The European Academy of Allergy and Clinical Immunology (EAACI) owns three journals: Allergy, Pediatric Allergy and Immunology and Clinical and Translational Allergy. One of the major goals of EAACI is to support health promotion in which prevention of allergy and asthma plays a critical role and to disseminate the knowledge of allergy to all stakeholders including the EAACI junior members. There was substantial progress in 2019 in the identification of basic mechanisms of allergic and respiratory disease and the translation of these mechanisms into clinics. Better understanding of molecular and cellular mechanisms, efforts for the development of biomarkers for disease prediction, novel prevention and intervention studies, elucidation of mechanisms of multimorbidities, entrance of new drugs in the clinics as well as recently completed phase three clinical studies and publication of a large number of allergen immunotherapy studies and meta-analyses have been the highlights of the last year.

An amendment to this paper has been published and can be accessed via the original article.

The European Academy of Allergy and Clinical Immunology (EAACI) supports three journals: Allergy, Paediatric Allergy and Immunology as well as Clinical and Translational Allergy. The major goals of EAACI include (i) supporting health promotion in which the prevention of allergy and asthma plays a critical role and (ii) disseminating the knowledge of allergy to all stakeholders including the EAACI junior members. Substantial progress was made in 2018 in the identification of basic mechanisms of atopic dermatitis and urticaria and the translation of these mechanisms into clinics. Many large epidemiologic studies and meta-analyses have been the highlights of the last year.

BACKGROUND:GA²LEN, the Global Allergy and Asthma European Network, has recently launched a program for the development, interaction, and accreditation of centers of reference and excellence in special areas of allergy embedded in its overall quality management of allergy centers of excellence. The first area chosen is urticaria. Urticaria is a common and debilitating condition and can be a challenge for both patients and treating physicians, especially when chronic. Centers of reference and excellence in urticaria (UCAREs) can help to improve the management of hard-to-treat conditions such as urticaria.AIMS:Here, we describe the aims, the requirements and deliverables, the application process, and the audit and accreditation protocol for GA²LEN UCAREs.RESULTS:The main aims of GA²LEN UCAREs are to provide excellence in urticaria management, to increase the knowledge of urticaria by research and education, and to promote the awareness of urticaria by advocacy activities. To become a certified GA²LEN UCARE, urticaria centers have to apply and fulfill 32 requirements, defined by specific deliverables that are assessed during an audit visit.DISCUSSION AND CONCLUSION:The GA²LEN UCARE program will result in a strong network of urticaria specialists, promote urticaria research, and harmonize and improve urticaria management globally.

Clinical and Experimental DermatologyVolume 39, Issue 5 p. 651-652 Viewpoints in dermatology ● Correspondence Improvement in quality of life impairment followed by relapse with 6-monthly periodic administration of omalizumab for severe treatment-refractory chronic urticaria and urticarial vasculitis A. C. Kai, A. C. Kai Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London, SE1 7EH, UKSearch for more papers by this authorC. Flohr, C. Flohr Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London, SE1 7EH, UKSearch for more papers by this authorC. E. Grattan, C. E. Grattan clive.e.grattan@nnuh.nhs.uk Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London, SE1 7EH, UKSearch for more papers by this author A. C. Kai, A. C. Kai Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London, SE1 7EH, UKSearch for more papers by this authorC. Flohr, C. Flohr Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London, SE1 7EH, UKSearch for more papers by this authorC. E. Grattan, C. E. Grattan clive.e.grattan@nnuh.nhs.uk Cutaneous Allergy, St John's Institute of Dermatology, St Thomas' Hospital, London, SE1 7EH, UKSearch for more papers by this author First published: 23 April 2014 https://doi.org/10.1111/ced.12320Citations: 17 Conflict of interest: the authors declare that they have no conflicts of interest. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume39, Issue5July 2014Pages 651-652 RelatedInformation

Recurrent fever can be the sole or leading manifestation of a variety of diseases including malignancies, autoimmune diseases and infections. Because the differential diagnoses are manifold, no formal guidelines for the approach of patients with recurrent fever exists. The newly recognized group of autoinflammatory diseases are often accompanied by repetitive fever attacks. As these episodes are frequently associated by a variety of divergent presentations, the differentiation of other causes for febrile illnesses can be difficult. In this article, we first review disease entities, which frequently present with the symptom of recurrent fever. In a next step, we summarize their characteristic pattern of disease presentation. Finally, we analyse key features of autoinflammatory diseases, which are helpful to distinguish this group of diseases from the other causes of recurrent fever. Recognizing these symptom patterns can provide the crucial clues and, thus, lead to the initiation of targeted specific diagnostic tests and therapies.

