Inconsistent documentation of known allergies in electronic patient records (EPRs) poses a major patient safety risk. Unlike drug allergies, food and non-drug allergens lack standardised documentation frameworks. This study evaluated how such allergies are recorded across NHS Trusts and the extent of avoidable harm from exposures.
We conducted a national cross-sectional, study. Freedom of Information (FOI) requests were sent to all 209 public (NHS) hospital Trusts (December 2024) to collect data on allergy-related incidents, EPR availability, training and governance. An online survey was distributed to British Society for Allergy & Clinical Immunology (BSACI) members (February 2025) to capture clinician experiences, challenges and suggestions. Quantitative data were analysed using non-parametric statistics; qualitative data were analysed using thematic analysis.
Responses were received from 194 Trusts (93%), with 145 providing complete datasets (582 hospitals). Sixty-one different EPR platforms were identified, with 44 Trusts operating multiple systems. Across a median 10-year span, 12,385 allergy-related incidents were reported: 7724 (62%) drugs and 1277 (10%) food/non-drug allergens. Over half of Trusts (54%) lacked a dedicated incident-reporting category for food/non-drug allergens, suggesting underestimation. Trusts without EPRs reported 140% more incidents than those with EPRs (p = 0.002). Those with in-house allergy services, training and guidance recorded higher incident rates, consistent with enhanced recognition and reporting. The BSACI survey revealed challenges including poor EPR usability, limited coding options, weak alert systems and reliance on free text. Ninety percent of respondents supported national guidance on allergy documentation.
Marked heterogeneity exists in NHS EPR systems and food/non-drug allergy documentation practices. Trusts without EPRs experience higher reporting rates, while training and specialist services are associated with improved recognition. The absence of dedicated categories for food and non-drug allergies contributes to systematic underreporting. These findings demonstrate how fragmented systems and inconsistent governance directly compromise allergy safety across UK hospitals.
Background: Flow cytometry studies have reported an association between lower regulatory T cells (Treg) in cord blood and subsequent food allergy. Flow cytometry, however, is a resource-intensive technique. We therefore aimed to develop an epigenetic biomarker (nTregepi) that correlates with the proportion of naïve regulatory T cells (nTreg) in cord blood white cells (CBWCs) measured by flow cytometry. We then investigated the association between nTregepi and subsequent food allergy.
Methods: The Barwon Infant Study (BIS) is a prebirth cohort study (n = 1074 infants). Illumina Infinium MethylationEPIC v1.0 BeadChips were used to assess DNA methylation in cord whole blood (n = 936). In a subgroup, flow cytometry was used to measure the proportion of nTregs (CD4 + CD45RA + FOXP3+) in CBWCs (n = 450). In a training set (n = 338), we assessed the correlation between methylation at 78 probes in the FOXP3 and TIGIT genes and the proportion of nTregs in CBWCs. LASSO regression was then used to develop a linear methylation predictor of nTregs as a proportion of CBWCs, denoted 'nTregepi', which was then tested in a validation set (n = 112). The association between nTregepi and subsequent IgE-mediated food allergy was evaluated using logistic regression.
Results: Methylation levels of 23/78 sites in FOXP3 and TIGIT were associated with the proportion of nTregs in CBWCs (q < 0.05 for each). LASSO regression of methylation levels for these 21 probes was used to derive a linear predictor (nTregepi) which correlated with the log proportion of nTregs in the validation set (R2 = 0.22, p < 0.001). In the complete cohort with relevant data available (n = 693), a higher nTregepi was associated with decreased odds of food allergy (odds ratio 0.65 (95% CI 0.48-0.88, p = 0.005)).
Conclusions: A composite epigenetic biomarker in cord whole blood correlates with the proportion of nTreg in CBWCs and is strongly associated with the absence of subsequent food allergy.
Background: Non-steroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) is characterised by the clinical triad of hypersensitivity to NSAIDs, nasal polyposis, and asthma. The cells and mediators causing acute symptoms when driving the hypersensitivity reaction to acetylsalicylic acid (ASA) ingestion, remain poorly defined.
