Background Contact allergy is a common condition and can severely interfere with daily life or professional activities. Due to changes in exposures, such as introduction of new substances, new products or formulations and regulatory intervention, the spectrum of contact sensitization changes. Objective To evaluate the current spectrum of contact allergy to allergens present in the European baseline series (EBS) across Europe. Methods Retrospective analysis of data collected by the European Surveillance System on Contact Allergies (ESSCA, www.essca-dc.org) in consecutively patch-tested patients, 2013/14, in 46 departments in 12 European countries. Results Altogether, 31 689 patients were included in the analysis. Compared to a similar analysis in 2004, the prevalence of contact allergy to methylisothiazolinone went up to around 20% in several departments. In comparison, contact allergy to the metals nickel, cobalt and chromium remained largely stable, at 18.1%, 5.9% and 3.2%, respectively, similar to mostly unchanged prevalence with fragrance mix I, II and Myroxylon pereirae (balsam of Peru) at 7.3%, 3.8% and 5.3%, respectively. In the subgroup of departments diagnosing (mainly) patients with occupational contact dermatitis, the prevalence of work-related contact allergies such as epoxy resin or rubber additives was found to be increased, compared to general dermatology departments. Conclusion Continuous surveillance of contact allergy based on network data offers the identification of time trends or persisting problems, and thus enables focussing in-depth research (subgroup analyses, exposure analysis) on areas where it is needed.

Until recently, food allergies to mammalian meats have been considered to be very rare. The observation that patients not previously exposed to the monoclonal chimeric antibody cetuximab suffered from severe anaphylaxis upon first exposure, led to the identification of galactosealpha- 1,3-galactose as a new relevant carbohydrate allergen. These patients later often suffered from anaphylactic reactions to red meat. Epidemiological data indicated that bites by the tick Amblyomma americanum in the USA, later also by Ixodes species in other continents, resulted in sensitisation to alpha-gal. On the other hand, in African patients with parasitic disorders, a high prevalence of anti-alpha-gal IgE, without clinical relevance, has been reported. In our four cases, one patient with a late onset of meat allergy had a history of a tick bite. The other three patients had symptoms from childhood or at a juvenile age. This indicates that in some patients, other ways of sensitisation may also take place. However, in patients without atopy, tick bite-induced IgE to alpha-gal may be more relevant. Diagnosis is based on a history of delayed onset of anaphylaxis. Skin tests with commercially available meat test solutions are often equivocal or negative; skin tests with raw meat and particularly pork kidney are more sensitive. Determination of specific IgE to alpha-gal is commercially available. The highest sensitivity is observed with skin and basophil activation tests with cetuximab which is, however, limited by its high costs.

The strongest and best-documented risk factor for drug hypersensitivity (DH) is the history of a previous reaction. Accidental exposures to drugs may lead to severe or even fatal reactions in sensitized patients. Preventable prescription errors are common. They are often due to inadequate medical history or poor risk assessment of recurrence of drug reaction. Proper documentation is essential information for the doctor to make sound therapeutic decision. The European Network on Drug Allergy and Drug Allergy Interest Group of the European Academy of Allergy and Clinical Immunology have formed a task force and developed a drug allergy passport as well as general guidelines of drug allergy documentation. A drug allergy passport, a drug allergy alert card, a certificate, and a discharge letter after medical evaluation are adequate means to document DH in a patient. They are to be handed to the patient who is advised to carry the documentation at all times especially when away from home. A drug allergy passport should at least contain information on the culprit drug(s) including international nonproprietary name, clinical manifestations including severity, diagnostic measures, potential cross-reactivity, alternative drugs to prescribe, and where more detailed information can be obtained from the issuer. It should be given to patients only after full allergy workup. In the future, electronic prescription systems with alert functions will become more common and should include the same information as in paper-based documentation.

BackgroundHand eczema (HE) is a common skin disease with major medical psychological and socio-economic implications. Onset and prognosis of HE are determined by individual as well as environmental factors. So far, most epidemiological data on HE have been reported from Scandinavian and recently German studies.ObjectiveTo investigate the characteristics and medical care of patients with chronic HE (CHE) in Switzerland, and identify risk factors.MethodsIn this cross-sectional study, data from patients with chronic HE were obtained by means of medical history, dermatological examination and patient questionnaires. Multiple logistic regression analysis was applied to identify risk factors for high severity and dermatology life quality index (DLQI).ResultsIn seven dermatology departments, 199 patients (mean age 40.4years, 50.8% female) with CHE (mean duration 6.6years) were enrolled. Moderate to severe HE was reported by 70.9% of patients, and was associated with age <30 or >50years, localization of lesions and pruritus. Because of the CHE, 37.3% of patients were on sick leave over the past 12months, 14.8% had changed or lost their job. Practically all patients applied topical therapy, 21% were treated with alitretinoin, and 21% with psoralen plus UVA light (PUVA). The effects on the health-related quality of life was moderate to large in 33.7% and 39.4% of CHE patients, respectively. Factors associated with a high impact on DLQI (mean 9.75.8) were female sex, lesions on back of the hands and pruritus as well as mechanical skin irritation and wearing gloves.ConclusionIn agreement with recent studies, the Swiss data demonstrate the high impact of CHE on medical well-being, patient quality of life and work ability. As it is associated with an intense use of health care services, high rate of sick leave, job loss and change, CHE may cause a high socio-economic burden.

