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Résumé Après les antibiotiques, les AINS sont les médicaments les plus souvent responsables de réaction d’hypersensibilité (1 à 3 % parmi la population générale et jusqu’à 30 % dans la population présentant un asthme, une rhinosinusite chronique ou une urticaire chronique spontanée). Ces réactions peuvent être allergiques (médiées par les IgE ou par des lymphocytes T) ou non allergiques (liées à la libération de médiateurs par les mastocytes, les basophiles notamment). Les premières réactions (allergiques) sont spécifiques d’un AINS ou d’une famille chimique d’AINS tandis que les secondes (non allergiques) sont induites par des AINS de familles chimiques différentes (réactivité croisée pharmacologique ou « cross-intolérants »). Les différents phénotypes cliniques ont ainsi été redéfinis récemment par le groupe ENDA/EAACI dans l’objectif de préciser les moyens diagnostiques à mettre en œuvre et une prise en charge standardisée pour chaque patient ; la méthodologie est reprise dans cet exposé. After antibiotics, NSAIDs are the drugs most often responsible for drug hypersensitivity reactions, involving 1–3% of the general population and up to 30% of people with asthma, chronic rhinosinusitis or spontaneous chronic urticaria. These reactions may be allergic (IgE- or T cell-mediated) or non-allergic (due to the release of mediators from mast cells and basophils). The allergic reactions are specific to an NSAID or to a chemical family of NSAIDs, while the non-allergic reactions are induced by NSAIDs of different chemical families (pharmacological cross-reactivity or “cross-intolerance”). The different clinical phenotypes have been redefined recently by the ENDA/EAACI group aiming to clarify the diagnostic methods and to implement standardized management for each patient; the methodology is included in this presentation. [ABSTRACT FROM AUTHOR]

Fixed drug eruption (FDE) is a well-recognized, non-immediate, drug hypersensitivity reaction, often attributed to the use of various medications, most commonly non-steroidal anti-inflammatory drugs (NSAIDs) and antibiotics. Cross-reactivity between related NSAIDs in FDE has been reported, but among chemically unrelated NSAIDs, is rare. Herein, we present a rare well-documented case where a patient initially displayed tolerance to etoricoxib after experiencing a nimesulide-induced FDE. Subsequently, the patient developed an etoricoxib-induced FDE, accompanied by the development of bullous lesions. This case report and the literature review on comparable FDE occurrences shed light on the intricate nature of FDEs, suggesting the possibility of cross-reactivity between chemically related and unrelated NSAIDs or the emergence of new drug-specific T cells without cross-reactivity after multiple exposures to a drug in a susceptible patient. Our case underscores the importance of increased awareness and vigilance among both physicians and patients in the realm of personalized medicine. Further research is needed to unravel the intricate mechanisms behind these drug eruptions, improve diagnostic approaches, and enhance patient care. [ABSTRACT FROM AUTHOR]

The article presents a case study of 88 year old patient with hypersensitivity reactions to iodinated contrast media (ICM) with acute exanthema, temperature and intraepidermal pustule with numerous polymorphonuclear cells. Patch test confirmed acute generalized exanthematous pustulosis (AGEP), hence coronary stenting and endovascular valvuloplasty, including ICM administration of iopromide and oral prednisone was recommended.

Nonsteroidal anti‐inflammatory drugs (NSAIDs) are among the main causes of fixed drug eruption (FDE). Cross‐sensitivity between chemically unrelated NSAIDs has been rarely described in FDE. We report herein two cases of NSAID‐induced FDE confirmed by oral provocation test (OPT) with a literature review. Case 1 is a 49‐year‐old woman who took mefenamic, naproxen and acetaminophen for lumbago. On the second day, she noticed three erythematous plaques, located in the upper lip, chin and the right hand, which faded spontaneously, leaving residual patches. Three months later, she took mefenamic acid with reactivation of the same plaques. She received naproxen. On the same day, she exhibited a reactivation of lesions with the development of a new one. These lesions have disappeared leaving hyperpigmented sequelae. After negative patch test to naproxen, an OPT was performed with positive reaction, observed on the third day. To establish the cross‐reactivity, she underwent OPTs, which gave positive results to indomethacin, ketoprofen and tiaprofenic acid. Case 2 is a 52‐year‐old woman who presented painful dusky‐red macules, located in the right and left wrists, 24 hours after taking mefenamic acid. She described two similar events that occurred in the past with an undefined drug and piroxicam. Patch tests to lysine acetylsalicylate, mefenamic acid, piroxicam, naproxen and celecoxib were negative. OPTs to the same NSAIDs gave positive results to lysine acetylsalicylate, piroxicam and mefenamic acid. Thirteen case reports, seven case series and one retrospective analysis, including cases with confirmed cross‐reactivity between NSAIDs, were reported in literature. Clinicians should be aware of such phenomenon. [ABSTRACT FROM AUTHOR]

