Abstract
Introduction
In adults, IgE-mediated food allergy is associated with clinically relevant allergic reactions of variable severity. Omalizumab has been shown to reduce food-related reactions in selected populations; however, evidence in adults, particularly those with chronic spontaneous urticaria (CSU), remains limited.
Aim
To evaluate whether omalizumab treatment reduces the severity of food-related allergic reactions upon re-exposure in adult patients with chronic spontaneous urticaria and concomitant IgE-mediated food allergy.
Material and methods
Adult patients with CSU receiving omalizumab and a documented history of IgE-mediated food allergy were retrospectively evaluated with a limited prospective component. Reaction severity before and after omalizumab treatment was assessed using the EAACI, Brown, and Ring–Messmer classification systems. Analyses were restricted to patients who were re-exposed to the culprit food after treatment. Baseline clinical and laboratory parameters were compared between responders and non-responders.
Results
Forty adult patients were included (median age: 42 years; 70% were female). Anaphylaxis history was more frequent in patients with chronic spontaneous urticaria and concomitant IgE-mediated food allergy than in CSU patients without food allergy (p = 0.040). Thirty-one patients were re-exposed to the culprit food after initiation of omalizumab treatment. Reaction severity was significantly reduced following treatment across the EAACI, Brown, and Ring–Messmer classification systems (all p < 0.001). Baseline total IgE levels, eosinophil counts, serum tryptase levels, and atopy status were not associated with clinical response. Higher baseline C-reactive protein levels were observed among responders (p = 0.039).
Conclusions
Omalizumab treatment was associated with a consistent reduction in the severity of food-related allergic reactions upon re-exposure in adults with CSU and IgE-mediated food allergy. Clinical improvement occurred largely independently of conventional allergic biomarkers.
Keywords: IgE-mediated food allergy, chronic spontaneous urticaria, omalizumab, anaphylaxis, adult patients, total IgE
Introduction
Omalizumab is an anti-IgE monoclonal antibody that binds to free IgE and reduces FcεRI expression, and it has long been used as a biologic agent with proven efficacy in the treatment of chronic spontaneous urticaria. Recent clinical studies have shown that omalizumab can reduce the severity of reactions to multiple foods in children and adolescents, as well as decrease the risk of adverse events related to food exposure [1]. However, almost all of these findings are based on paediatric populations, and it remains unclear whether a similar effect exists in adults – particularly those with chronic urticaria who also have IgE-mediated food allergy.
According to the European Academy of Allergy and Clinical Immunology (EAACI) guidelines for IgE-mediated food allergy, management is not limited to strict allergen avoidance; rather, it encompasses a multidimensional approach that includes individualised dietary counselling, emergency preparedness, psychological support, and immunomodulatory treatments in selected patients [2]. In this context, biologic therapies such as omalizumab are gaining increasing importance not only for controlling symptoms of allergic diseases, but also as agents with potential roles in reducing reaction severity and improving patient safety during unavoidable allergen exposure.
Systematic reviews indicate that evidence regarding the safety and clinical impact of biologic therapies for IgE-mediated food allergy remains limited, particularly in adult populations [3]. This uncertainty clearly highlights the lack of data regarding the impact of omalizumab on the likelihood or severity of clinical reactions following food exposure in the adult population.
Aim
The aim of this study was to evaluate the effects of omalizumab treatment on the severity of food-related allergic reactions upon re-exposure, according to the EAACI, Ring–Messmer, and Brown anaphylaxis classification systems, in adult patients diagnosed with chronic spontaneous urticaria (CSU) and concomitant IgE-mediated food allergy.
Material and methods
Study design
This study was designed as a retrospective cohort analysis with a prospective assessment component. Medical records were retrospectively reviewed to identify eligible patients, and patients were subsequently contacted by telephone to prospectively evaluate post-treatment clinical outcomes following omalizumab therapy. The primary aim was to determine the prevalence of IgE-mediated food allergy among patients with chronic spontaneous urticaria treated with omalizumab and to assess changes in the severity of anaphylactic reactions before and after treatment. A total of 262 patients receiving omalizumab for chronic spontaneous urticaria were screened through a medical record review. Among them, 40 adult patients with concomitant IgE-mediated food allergy met the inclusion criteria and were included in the analysis.