Skin tests are of paramount importance for the evaluation of drug hypersensitivity reactions. Drug skin tests are often not carried out because of lack of concise information on specific test concentrations. The diagnosis of drug allergy is often based on history alone, which is an unreliable indicator of true hypersensitivity.To promote and standardize reproducible skin testing with safe and nonirritant drug concentrations in the clinical practice, the E uropean N etwork and E uropean A cademy of A llergy and C linical I mmunology ( EAACI ) Interest Group on Drug Allergy has performed a literature search on skin test drug concentration in MEDLINE and EMBASE , reviewed and evaluated the literature in five languages using the GRADE system for quality of evidence and strength of recommendation. Where the literature is poor, we have taken into consideration the collective experience of the group.We recommend drug concentration for skin testing aiming to achieve a specificity of at least 95%. It has been possible to recommend specific drug concentration for betalactam antibiotics, perioperative drugs, heparins, platinum salts and radiocontrast media. For many other drugs, there is insufficient evidence to recommend appropriate drug concentration. There is urgent need for multicentre studies designed to establish and validate drug skin test concentration using standard protocols. For most drugs, sensitivity of skin testing is higher in immediate hypersensitivity compared to nonimmediate hypersensitivity.

Paul M. O’Byrne obtained his medical degree at University College, Dublin, and his training in internal medicine and respiratory medicine at McMaster University. He undertook research training under the supervision of Dr. Freddy Hargreave at McMaster University and then of Dr. Jay A. Nadel at the Cardiovascular Research Institute in San Francisco. His research interests are in the mechanisms and treatment of asthma, with particular reference to the role of environmental allergens and the mechanisms by which these cause airway inflammation. Dr. O’Byrne is currently the E.J. Moran Campbell Professor of Medicine, and Chair of the Department of Medicine at the Michael G. DeGroote School of Medicine, McMaster University. He is also the Executive Director of the Firestone Institute for Respiratory Health at St. Joseph’s Healthcare. He has published more than 360 peer-reviewed papers, including papers in the New England Journal of Medicine , Lancet , Nature Medicine , AJRCCM , JACI and the Journal of Immunology . He has authored 90 book chapters and edited 12 books. Dr. O’Byrne has received the James H. Graham Award of Merit, Royal College of Physicians and Surgeons of Canada, and has been the Distinguished Lecturer in Respiratory Sciences for the Institute of Circulatory and Respiratory Health of the Canadian Institutes of Health Research. Furthermore, he was elected Fellow of the Royal Society of Canada in 2010. Dr. O’Byrne is the past Chair of the Executive Committee of the Global Initiative for Asthma (GINA), an Associate Editor of the medical journals Chest and International Archives of Allergy and Immunology , and he is on the Editorial Board of the American Journal of Respiratory and Critical Care Medicine and Thorax . Published online: July 31, 2013

Summary Background Experimental studies suggest that glutathione S‐transferase (GST) genotypes modify nasal allergen responses induced by secondhand smoke (SHS) exposure. Objective We aimed to investigate whether GSTs affected systemic IgE and allergic rhinitis (AR) in SHS‐exposed individuals from a population‐based cohort. Methods Analyses comprised 2309 never‐smokers from the Swiss study on air pollution and health in adults cohort, reporting SHS status at baseline and 11 years later. Outcomes were defined by total serum IgE⩾100 kU/L, specific serum IgE determined by Phadiatop® ⩾0.35 kU/L and self‐reported AR. GSTP1 Ile105Val, GSTM1 and GSTT1 gene deletion genotypes were identified at the follow‐up survey. Results After adjustment for relevant covariates, the homozygous GSTP1 105‐Val genotype was negatively associated with high total IgE and high‐specific IgE by Phadiatop®, notably in subjects persistently exposed to SHS (OR: 0.20, 95% CI 0.05–0.75; P=0.02, for high total IgE and OR: 0.29, 95% CI 0.10–0.89; P=0.03, for high specific IgE by Phadiatop®). Carrying at least one copy of the GSTM1 gene (non‐null) showed a similar association for high specific IgE by Phadiatop® (OR: 0.41, 95% CI 0.22–0.76; P=0.004). No significant associations were found between GSTs and rhinitis. Conclusion and Clinical Relevance In this large cohort, homozygosity for GSTP1 105‐Val or carrying the GSTM1 non‐null genotype decreased the risk of high total IgE or high specific IgE using Phadiatop® by nearly half in subjects exposed to SHS, as compared with subjects carrying opposite alleles. These findings underline the value of genetic susceptibility when evaluating the effects of environmental exposure on allergic illness. The potential long‐term effects of persistent SHS exposure in genetically vulnerable individuals may be of public health relevance. Cite this as: M. W. Gerbase, D. Keidel, M. Imboden, A. Gemperli, A. Bircher, P. Schmid‐Grendelmeier, P.‐O. Bridevaux, W. Berger, C. Schindler, T. Rochat and N. Probst‐Hensch, Clinical & Experimental Allergy, 2011 (41) 1579–1586.