Drug reaction with eosinophilia and systemic symptom (DRESS) is a severe adverse drug‐induced reaction. Commonly related to anticonvulsant and allopurinol, DRESS can affect both adults and children. Cefotaxime is rarely associated with DRESS, especially with children. We report a cefotaxime‐induced DRESS in a child and emphasize the role of allergological work‐up to point out the culprit drug in exploring cross‐reactivity and identifying a possible cosensitization. A 2‐year‐old boy was treated with cefotaxime, vancomycin and metronidazole for acute otomastoiditis. Metronidazole was withdrawn and vancomycin was changed by teicoplanin 10 and 15 days later, respectively. Nineteen days after ongoing cefotaxime and 4 days after teicoplanin intake, the patient developed hyperthermia, a widespread exanthema, facial oedema with neither mucosal involvement nor palpable lymphadenopathy. Biological tests revealed eosinophilia, atypical lymphocytes, mild cytolysis and a high lactate dehydrogenase level. Serological tests for viral and bacterial infections were negative. DRESS was suspected and the 2 antibiotics were withdrawn. Intradermal tests (IDT) were carried out 2 months later with cefotaxime and teicoplanin. They revealed a positive result at 48‐hour reading. To assess cross‐reactivity among β‐lactams, IDT to penicillins (benzylpenicillin, amoxicillin and oxacillin) was performed showing negative results at 48‐hour reading. Nevertheless, IDT to cephalosporins (cefazolin, cefuroxime, ceftazidime and ceftriaxone) displayed positive results at 48‐hour reading. As a result, IDT are of great interest and should be performed to confirm the role of cefotaxime and detect a potential cross‐reactivity with chemically similar drugs and drugs taken before and during the episode of DRESS. [ABSTRACT FROM AUTHOR]

We report a 26-year-old female patient who developed anaphylaxis after the use of pantoprazole and esomeprazole and was successfully desensitized with rabeprazole. The patient, who was diagnosed with duodenal ulcer by gastroscopy, was prescribed pantoprazole 40 mg tablet for treatment. Thirty minutes after taking the first dose of pantoprazole, generalized urticaria, angioedema of the lips, abdominal pain, diarrhea, shortness of breath and hypotension (blood pressure: 80/40 mmHg) developed. No loss of consciousness developed. Since dyspeptic complaints continued, esomeprazole 40 mg tablet was prescribed to the patient 1 month later. Generalized urticaria, abdominal pain, diarrhea and dyspnea developed 40 minutes after taking the first dose of esomeprazole. As hypersensitivity to PPIs was considered, skin tests were performed with all PPIs to detect alternative PPIs, as skin tests are safe and specific. A positive reaction was detected to all PPIs in the skin tests, so no oral provocation was performed with PPIs. Desensitization was planned because treatment with PPI was necessary and there was no alternative treatment. This patient who developed anaphylaxis with pantoprazole and esomeprazole was successfully desensitized with rabeprazole. In conclusion, in cases of hypersensitivity to PPIs, the possibility of cross-reactivity should be kept in mind and skin tests with PPIs should be performed before performing oral provocation testing. If no alternative is found, a PPI desensitization protocol can be applied. [ABSTRACT FROM AUTHOR]

Beta-lactam antibiotics are the most commonly reported drug allergy in adults and children. More than 95% of those with reported allergy labels to beta lactams are not confirmed when subjected to allergy testing. Beta lactam antibiotics are associated with a wide spectrum of immediate and delayed drug hypersensitivity reactions. The latency period to symptoms and clinical presentation aids in the causality assessment. Risk stratification based on diagnosis and timing then allows for appropriate management and evaluation. Skin prick testing, intradermal testing and oral challenge are well established for evaluation of immediate reactions. Delayed intradermal testing, patch testing and oral challenge can also be considered for evaluation of mild to moderate delayed reactions. Cross-reactivity between beta-lactams appears to be driven most commonly by a shared R1 side-chain. Standardized algorithms, protocols and pathways are needed for widespread implementation of a pragmatic and effective approach to patients reporting beta lactam allergy. [ABSTRACT FROM AUTHOR]