Data collection and outcome measures
Demographic characteristics and clinical features of chronic spontaneous urticaria were obtained from medical records. Data regarding omalizumab treatment duration and history of IgE-mediated food allergy were recorded. The severity of food-related anaphylactic reactions was assessed before and after omalizumab treatment and classified according to the EAACI anaphylaxis guidelines, the Ring–Messmer classification, and the Brown grading system, all of which are widely used and validated tools for assessing anaphylaxis severity in clinical practice [2, 4, 5].
Adult patients aged 18 years and older with a diagnosis of chronic spontaneous urticaria who remained uncontrolled despite receiving second-generation antihistamine treatment for at least 6 months and subsequently initiated omalizumab therapy were eligible for inclusion. Patients were included if they had a documented history of IgE-mediated food allergy and if sufficient medical records were available to allow assessment of food-related anaphylaxis severity before and after omalizumab treatment.
Patients younger than 18 years, those with inducible (physical) urticaria without chronic spontaneous urticaria, those without a documented history of IgE-mediated food allergy, patients with incomplete medical records regarding food allergy history or anaphylaxis severity, and those receiving concomitant biologic therapies for allergic or immunologic diseases were excluded from the study. Atopy was defined as at least one positive skin prick test and/or specific IgE to aeroallergens. Patients were classified as responders if they demonstrated a reduction in the severity of food-related allergic reactions upon re-exposure after initiation of omalizumab treatment, as assessed by at least one-grade improvement in anaphylaxis severity according to the EAACI, Brown, or Ring–Messmer classification systems, or complete absence of reaction upon re-exposure (severity score = 0). Patients who experienced no change or worsening in reaction severity after re-exposure were classified as non-responders.
Statistical analysis
Statistical analyses were performed using SPSS software, version 22.0 (IBM Corp., Armonk, NY, USA). Categorical variables were summarised as frequencies and percentages, and continuous variables were expressed as median (interquartile range) or mean ± standard deviation, as appropriate. Normality of continuous variables was assessed using visual inspection of histograms and Q–Q plots.
Categorical variables were compared using the χ2 test or Fisher’s exact test, as appropriate. Continuous variables were compared using the independent-samples t-test or the Mann–Whitney U test, depending on data distribution. Changes in anaphylaxis severity before and after omalizumab treatment were evaluated using the Wilcoxon signed-rank test. A p-value < 0.05 was considered statistically significant.
Results
This retrospective review included 262 patients treated with omalizumab for chronic spontaneous urticaria, of whom 40 adult patients with concomitant IgE-mediated food allergy met the inclusion criteria and were enrolled in the study. The median age was 42 years (IQR: 33–50), and 70.0% were female. Asthma and rhinitis were present in 27.5% and 42.5% of patients, respectively (Table 1).
Table 1.
Clinical characteristics of patients diagnosed with CSU receiving omalizumab treatment and having a history of food allergy (n = 40)
| Parameter | n (%) |
|---|---|
| Female sex | 28 (70.0) |
| Asthma | 11 (27.5) |
| Rhinitis | 17 (42.5) |
| Drug allergy | 18 (45.0) |
| CIndU subtypes coexisting with CSU | 24 (60.0) |
| Dermographic urticaria | 18 (45.0) |
| Cold-induced urticaria | 2 (5.0) |
| Heat-induced urticaria | 11/39 (28.2)* |
| Delayed pressure urticaria | 6/38 (15.8)* |
| Cholinergic urticaria | 1/35 (2.9)* |
Valid percentages are reported due to missing data.
The baseline laboratory characteristics of patients with CSU and concomitant food allergy are presented in Table 2.
Table 2.