Le terme «anaphylaxie» n’est pas utilisé de façon uniforme. En général, il fait référence à une réaction d’hypersensibilité systémique grave et potentiellement fatale, de survenue rapide [1]. Seuls quelques minutes peuvent s’écouler entre le début des symptômes et l’obtention d’un tableau clinique complet d’anaphylaxie, qui peut se solder par le décès du patient [2, 3]. Même si la plupart des réactions anaphylactiques se déroulent en l’espace de 30 minutes, un état de choc peut également se manifester 1–2 heures après le premier contact [2]. Dans ce cas, des substances ingérées par voie orale sont le plus souvent en cause. Les déclencheurs les plus fréquents de réactions anaphylactiques sont les piqures d’hyménoptères, les médicaments et les denrées alimentaires [2–6]. Il n’est pas rare que des cofacteurs soient également impliqués (par ex. anaphylaxie alimentaire induite par l’effort; alcool ou anti-inflammatoires non stéroïdiens [y compris Aspirin®] conjointement avec protéines alimentaires et activité physique, infection virale et contact avec des allergènes) [2, 5, 7]. Les manifestations cliniques, qui concernent tout l’organisme (tab. 1 p), reposent sur une activation aiguë des mastocytes et des basophiles. Le mécanisme peut être IgE-médiée ou non IgE-médiée, ce qui n’est pas différentiable d’après les manifestations cliniques. L’incidence des chocs anaphylactiques potentiellement fatals est estimée à environ 10 cas pour 100000 habitants par an en Suisse [3]. Par tranche d’1 million d’habitants, 1–3 personnes décèdent suite à une réaction allergique grave. L’anaphylaxie constitue une urgence médicale, d’où l’importance déterminante d’une prise en charge médicale précoce. Différentes analyses rétrospectives ont révélé que le traitement aigu des réactions allergiques graves différait souvent des directives et recommandations nationales et internationales [5, 6, 8–11]. Il est regrettable que l’adrénaline, qui est un médicament essentiel dans le traitement des réactions allergiques graves, soit utilisée trop rarement et trop tardivement. Par ailleurs, après un premier choc anaphylactique traité avec succès, les victimes sont souvent insuffisamment formées à l’auto-traitement d’urgence et elles ne sont pas assez rendues attentives à l’importance d’un suivi avec évaluation allergologique [10–12]. L’anaphylaxie constitue un évènement marquant, à l’issue duquel la qualité de vie peut être massivement altérée. Pour la grande majorité (~94%) des réactions anaphylactiques, les causes parviennent à être élucidées par le biais d’un bilan allergologique [2, 3]. Il est primordial que les personnes concernées soient correctement conseillées et informées sur la manière d’éviter une nouvelle réaction anaphylactique afin qu’elles ne vivent pas constamment dans la peur [12].

To cite this article:Cernadas JR, Brockow K, Romano A, Aberer W, Torres MJ, Bircher A, Campi P, Sanz ML, Castells M, Demoly P, Pichler WJ, for the European Network of Drug Allergy and the EAACI interest group on drug hypersensitivity. General considerations on rapid desensitization for drug hypersensitivity – a consensus statement.Allergy2010;65: 1357–1366.AbstractDrug hypersensitivity reactions can occur with most drugs, are unpredictable, may affect any organ or system, and range widely in clinical severity from mild pruritus to anaphylaxis. In most cases, the suspected drug is avoided in the future. However, for certain patients, the particular drug may be essential for optimal therapy. Under these circumstances, desensitization may be performed. Drug desensitization is defined as the induction of a temporary state of tolerance of a compound responsible for a hypersensitivity reaction. It is performed by administering increasing doses of the medication concerned over a short period of time (from several hours to a few days) until the total cumulative therapeutic dose is achieved and tolerated. It is a high‐risk procedure used only in patients in whom alternatives are less effective or not available after a positive risk/benefit analysis. Desensitization protocols have been developed and are used in patients with allergic reactions to antibiotics (mainly penicillin), insulins, sulfonamides, chemotherapeutic and biologic agents, and many other drugs. Desensitization is mainly performed in IgE‐mediated reactions, but also in reactions where drug‐specific IgE have not been demonstrated. Desensitization induces a temporary tolerant state, which can only be maintained by continuous administration of the medication. Thus, for treatments like chemotherapy, which have an average interval of 4 weeks between cycles, the procedure must be repeated for every new course. In this paper, some background information on rapid desensitization procedures is provided. We define the drugs and drug reactions indicated for such procedures, describe the possible mechanism of action, and discuss the indications and contraindications. The data should serve as background information for a database (accessible via the EAACI‐homepage) with standardized protocols for rapid desensitization for antibiotics, chemotherapeutic agents, monoclonal antibodies/fusion proteins, and other drugs.