This Week in Allergy & Immunology — Aug 21, 2026

Welcome to This Week in Allergy and Immunology. This week we're covering 10 notable papers spanning drug hypersensitivity and perioperative anaphylaxis, asthma and upper airway treatment strategies, and new mechanistic work on food allergy trajectories. Let's dive in.

We start with drug allergy, where the European Academy of Allergy and Clinical Immunology has published two companion documents in Allergy that together reset how we diagnose and describe these reactions. The updated statement on drug hypersensitivity skin testing, led by Barbaud and colleagues, standardises methodology and gives validated non-irritant concentrations across the major drug classes we actually test, including antibiotics, contrast media, anaesthetics, proton pump inhibitors, chemotherapies and biologicals [1]. Several points matter at the bedside. For immediate reactions, the optimal testing window is four to six weeks after the reaction, and testing beyond six months increases false negatives, although chemotherapy reactions still need earlier assessment, within about two weeks, because treatment cannot wait. The reference method for reading a positive immediate intradermal test is now explicit: inject exactly zero point zero two millilitres, and call it positive when the wheal at twenty minutes is at least three millimetres larger than the initial wheal. For patch testing, the guidance warns that crushing tablets and diluting them at thirty percent in petrolatum produces substantial variability in the actual concentration delivered, so active ingredient concentrations should be documented systematically. Critically for delabelling practice, risk stratification now permits direct drug provocation for mild maculopapular exanthema without preliminary skin testing, while anaphylaxis still requires skin testing first, and skin tests are described as useful and safe for identifying the culprit in severe delayed reactions including DRESS, acute generalised exanthematous pustulosis, and Stevens-Johnson syndrome or toxic epidermal necrolysis. Alongside this, a position paper from Torres and colleagues proposes a new nomenclature for immune-mediated drug reactions [2]. Their argument is that the Gell and Coombs framework no longer explains what we see in contemporary practice, and that phenotype alone cannot tell you the endotype. They split immune-mediated reactions into drug allergy, meaning antigen-driven reactions diagnosed by tests that detect sensitisation, and drug hypersensitivity, meaning the broader group of reactions driven directly by the drug's interaction with immune or inflammatory pathways. Expect this vocabulary to start appearing in journals, pharmacovigilance reports and trial protocols.

Staying with severe reactions, the Journal of Allergy and Clinical Immunology In Practice reports a prespecified analysis from Dewachter and colleagues of perioperative IgE-mediated anaphylaxis across two academic centres [5]. Among 72 patients with grade three or four reactions, 27 showed what the authors call the early cutaneous vasoconstriction phenotype, and all six fatal or near-fatal outcomes in the cohort occurred in that group. That works out to roughly one in five patients with early vasoconstriction dying or requiring mechanical circulatory support, against none of the 45 patients with vasodilation or no cutaneous signs. In every one of those six cases, vasoconstriction was accompanied by bradycardia, with a median heart rate in the mid-forties. The authors interpret this as a marker of profound hypovolaemia and greater initial severity, and they suggest that purely symptomatic treatment, given without regard to the underlying mechanism, may have contributed to the poor outcomes. The practical message for anyone who consults on perioperative reactions, or who teaches anaesthesia colleagues, is that a pale, cold, bradycardic patient is not having a milder reaction than a flushed one. It may well be the opposite.

Turning to asthma, three papers this week question how well our current strategies actually work. In the Journal of Allergy and Clinical Immunology In Practice, Kang and colleagues report a multicentre, open-label, randomised crossover trial asking whether a long-acting muscarinic antagonist could substitute for inhaled corticosteroid in type 2-low mild asthma, defined by blood eosinophils under 300 and either low fractional exhaled nitric oxide or low sputum eosinophils [3]. Of 150 patients randomised, 89 completed both six-month phases. In the per-protocol analysis, treatment success was about eight percentage points higher with the muscarinic antagonist, and non-inferiority held in two intention-to-treat analyses. But the result is not uniformly positive: in the most conservative intention-to-treat analysis, where every incomplete phase was counted as a failure, non-inferiority was not established. Exacerbation rates did not differ, and symptom control and lung function were stable in both phases. So this is a signal worth watching rather than a licence to drop inhaled steroids, and the authors themselves frame it as an option for selected patients. That caution is reinforced by the French FASE2 study published in the same journal, in which Portel and colleagues surveyed 970 adults with GINA step five asthma treated in non-academic hospitals [8]. Roughly seven in ten were on a biologic, most commonly omalizumab, yet close to sixty percent OF PATIENTS had partially controlled or uncontrolled disease by asthma control test, and about six in ten had at least one exacerbation in the preceding year. The most striking finding is a perception gap: only about a third OF PATIENTS reported full adherence, while physicians judged nearly nine in ten to be adherent. Anxiety symptoms were present in close to half OF PATIENTS and depressive symptoms in about a quarter. The authors argue that closing these gaps, in adherence, inhaler optimisation and comorbidity management, could deliver gains comparable to introducing another new biologic. Finally, in the Journal of Allergy and Clinical Immunology, Szatkowski and colleagues report a randomised, double-blind, placebo-controlled crossover trial of high-dose aspirin at 600 milligrams daily after desensitisation in 14 patients with aspirin-exacerbated respiratory disease, with 13 controls [9]. Eight patients responded to aspirin, but exactly the same number responded to placebo, with substantial overlap, and there were no consistent molecular changes after either treatment. Clinical improvement during aspirin therapy was, in short, comparable to placebo in this small trial. The positive finding was biomarker-related: higher baseline sputum SERPINB9 expression strongly predicted clinical improvement, making it a candidate for selecting who is worth desensitising.

