Special Issue "Clinical Diagnosis and Treatment for Chronic Urticaria"
Deadline for manuscript submissions: 31 October 2020.
Interests: Urticaria; chronic spontaneous urticaria; inducible urticaria; contact urticaria; contact dermatitis; eczema; atopic dermatitis
“The history of urticaria represents a fascinating account of man´s gradually increasing understanding of medicine as such, and of the unique clinical features of the pathomechanisms of urticaria in particular” (“Urticaria,” 1986). We can affirm with forcefulness that the most recent pathogenic and therapeutic advances in urticaria constitute a true revolution. Currently, the expectations of therapeutic success for the patient and for the doctor are frankly much better than 10 years ago, and will be even better in the immediate future. The success of the management of chronic spontaneous urticarial (CSU) lies on a perfect strategic plan. The EAACI; GA2LEN; EDF; WAO Urticaria guidelines (2018) define successful therapy as the complete resolution of signs (hives and angioedema) and symptoms (itch and pain). A basic principle of efficacy and safety is desirable; it is the therapeutic goal, as the clinical experience holds that treatment should continue for extended periods of time, with adaptations according to changes in symptoms. Nowadays, the unique recommended third line of treatment consists of adding to the antihistamines an incredible drug for CSU, omalizumab. We learned from our practice and we have data about how omalizumab behaves: prediction of CSU fast-slow and no response, the need to up dose, relapse and retreatment, use in special populations, efficacy for angioedema and chronic inducible urticarias (CIndUs), or safety of long term treatment. The wheal is a consequence of mast cell degranulation through different keys, including cross-linkage of immunoglobulin (Ig)E and IgG bound to the high-affinity IgE receptors (FcɛRI) on the surface of the mast cells and basophiles. Histamine and other mediators such as the Platelet Activating Factor or PGD2 leads to hives and angioedema. Vasodilatation induces erythema and the oedema is a consequence of neutrophils, lymphocytes, basophils, and mainly eosinophils’ chemoattraction through leaky capillaries. Based in molecular and genetic pathogenic findings, several new treatments could also be proposed for CU. The identification and validation of reliable biomarkers in CSU and CIndU would be useful to define the patient's disease status leading to a more individualized and personalized treatment and follow-up, improving symptom control and quality of life and decreasing the burden of the disease. This urticaria supplement will update diagnosis and clinical management of chronic urticaria. The disease improvement means a worldwide continuous medical education for which active CU networks (e.g., UCARE) are crucial.
Prof. Ana M. Giménez-Arnau
Manuscript Submission Information
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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Chronic Spontaneous Urticaria
- Chronic Inducible Urticaria
- Contact Urticaria