β-Lactams which include penicillins, cephalosporins, carbapenems, and monobactams are the most common antibiotic classes reported to cause allergic reactions to drugs. This review is mainly about published studies assessing the cross-reactivity among β-lactams in penicillin- or cephalosporin-allergic subjects by carrying out diagnostic tests with alternative β-lactams and, if appropriate, graded challenges. Several studies demonstrated that cross-reactivity connected with the β-lactam ring, causing positive responses to allergy tests with all β-lactams, is infrequent in subjects with an IgE-mediated allergy and anecdotal in those with a T-cell-mediated allergy. Identities or similarities of β-lactam side-chain structures are mainly responsible for cross-reactivity among these antibiotics. For example, in aminopenicillin-allergic subjects, cross-reactivity with aminocephalosporins could possibly be over 30%. On the other hand, in a few prospective studies of penicillin-allergic individuals, less than 1% of cases show a cross-reactivity between penicillins and both aztreonam and carbapenems. Particular patterns of allergy-test positivity observed in some studies that assessed cross-reactivity among β-lactams seem to indicate that prior exposures may be responsible for coexisting sensitivities. Therefore, pre-treatment skin tests with the related β-lactams are suggested before administering them via graded challenges to β-lactam-allergic patients who need alternative β-lactams. [ABSTRACT FROM AUTHOR]

Background: Analysis of cross-reactivity is necessary for prescribing safe cephalosporins for penicillin allergic patients. Amoxicillin (AX) is the betalactam most often involved in immediate hypersensitivity reactions (IHRs), and cefadroxil (CX) the most likely cephalosporin to cross-react with AX, since they share the same R1 side chain, unlike cefuroxime (CO), with a structurally different R1. We aimed to analyse cross-reactivity with CX and CO in patients with confirmed IHRs to AX, including sIgE recognition to AX, CX, CO, and novel synthetic determinants of CX. Methods: Fifty-four patients with confirmed IHRs to AX based on skin test (ST) and/or drug provocation test (DPT) were included. Serum sIgE to AX and benzylpenicillin was determined by Radioallergosorbent test (RAST). Two potential determinants of CX, involving intact or modified R1 structure, with open betalactam ring, were synthesised and sIgE evaluated by RAST inhibition assay. Results: Tolerance to CX (Group A) was observed in 64.8% cases and cross-reactivity in 35.2% cases (Group B). Cross-reactivity with CO was only found in 1.8% cases from Group B. ST to CX showed a negative predictive value of 94.6%. RAST inhibition assays showed higher recognition to CX as well as to both synthetic determinants (66% of positive cases) in Group B. Conclusions: Cross-reactivity with CX in AX allergic patients is 35%, being ST not enough for prediction. R1, although critical for recognition, is not the unique factor. The synthetic determinants of CX, 1-(HOPhG-Ser-Bu) and 2-(pyrazinone) are promising tools for determining in vitro cross-reactivity to CX in AX allergic patients. [ABSTRACT FROM AUTHOR]

Background: Analysis of cross‐reactivity is necessary for prescribing safe cephalosporins for penicillin allergic patients. Amoxicillin (AX) is the betalactam most often involved in immediate hypersensitivity reactions (IHRs), and cefadroxil (CX) the most likely cephalosporin to cross‐react with AX, since they share the same R1 side chain, unlike cefuroxime (CO), with a structurally different R1. We aimed to analyse cross‐reactivity with CX and CO in patients with confirmed IHRs to AX, including sIgE recognition to AX, CX, CO, and novel synthetic determinants of CX. Methods: Fifty‐four patients with confirmed IHRs to AX based on skin test (ST) and/or drug provocation test (DPT) were included. Serum sIgE to AX and benzylpenicillin was determined by Radioallergosorbent test (RAST). Two potential determinants of CX, involving intact or modified R1 structure, with open betalactam ring, were synthesised and sIgE evaluated by RAST inhibition assay. Results: Tolerance to CX (Group A) was observed in 64.8% cases and cross‐reactivity in 35.2% cases (Group B). Cross‐reactivity with CO was only found in 1.8% cases from Group B. ST to CX showed a negative predictive value of 94.6%. RAST inhibition assays showed higher recognition to CX as well as to both synthetic determinants (66% of positive cases) in Group B. Conclusions: Cross‐reactivity with CX in AX allergic patients is 35%, being ST not enough for prediction. R1, although critical for recognition, is not the unique factor. The synthetic determinants of CX, 1 ‐(HOPhG‐Ser‐Bu) and 2 ‐(pyrazinone) are promising tools for determining in vitro cross‐reactivity to CX in AX allergic patients. [ABSTRACT FROM AUTHOR]