On the upper airway, two studies address how much treatment is enough. In Annals of Allergy, Asthma and Immunology, Chatmaitri and colleagues randomised 70 children aged six to eighteen with perennial allergic rhinitis to regular versus as-needed intranasal fluticasone furoate in an eight-week double-dummy trial [6]. Regular dosing gave better symptom scores, visual analogue scores and peak nasal inspiratory flow at early time points, and greater reductions in mucosal eosinophils and metachromatic cells at week eight, but the clinical differences between groups were no longer apparent by the end of the trial. Cumulative steroid exposure was lower with as-needed use, adverse events were comparable, and epistaxis actually occurred only in the as-needed group. As-needed dosing improved symptoms from baseline too, so it is a defensible option for selected children who cannot manage daily therapy. At the other end of the severity spectrum, the World Allergy Organization Journal reports real-world experience with stapokibart, an interleukin-4 receptor alpha blocking antibody, in 37 adults in Northern China with Artemisia-driven seasonal allergic rhinitis uncontrolled on standard therapy [7]. Using just two doses, 600 milligrams at baseline and 300 milligrams at week two, total nasal symptom scores fell from around nine at baseline to under one by week four and stayed low through week sixteen, with parallel improvements in quality of life, a marked drop in rescue medication and suppression of nasal nitric oxide. This is an uncontrolled case series in a season-limited disease, so placebo and natural pollen decline both contribute, but a short-course, season-oriented biologic strategy is a pragmatic idea worth formal testing. Complementing all of this, a review in Allergy from van Wijk and colleagues dissects why allergen immunotherapy trials succeed or fail, pointing to unvalidated primary endpoints, heterogeneous patient selection, low or variable allergen exposure, and large placebo effects, and calling for an internationally agreed minimal clinically important difference and publication of negative studies [4].

Finally, on mechanisms, Choi and colleagues in Allergy analysed 1518 children from the Korean COCOA birth cohort followed to age seven, and identified four food allergy trajectories: no allergy in the large majority, early remission, early persistent in under five percent, and late remission [10]. Children on the early persistent path had higher interleukin-4, 5 and 6 at ages three and seven, lower interleukin-10 at age three than the late remission group, and hypermethylation of two placental genes, RPS6KA2 and GCSAML. GCSAML methylation tracked with total and egg white specific IgE, early-life eosinophils and interleukin-5. It is association rather than causation, but it points to prenatal programming of who outgrows food allergy and who does not.

If you only have time for one paper this week, make it the updated EAACI statement on drug hypersensitivity skin testing [1]. It is the document you will actually reach for in clinic, and its risk-stratified pathway allowing direct provocation for mild maculopapular exanthema will change how quickly you can delabel.

Here are the key takeaways from this week in Allergy and Immunology. First, test immediate drug reactions at four to six weeks, use the standardised zero point zero two millilitre intradermal technique with a three millimetre wheal increase as the threshold, and reserve preliminary skin testing for anaphylaxis rather than mild exanthema. Second, in perioperative anaphylaxis, early cutaneous vasoconstriction with bradycardia identifies the patients most likely to die, not the mildest ones. Third, before adding or switching a biologic in uncontrolled severe asthma, verify adherence directly with the patient, because physician estimates substantially overestimate it, and screen for anxiety and depression. Fourth, aspirin therapy after desensitisation performed no better than placebo in a small crossover trial, and sputum SERPINB9 is an early candidate for identifying who benefits. And fifth, in mild type 2-low asthma, muscarinic antagonist monotherapy looks like a plausible alternative to inhaled corticosteroid for selected patients, but the evidence is not yet definitive.

That's your roundup for This Week in Allergy and Immunology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

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This is an automated summary generated by artificial intelligence, which can make mistakes. Always review the original source materials.