Objective: To investigate the dynamics of nasal mediators during ASA provocation in N-ERD patients before and 24 weeks after therapy with the IL-4 receptor alpha-blocking antibody dupilumab (EudraCT (2019-004889-18) and ClinicalTrials.gov (NCT04442256)).
Methods: Nasal mucosal lining fluids of patients with N-ERD, chronic rhinosinusitis patients with nasal polyp (CRSwNP) and healthy disease controls were collected at selected time points up to 2 h after ASA provocation. Analysis of thirty-three different inflammatory mediators as well as transcriptomic profiling was performed. In N-ERD patients, provocation was repeated after 24 weeks of dupilumab therapy.
Results: Sixty minutes after provocation with ASA, N-ERD patients showed a significant increase in type 2 associated cytokines (i.e., TSLP, IL-5 and eotaxin-3) as compared to the other patient groups. This effect was diminished after 24 weeks of dupilumab therapy and was independent of the development of ASA tolerance. Transcriptomics revealed dampened upregulation of type 2 associated pathway genes (i.e., AREG) as well as enhanced downregulation of lipid (i.e., ALOX15) and peroxisome metabolisms (i.e., NOS2) at ASA provocation after dupilumab therapy.
Conclusion and clinical relevance: Treatment with dupilumab leads to reduced nasal type 2 cytokine secretion and distinct changes in transcriptomic profile during ASA provocation, but changes in type 2 mediators show no association with tolerance development.
Trial registration: EudraCT (2019-004889-18) and ClinicalTrials.gov (NCT04442256).
Introduction: Peanut allergy is the most common food allergy in Australian school-aged children and is rarely outgrown. Access to oral immunotherapy (OIT), a disease-modifying treatment for food allergy, is limited in many regions of the world, including Australia. Clinical trials show high rates of allergic desensitisation and remission are being achieved, particularly in young children, but significant variability in protocols and implementation prevents large-scale evaluation of clinical and patient-reported safety, effectiveness and long-term outcomes. A standardised national model of care OIT program has not been previously attempted. In Australia, the National Allergy Centre of Excellence partnered with 10 paediatric hospitals to develop and implement the ADAPT OIT Program, which aims to change the trajectory from 'Allergy Development to an Accelerated Pathway to Tolerance'. The Program was designed after extensive international expert and consumer consultation, and attempts to be pragmatic, feasible by using existing resources, and equitable, with out-of-pocket costs to families limited to the purchase of the OIT product, store-bought peanut flour.
Methods: In July 2024, the ADAPT OIT Program was launched. Infants were considered if they had a history consistent with an IgE-mediated allergic reaction to peanut < 12 months of age and evidence of sensitisation (peanut SPT ≥ 3 mm; peanut sIgE or ara h 2 sIgE ≥ 0.35kUA/L). A threshold oral food challenge (OFC) was done to confirm a diagnosis of peanut allergy using teaspoon measures (1/64th, 1/32nd, 1/16th, 1/8th, ¼, ½, 1 tsp. peanut flour, cumulative dose of 2435 mg peanut protein), and to determine the OIT starting dose unless the index reaction was a CoFAR Grade 3+. In this case, infants started OIT with a microdose escalation commencing with a red microspoon of peanut flour (3 mg peanut protein) up to a maximum of 1/64th tsp. (15 mg). Up-dose stage visits were conducted every 4 weeks until the maintenance stage was achieved (1/2 tsp. of peanut flour: 650 mg peanut protein). After 2 years of OIT, infants had an 8-week period of strict peanut avoidance followed by an OFC to assess for sustained unresponsiveness (SU). Infants were followed up for a minimum of 12 months post SU OFC.
Conclusion: The ADAPT OIT Program aims to make best-practice peanut OIT accessible to a significant proportion of infants with peanut allergy in Australia. Under a national standardised model, with rigorous and timely evaluation, the Program design enables optimisation over time for maximal impact.
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：