Background: Proton pump inhibitors (PPIs) can trigger immediate-type hypersensitivity reactions (HSRs). Three main patterns of cross-reactivity have been identified: reactions to a single PPI, selective cross-reactions, and cross-reactions with all PPIs. Several hypotheses have been advanced, but no consensus has been reached. Objective: We sought to identify immediate-type hypersensitivity cross-reactions to PPIs using real-world data about hypersensitivity testing from French pharmacovigilance cases. Methods: Potentially relevant immediate-type HSRs reported from January 1985 to February 2015 were extracted from the French pharmacovigilance database using a standardized MedDRA query (SMQ). Cases describing skin tests or oral provocation tests (OPTs) performed with several PPIs that yielded at least one positive result were included. Results: The SMQ extracted 2,119 cases, 38 of which were included in our study. Data collected from skin tests and OPTs indicated cross-reactions with all PPIs (n = 1), reactions to a single PPI (n = 14), or selective cross-reactions (n = 23). Esomeprazole, omeprazole, and pantoprazole concerned 78% of all selective cross-reactions. In more than half of the cases (55.3%), only 2 PPIs were tested. Conclusion: To the best of our knowledge, this PPI cross-reactivity study is the largest to date in terms of population size, describing 38 immediate-type HSRs to PPIs explored by skin tests or OPTs. This paucity of data belies the lack of standardized procedures for PPI hypersensitivity testing. It is likely that PPI HSR workups in everyday clinical practice are often incomplete. Further research to gain insight into selective cross-reactions between PPIs is needed. In the meantime, thorough workups should be completed when a PPI is suspected to have triggered an HSR, instead of routine contraindication to all PPIs. [ABSTRACT FROM AUTHOR]

Cutaneous adverse drug reaction induced by oral dexamethasone with possible cross-reactivity to Group 1 corticosteroids confirmed by patch testing and intradermal testing Here, we report, to the best of our knowledge, the first case of a CADR induced by oral dexamethasone with evidence of possible Group 1 corticosteroid cross-reactivity confirmed by patch testing and intradermal testing. Case report, corticosteroids, cross-reactivity, cutaneous adverse drug reaction, dexamethasone, intradermal testing, patch testing. [Extracted from the article]

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Introduction: Diagnosing and managing drug hypersensitivity is challenging because there are no clear limits between different types of drug reactions. Distinguishing between type A (predictable) and type B (hypersensitivity) reactions when a drug is introduced on the market is not easy. When many people use a drug, adverse reactions can occur, conditioned by diverse genetic profiles, viral infections or concomitant therapy. Occasionally the only tool clinicians have on which to base the diagnosis is the clinical history. Skins tests orin vitrotests sometimes have low sensitivity or are unavailable, and drug provocation tests may be dangerous or strictly forbidden in case of severe cutaneous reactions. Areas covered: This paper reviews the diagnosis and management of the two main types of immunological reactions: IgE-mediated immediate drug hypersensitivity reactions (IDHRs) and non-immediate drug hypersensitivity reactions (NIDHRs). Expert commentary: Although Europe and the United States use different diagnostic methods, patients with history of drug hypersensitivity must avoid the suspicious drug, and clinicians must assess tolerance to safe alternatives under medical surveillance. Sometimes desensitization may be required. There is a consensus about the need to perform genetic testing for specific drugs and give patients proper documentation to prevent future exposure to culprit drugs. [ABSTRACT FROM AUTHOR]

