involved did not correlate with serum tryptase levels [6].…”

Section: Clinical Classification Of Urticariamentioning

confidence: 99%

Urticaria and Angioedema: an Update on Classification and Pathogenesis

Radonjic-Hoesli

Scherer

Micaletto

et al. 2017

Clinic Rev Allerg Immunol

119

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Urticaria is a common, mast cell-driven disease presenting with wheals or angioedema or both. In the last years, urticaria has increasingly attracted notice to clinicians and researchers, last but not least inspired by the approval of omalizumab, an anti-IgE antibody, for urticaria treatment. There is wide consensus on the clinical classification based on duration and elicitation. However, the pathogenesis is incompletely understood. This review summarizes current guidelines for the management and novel insights in the pathogenesis of urticaria with special focus on their impact on clinical praxis. The classification of urticaria subgroups is mainly based on clinical criteria: acute and chronic urticaria (CU). Chronic urticaria comprises both chronic spontaneous urticaria (CSU) and chronic inducible urticaria (CIndU) that includes physical and non-physical urticarias. Recent research focused on characterizing the role of cells and mediators involved in the pathogenesis of urticaria, identifying the mechanisms of mast cell activation, and investigating underlying autoimmune processes in chronic spontaneous urticarial. Currently, non-sedating antihistamines and omalizumab, an antiimmunoglobulin E antibody, are recommended for the therapy of chronic urticaria, as both exhibit a favorable efficacy and safety profile. Novel therapeutic strategies aim at specifically targeting cells and mediators involved in the pathogenesis of urticaria.

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Section: Clinical Classification Of Urticariamentioning

confidence: 99%

Urticaria and Angioedema: an Update on Classification and Pathogenesis

Radonjic-Hoesli

Scherer

Micaletto

et al. 2017

Clinic Rev Allerg Immunol

119

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“…It is thought that IL-1 plays a major role in the pathogenesis of Schnitzler’s syndrome largely due to the observation that IL-1 receptor antagonists can induce symptom remission in patients who have failed other immunomodulatory regimens 3 18 19. Moreover, the pathogenesis is thought to be mast-cell independent.…”

Section: Discussionmentioning

confidence: 99%

“…CSU is a common condition with a point prevalence of 0.5%–1% and is clinically diagnosed based on the presence of recurrent pruritic, migratory, raised, non-scarring, erythematous plaques 2. Laboratory investigations are normal, and lesions are responsive to standard CSU therapy 3. CSU is a benign and self-limiting disease lasting between 2 and 5 years 1.…”

Section: Introductionmentioning

confidence: 99%

Refractory urticaria and the importance of diagnosing Schnitzler’s syndrome

et al. 2019

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A 52-year-old man presented with chronic urticaria that was refractory to standard chronic spontaneous urticaria (CSU) treatment. Over time, he developed systemic symptoms including fatigue, weight loss, arthralgia and bone pain. His laboratory investigations also became significant for microcytic anaemia, neutrophilia and elevated C reactive protein, erythrocyte sedimentation rate and IgE levels, in addition to an IgM monoclonal protein. He achieved only partial remission with typical medications for CSU including omalizumab, cyclosporine and cetirizine. After 6 years, his worsening symptoms and abnormal investigations led to a rare diagnosis of Schnitzler’s syndrome and a trial of the interleukin 1 receptor antagonist, anakinra, which caused a rapid and complete resolution of his symptoms.

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“…Additional study of tryptase expression and function in these patients may yield important insights into the effects of specific tryptase isoforms on mast cell-mediated reactions and cellular homeostasis. Importantly, the majority of BST elevations, present in 4–6% of the general population ( Gonzalez-Quintela et al, 2010 ; Fellinger et al, 2014 ), appears to be attributable to increased TPSAB1 copy number, suggesting that this genetic trait may commonly contribute to some of the clinical phenotypes initially reported, as well as to others clinically associated with elevated BST ( Kucharewicz et al, 2007 ; Fellinger et al, 2014 ; Sahiner et al, 2014 ; Doong et al, 2017 ; Valent et al, 2017 ).…”

Section: Mast Cell Deregulationmentioning

confidence: 99%