Laboratory characteristics of 40 patients with CSU and concomitant food allergy history
| Variable | N | Median (IQR) | Min.–max. |
|---|---|---|---|
| Age [years] | 40 | 42 (33–50) | 20–66 |
| Total IgE [IU/ml] | 39 | 232 (65–367) | 11–3000 |
| TPOAb [IU/ml]* | 34 | 8 (3–11) | 0.25–210 |
| TgAb [IU/ml]* | 33 | 11 (5–14) | 0–302 |
| Eosinophils [× 106/l] | 40 | 100 (55–200) | 0–730 |
| Basophils [× 106/l] | 40 | 20 (10–40) | 0–100 |
| Tryptase [μg/l] | 37 | 4.9 (3.3–7.7) | 1.5–23.7 |
| ECP [ng/ml] | 6 | 88 (31–134) | 19–200 |
Reference ranges: TPOAb 0–9 IU/ml, TgAb 0–4 IU/ml (institutional standards).
Patients with IgE-mediated food allergy had a significantly higher history of anaphylaxis compared with CSU patients without food allergy (37.5% vs. 22.3%, p = 0.040; OR = 2.09, 95% CI: 1.03–4.28) (Table 3). No significant differences were observed between groups regarding age, sex, atopy, asthma, rhinitis, drug allergy, CRP, D-dimer, total IgE, or serum tryptase levels (all p > 0.05). Among food-allergic patients, 52.5% had multiple food allergies. The most frequently implicated food groups were vegetables (32.5%), spices (27.5%), nuts (20.0%), meat (20.0%), and eggs (12.5%). Objective diagnostic testing was performed in 47.5% of patients, with confirmed positivity in 36.8% of those tested (Table 4).
Table 3.
Comparison of clinical characteristics between patients with and without a history of IgE-mediated food allergy prior to omalizumab treatment
| Variable | Food allergy (+) n = 40 | Food allergy (–) n = 222 | P-value |
|---|---|---|---|
| Gender (female) | 28 (70.0%) | 142 (64.0%) | 0.462 |
| Asthma | 11 (27.5%) | 58 (26.1%) | 0.856 |
| Rhinitis | 17 (42.5%) | 108 (48.6%) | 0.474 |
| Drug allergy | 18 (45.0%) | 78 (35.3%) | 0.241 |
| History of anaphylaxis | 15 (37.5%) | 49 (22.3%) | 0.040* |
| Atopy | 15 (37.5%) | 85 (38.2%) | 0.960 |
| Age [years] median (IQR) | 42 (33-50) | 43 (35-52.5) | 0.400 |
| CRP [mg/l] median (IQR) | 3.0 (1.0–7.9) | 3.85 (2.0–7.0) | 0.222 |
| D-dimer [ng/ml] median (IQR) | 0.4 (0.2–0.6) | 0.3 (0.2–0.6) | 0.852 |
| Total IgE [IU/ml] median (IQR) | 232 (65–349.5) | 140 (63.5–292) | 0.241 |
| Serum tryptase [μg/l] median (IQR) | 4.9 (3.3–7.7) | 5.6 (4.3–7.6) | 0.328 |
p < 0.05 is considered statistically significant. Odds ratio (OR) for history of anaphylaxis in patients with food allergy compared with those without food allergy was 2.09 (95% CI: 1.03–4.28).
Table 4.
Clinical and diagnostic characteristics of patients with food allergy
| Variable | Present, n (%) |
|---|---|
| Multiple food allergy | 21/40 (52.5%) |
| Food groups* | |
| Legumes | 0/40 (0%) |
| Cereals | 1/40 (2.5%) |
| Spices | 11/40 (27.5%) |
| Fruits | 3/40 (7.5%) |
| Vegetables | 13/40 (32.5%) |
| Nuts | 8/40 (20.0%) |
| Seeds | 1/40 (2.5%) |
| Milk | 4/40 (10.0%) |
| Eggs | 5/40 (12.5%) |
| Seafood | 4/40 (10.0%) |
| Meat | 8/40 (20.0%) |
| Chocolate | 6/40 (15.0%) |
| Coffee | 1/40 (2.5%) |
| Processed meat (salami/sucuk/sausage) | 1/40 (2.5%) |
| Diagnostic test performed | 19/40 (47.5%) |
| Diagnostic test positive (among those tested) | 7/19 (36.8%) |
| If positive, diagnostic test method (n = 7) | |
| Specific IgE | 4 /7 (57.1%) |
| Prick test | 3/7 (42.9%) |
| Positive food group (n = 7) | |
| Milk | 2/7 (28.6%) |
| Egg | 3/7 (42.9%) |
| Meat | 1/7 (14.3%) |
| Vegetables + nuts | 1/7 (14.3%) |
Patients may be represented in more than one food category.