Non-immediate cutaneous reactions (i.e., occurring at least 1 h after the initial drug administration), particularly maculopapular exanthemas and urticarial eruptions, are common during beta-lactam treatments. A T cell-mediated pathogenic mechanism has been demonstrated in some cutaneous reactions, such as maculopapular exanthema, fixed drug eruption, acute generalized exanthematous pustulosis, and drug-induced hypersensitivity syndrome. In the diagnostic work-up, patch testing is useful, together with delayed-reading intradermal testing. Patch tests are a simple and safe diagnostic tool, which in the case of severe reactions should be used as the first line of investigation. However, patch tests are less sensitive than intradermal tests, which are preferable in subjects with mild reactions. Lymphocyte transformation or activation tests and enzyme-linked immunosorbent spot assays can be used as complementary tests. In selected cases of mild or moderate reactions, displaying negative results in the aforesaid allergy tests, a graded challenge with the implicated beta-lactam can be performed. [ABSTRACT FROM AUTHOR]

Background: We previously reported perfect specificity and low sensitivity of skin tests in proton pump inhibitor (PPI)- induced immediate hypersensitivity reactions in a prospective multicenter study. Here, in a retrospective study, we aimed to further evaluate the diagnostic workup procedures and characteristics of the patients with suspected PPI hypersensitivity. Methods: This national multicenter study was conducted as a retrospective chart review of patients with a history of PPI-induced immediate hypersensitivity reaction. A total of 60 patients were included. Results of diagnostic workup procedures (standardized skin-prick, intradermal, and oral-provocation tests with PPIs) and the characteristics of the patients were analyzed. Results: Lansopra zole was the most commonly suspected drug with 41 patients (68.3%), followed by pantoprazole in 12 patients (20.0%), esomeprazole in 6 (10.0%), rabeprazole in 4 (6.7%), and omeprazole in 1 (1.7%). Anaphylaxis (40 patients, 66.7%) was the most common clinical presentation followed by urticaria (17 patients, 28.3%). Diagnostic skin tests with the culprit PPI were positive in 13/26 patients (50.0%). Diagnostic oral-provocation tests were negative in 6/8 patients; 5 of these 6 patients had skin test results with the culprit PPI, and all were negative. Ten patients had at least 1 cross-reactivity. Extensive cross-reactivity (between >2 PPIs) was detected in 4 patients. Conclusions: Lansoprazole was the most frequently implicated drug and anaphylaxis was the most frequent manifestation of PPI-induced hypersensitivity reactions. Physicians should be aware of the possible crossreactivity among PPIs; however, a safe, alternative PPI can usually be detected by a thorough drug allergy workup. [ABSTRACT FROM AUTHOR]

The Standards of Care Committee of the British Society for Allergy and Clinical Immunology ( BSACI) and an expert panel have prepared this guidance for the management of immediate and non-immediate allergic reactions to penicillins and other beta-lactams. The guideline is intended for UK specialists in both adult and paediatric allergy and for other clinicians practising allergy in secondary and tertiary care. The recommendations are evidence based, but where evidence is lacking, the panel reached consensus. During the development of the guideline, all BSACI members were consulted using a Web-based process and all comments carefully considered. Included in the guideline are epidemiology of allergic reactions to beta-lactams, molecular structure, formulations available in the UK and a description of known beta-lactam antigenic determinants. Sections on the value and limitations of clinical history, skin testing and laboratory investigations for both penicillins and cephalosporins are included. Cross-reactivity between penicillins and cephalosporins is discussed in detail. Recommendations on oral provocation and desensitization procedures have been made. Guidance for beta-lactam allergy in children is given in a separate section. An algorithm to help the clinician in the diagnosis of patients with a history of penicillin allergy has also been included. [ABSTRACT FROM AUTHOR]

Background Data are limited about the value of skin tests in the diagnosis of proton pump inhibitor ( PPI)-induced hypersensitivity reactions and the cross-reactivity between PPIs. We aimed to assess the role of skin testing in the diagnosis of PPI-related immediate hypersensitivity reactions and the cross-reactivity patterns among PPIs. Methods The study was designed in a prospective, national, multicentre nature. Sixty-five patients with a suggestive history of a PPI-induced immediate hypersensitivity reaction and 30 control subjects were included. Standardized skin prick and intradermal tests were carried out with a panel of PPIs. Single-blind, placebo-controlled oral provocation tests ( OPTs) with the PPIs other than the culprit PPI that displayed negative results in skin tests ( n = 61) and diagnostic OPTs with the suspected PPI ( n = 12) were performed. Results The suspected PPIs were lansoprazole ( n = 52), esomeprazole ( n = 11), pantoprazole ( n = 9), rabeprazole ( n = 2), and omeprazole ( n = 1). The sensitivity, specificity, and negative and positive predictive values of the skin tests with PPIs were 58.8%, 100%, 70.8%, and 100%, respectively. Fifteen of the 31 patients with a hypersensitivity reaction to lansoprazole had a positive OPT or skin test result with at least one of the alternative PPIs (8/52 pantoprazole, 6/52 omeprazole, 5/52 esomeprazole, 3/52 rabeprazole). Conclusion Considering the high specificity, skin testing seems to be a useful method for the diagnosis of immediate-type hypersensitivity reactions to PPIs and for the evaluation of cross-reactivity among PPIs. However, OPT should be performed in case of negativity on skin tests. [ABSTRACT FROM AUTHOR]