Urticarial skin reactions are one of the most frequent problems seen by allergists and clinical immunologists in daily practice. The most common reason for recurrent wheals is spontaneous urticaria. There are, however, several less common diseases that present with urticarial rash, such as urticarial vasculitis and autoinflammatory disorders. The latter include cryopyrin-associated periodic syndrome and Schnitzler's syndrome, both rare and disabling conditions mediated by increased interleukin-1 secretion. Apart from the urticarial rash, patients are suffering from a variety of systemic symptoms including recurrent fever attacks, arthralgia or arthritis and fatigue. Autoinflammatory diseases are often associated with a diagnostic delay of many years and do not respond to antihistamines and other treatments of urticaria. Also, the chronic inflammation may lead to long-term complications such as amyloidosis. It is therefore important not to miss these diseases when diagnosing and treating patients with chronic recurrent urticarial rash. Here, we present clinical clues and tips that can help to identify autoinflammatory disorders in patients presenting with chronic urticarial rash and discuss their clinical picture and management.

Summary Background We have demonstrated previously mast cell histamine release upon incubation with chronic urticaria (CU) sera, presumably by degranulation. Objective To explore total and mature tryptase in order to assess whether any increase in total tryptase levels is due in part to mast cell degranulation or to mast cell burden. We also wanted to explore differences between the autoimmune groups called idiopathic (serum unable to activate basophils), and to correlate total and mature tryptase levels with different urticaria features. Methods We measured total and mature tryptase serum levels in 81 CU patients, 16 atopic donors and 21 healthy control sera. We assessed autoimmunity by measuring the CD63 expression in normal basophil donors upon incubation with CU sera. Results We found significantly higher levels of total tryptase in the sera of CU patients (6.6 ±4.1 μg/L) than in sera from healthy non‐atopic subjects (4.4 ±2.8 μg/L) and from atopic subjects (4.5 ±1.7 μg/L). Mature tryptase levels were undetectable (<1 ng/mL). Total tryptase levels in the autoimmune urticaria group were significantly higher (9.8 ±5.4 μg/L) than the idiopathic urticaria group (4.4 ±2.2 μg/L). A significant difference in total tryptase was found between symptomatic patients (7.3 ±4.1 μg/L) compared with asymptomatic ones (5.7 ±4.1 μg/L) at the time of venesection. No difference was found in mature tryptase levels either. Conclusion Total elevated tryptase levels are not accompanied by an elevated mature tryptase levels, as might be expected if the serum levels reflected mast cell degranulation. Cite this as : M. Ferrer, J. M. Nuñez‐Córdoba, E. Luquin, C. E. Grattan, J. M. De la Borbolla, M. L. Sanz, L. B. Schwartz, Clinical & Experimental Allergy , 2010 (40) 1760–1766.

Clinical and Experimental DermatologyVolume 34, Issue 6 p. 745-746 Yellow papules and plaques on the face of a young girl R. A. Abbott, R. A. Abbott St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorE. Calonje, E. Calonje St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorC. E. Grattan, C. E. Grattan St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorH. Kurwa, H. Kurwa St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorR. P. Sarkany, R. P. Sarkany St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this author R. A. Abbott, R. A. Abbott St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorE. Calonje, E. Calonje St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorC. E. Grattan, C. E. Grattan St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorH. Kurwa, H. Kurwa St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this authorR. P. Sarkany, R. P. Sarkany St John's Institute of Dermatology, Guy's and St Thomas’ NHS Foundation Trust, London, UKSearch for more papers by this author First published: 14 July 2009 https://doi.org/10.1111/j.1365-2230.2008.02979.x Dr Rachel Abbott, St John's Institute of Dermatology, Guy's and St Thomas' NHS Foundation Trust, London SE1 7EH, UK E-mail: rachel.abbott@nhs.net Conflict of interest: none declared. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume34, Issue6August 2009Pages 745-746 RelatedInformation

BACKGROUND Most urticarias are induced by vasoactive mediators such as histamine released from mast cells. Although mast cells are activated by allergens through cross-linking of cell-surface--bound IgE, this mechanism does not appear to explain most cases of chronic urticaria, which, when allergic, infectious, drug-induced, or physical causes cannot be identified, are classified as idiopathic. METHODS We recruited 26 patients with chronic idiopathic urticaria, in whom intradermal injection of autologous serum caused a wheal-and-flare response. Serum from four patients that induced marked histamine release from basophils from a donor with very low serum IgE levels was studied with respect to the IgE dependence of the histamine release, the activity of the IgG fractions, and the neutralizing effect of a recombinant preparation of the soluble extracellular domain of the alpha subunit of the high-affinity IgE receptor (sFc epsilon RI alpha). RESULTS The histamine-releasing activity of the serum was abolished by passive sensitization of basophils with myeloma IgE, enhanced after dissociation of IgE by treatment with lactic acid, and induced by IgG fractions from the serum of all four patients. Preincubation of the serum and isolated IgG with sFc epsilon RI alpha resulted in almost complete neutralization. CONCLUSIONS Histamine-releasing IgG autoantibodies against the alpha subunit of the high-affinity IgE receptor are present in the circulation of some patients with chronic urticaria. Autoantibody-induced cross-linking of IgE receptors may be an important mechanism in the pathogenesis of chronic urticaria and other diseases mediated by mast cells.