Thirty-one patients re-exposed to the culprit food after omalizumab initiation were included in the severity analysis. Of these, 17 (54.8%) were classified as responders and 14 (45.1%) as non-responders (Table 5). Reaction severity significantly decreased after treatment across all three anaphylaxis classification systems: EAACI (Z = −4.123, p < 0.001), Brown (Z = −4.123, p < 0.001), and Ring–Messmer (Z = −4.000, p < 0.001). Post-treatment non-reactivity was coded as severity score 0 (Figure 1). In responder versus non-responder analyses, baseline total IgE, eosinophil count, serum tryptase, D-dimer, atopy status, autologous serum skin test (ASST) positivity, and antinuclear antibody (ANA) positivity did not differ significantly; however, C-reactive protein (CRP) levels were higher in responders compared with non-responders (median 7.45 vs. 2.0 mg/l, p = 0.039) (Figure 2). No baseline laboratory parameter other than CRP was associated with response status, suggesting limited utility of conventional biomarkers in predicting changes in food-related reaction severity under omalizumab treatment.
Table 5.
Comparison of variables between omalizumab responders and non-responders
| Variable | Responder (n = 17) | Non-responder (n = 14) | Statistical test | P-value |
|---|---|---|---|---|
| Total IgE [IU/ml] | 231 (124–363) | 261 (22–520) | Mann–Whitney U = 111.5 | 0.983 |
| Eosinophil count [× 106/l] | 150 (65–225) | 80 (48–175) | Mann–Whitney U = 98.0 | 0.403 |
| CRP [mg/l] | 7.45 (2.80–12.50) | 2.0 (1.0–3.7) | Mann–Whitney U = 57.0 | 0.039* |
| D-dimer [ng/ml] | 0.5 (0.2–0.6) | 0.3 (0.15–0.85) | Mann–Whitney U = 32.5 | 0.733 |
| Tryptase [μg/l] | 6.20 (3.87–9.22) | 4.30 (3.30–8.30) | Mann–Whitney U = 90.5 | 0.554 |
| ASST positivity | 2 (11.8%) | 1 (7.1%) | Fisher’s exact | 0.505 |
| ANA positivity | 1 (5.9%) | 4 (28.6%) | Fisher’s exact | 0.087 |
| Atopy | 8 (47.1%) | 5 (35.7%) | Chi-square | 0.431 |
Values for continuous variables are expressed as median (interquartile range). Categorical variables are presented as n (%). MW – Mann–Whitney U test, χ2 or Fisher’s exact test was used for categorical variables. p < 0.05 is considered statistically significant.
Figure 1.
Distribution of reaction severity scores before and after omalizumab treatment. Severity was assessed using the EAACI (A), Brown (B), and Ring–Messmer (C) anaphylaxis classification systems. Post-treatment non-reactivity was coded as 0 for analytical purposes, as the original classification systems do not include a category for complete absence of reaction. Nine patients who were not re-exposed to the culprit food after omalizumab initiation were excluded from the analysis. Reaction severity was significantly reduced following omalizumab treatment according to the EAACI (Z = –4.123, p < 0.001), Brown (Z = –4.123, p < 0.001), and Ring–Messmer (Z = –4.000, p < 0.001) classifications
Figure 2.