Background After penicillins, cephalosporins are the betalactams that most often induce IgE-mediated reactions. The development of diagnostic tests has been delayed, however, because the cephalosporin allergenic determinants have not been properly identified. Objective To evaluate the usefulness of skin tests, serum specific IgE assays, and challenges in diagnosing immediate reactions to cephalosporins and to clarify the pathogenic mechanism of such reactions. Methods We studied 76 adults with immediate reactions to cephalosporins, mainly ceftriaxone, cefotaxime, and ceftazidime. Skin tests and serum specific IgE assays were performed for culprit cephalosporins and cefaclor, as well as for penicillin, amoxicillin, and ampicillin. Some subjects with negative results underwent challenges and re-evaluations. Responses to cephalosporins other than the culprit ones were also studied. Results In the first allergologic work-up, an IgE-mediated hypersensitivity to penicillins and/or cephalosporins was diagnosed in 63 (82.9%) of the 76 patients on the basis of skin-test and/or specific IgE assay positivity. Of the 13 negative patients, eight accepted challenges and underwent re-evaluations. Considering both first- and second-evaluation results, the skin-test-positivity rate increased from 76.3% to 85.5% and that of sepharose-radioimmunoassay positivity from 67.1% to 74.3%. Overall, an IgE-mediated hypersensitivity was diagnosed in 70 patients (in seven after retesting). On the basis of skin-test and CAP-FEIA results, we classified our 76 patients into five groups: group A (three patients), positive only to penicillin reagents; B (17), positive to both cephalosporin and penicillin reagents; C (24), positive to more than one cephalosporin; D (21), positive only to the responsible cephalosporin; E (11) negative to skin tests and CAP-FEIA, including five sepharose-radioimmunoassay positive. Conclusions Most immediate reactions to cephalosporins appear to be IgE-mediated. Cephalosporin skin testing and sepharose-radioimmunoassay are useful tools for evaluating these reactions. Cephalosporin IgE-mediated hypersensitivity may be a transient condition; therefore, allergologic exams should be repeated in patients with negative initial allergologic work-ups, including challenges. [ABSTRACT FROM AUTHOR]

Introduction. – Malassezia are lipophilic yeasts, saprophytic on human skin. For the past 20 years, Malassezia were thought to be involved in the pathogenesis of certain forms of head and neck dermatitis (HND). The aim of the present study was to investigate the role of this organism in HND. We also studied possible cross-reactivity with two other yeasts, Candida albicans and Saccharomyces cerevisiae.Patients and methods. – Fifty-three subjects were included: 25 patients with HND, 10 patients with generalized atopic dermatitis (AD) and 18 healthy controls. The 25 patients with HND had yeast cultures taken for Malassezia, and all 53 subjects had patch tests, skin prick tests and IgE antibody assays for Malassezia, C. albicans and S. cerevisiae. The HND patients were then treated with ciclopiroxolamine, a topical antimycotic.Results. – We found no statistically significant relationship between the results of yeast cultures, skin tests and the serological results or the results of the antimycotic treatment in these subjects. We did find increased sensitivity to Malassezia in patients with AD compared to the healthy controls, but there was no statistical difference between HND patients and patients with generalized AD. Nevertheless, for the entire group of patients, there was a significant relationship between results of skin prick tests and specific antibodies for Malassezia, C. albicans and S. cerevisiae, suggestive of possible cross-reactivity between these three yeasts.Conclusion. – The results lead us to propose two hypotheses: (1) Patients may be sensitized to yeast proteins but have no signs of an allergy requiring antifungal treatment, i.e. HND. (2) Patients with HND might be sensitized to several yeasts, and they would need systemic antifungal treatment that is active on Malassezia and C. albicans and, in addition, a S. cerevisiae-free diet. [Copyright &y& Elsevier]