Purpose of review
Urticaria is a frequent disorder that can present with erythema, edema, and pruritus involving the skin and mucous membranes. Early diagnosis and proper management of the urticaria according to the type (i.e., acute vs chronic) is of utmost importance to reduce the burden of the disease and prevent psychosocial comorbidities. In this review, we aim to summarize the diagnosis and management of acute and chronic urticaria with emphasis on the differences.
Recent findings
Autoimmune mechanisms (type I or type IIb autoimmunity) have been recently defined in the pathogenesis of chronic spontaneous urticaria. Despite the high rates of symptom control in both acute and chronic urticaria with the existing treatment options, new treatments are still needed in a subset of patients. Promising treatment targets in CSU include Bruton’s tyrosine kinase, Siglec-8, or IL-4/13.
Summary
Therapeutic management of acute and chronic urticaria is still challenging despite the highly effective treatments. In addition to symptomatic treatment, elicitation of the pathogenesis of both forms of urticaria and clear understanding of the nature of the disease by the patient are essential. Urticaria has still a high impact on the patients’ quality of life warranting the studies on the pathogenesis, novel treatment options, and the factors determining which patients with acute urticaria will likely develop chronic urticaria.
Background: We aim to investigate the effects of the Bruton’s tyrosine
kinase (BTK) inhibitor remibrutinib on human in vitro cell
activation induced by serum obtained from chronic spontaneous urticaria
(CSU) and chronic inducible urticaria (CIndU) patients. Methods: 22
patients with CSU (mean age 52 years, 27% women) and 22 with CIndU (46
years, 27% women) were included. A sex-equivalent control group was
enrolled. Total IgE serum levels and the FcεR1a expression on blood
basophils were determined before the initiation of omalizumab therapy.
Patients were then classified as responders or non-responders to
anti-IgE therapy, according to their clinical data and IgE and FcεR1a
receptor expression. Mast cell generation and stimulation and basophil
stimulation were performed. Flow cytometry was used to analyze samples.
Percentage of activation, degranulation and inhibition in basophils and
mast cells are studied. Results: Main results show that remibrutinib
inhibits mast cells and basophil degranulation induced by IgE
cross-linking. Also, serum from patients induced a greater degranulation
of mast cells and basophils compared to controls. We found that
activation of mast cells and basophils by patient sera was not related
to omalizumab responsiveness. Conclusion: Our results show that
remibrutinib is able to inhibit the degranulation of human basophils and
mast cells in vitro, independently of the patient’s expression of
FcεR1 expression and response to omalizumab.
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