Baseline C-reactive protein (CRP) levels in omalizumab responders and non-responders. Data are presented as median and interquartile range. CRP levels were significantly higher in responders compared with non-responders (Mann–Whitney U test, p = 0.039)
Discussion
In this real-life retrospective cohort of adult patients with chronic spontaneous urticaria and concomitant IgE-mediated food allergy, we demonstrated that omalizumab treatment was associated with a significant and consistent reduction in the severity of food-related allergic reactions upon re-exposure. Importantly, this improvement was observed across three validated anaphylaxis severity classification systems – EAACI, Brown, and Ring–Messmer – supporting the robustness of the findings. Although adult data on the effects of omalizumab in food allergy remain limited, particularly outside the context of oral immunotherapy, our results suggest a clinically meaningful reduction in reaction severity in adults with CSU at risk of accidental food exposure. Notably, the observed reduction in reaction severity occurred largely independently of baseline IgE levels, eosinophil counts, or serum tryptase, highlighting the limited predictive value of conventional allergic biomarkers in this setting.
IgE-mediated food allergy (FA) develops after unintentional exposure to food allergens and is driven by activation of the allergic cascade through high-affinity IgE receptors (FcεRI) on mast cells and basophils. This process leads to mediator release and multisystem involvement, including cutaneous, respiratory, gastrointestinal, cardiovascular, and neurological manifestations [6]. Omalizumab binds circulating IgE, thereby preventing its interaction with FcεRI and suppressing mast cell and basophil activation [7]. Given this mechanism of action, omalizumab represents a potential therapeutic option for IgE-mediated food allergy.
In line with recent evidence, omalizumab has been shown to increase reaction thresholds and reduce the severity of food-related allergic reactions, primarily by mitigating reactions following accidental exposure [8–11].
In the descriptive analysis of baseline patient characteristics, female predominance was observed in our adult cohort treated with omalizumab, which is consistent with the demographic distribution reported in adult allergic disease cohorts receiving omalizumab [12]. The presence of inducible urticaria subtypes in some patients further indicates that our study population represents a clinically heterogeneous adult cohort treated with omalizumab. The finding of elevated median total IgE levels in our study supports the importance of atopic predisposition and IgE-mediated mechanisms in patients with CSU and a concomitant history of food allergy. Although elevated serum tryptase levels were observed in a small number of patients, the majority had values within the normal range, suggesting that clonal mast cell disorders do not play a predominant role in this cohort.
In our cohort, patients with IgE-mediated food allergy were more likely to have a history of anaphylaxis than those without food allergies, highlighting the clinical importance of this group. Studies focusing on adult anaphylaxis have shown that food is a common trigger, accounting for about 22% of reactions [13]. Large international surveys conducted in specialised allergy centres report that approximately one-quarter of food-allergic patients experience food-induced anaphylaxis, underscoring the global relevance of severity-focused outcome assessment in adult populations [14].
Despite the higher baseline risk, omalizumab treatment was associated with a noticeable attenuation of reaction severity upon re-exposure, indicating a clinically meaningful effect.
Among the 40 patients with IgE-mediated food allergy, 21 (52.5%) had allergies to multiple foods. The most frequently reported food groups were vegetables (32.5%) and spices (27.5%), followed by nuts and meat (20.0%), chocolate (15.0%), and eggs (12.5%). In the literature, adult food allergy cohorts most commonly report shellfish and wheat as triggering foods, with proportions of 68.0% and 28.7%, respectively, in one adult cohort [15]. In contrast, the food distribution observed in our study reflects food exposures identified through clinical evaluation in a specific adult patient group with chronic spontaneous urticaria.
In this study, we observed a significant reduction in the severity of food-related allergic reactions after omalizumab treatment, as shown by the EAACI, Brown, and Ring–Messmer classification systems. The consistent reduction in reaction severity demonstrated across multiple validated anaphylaxis severity classification systems represents an important strength of the study. Expert opinion and current evidence emphasize that the use of omalizumab in food allergy should be guided by shared decision-making, taking into account patient preferences, comorbidities, and treatment burden, and should be considered particularly in patients with multiple food allergies or at high risk of severe reactions or accidental exposure, while continued allergen avoidance remains fundamental [16–18].
In the responder versus non-responder analysis, no significant differences were observed in baseline total IgE levels, eosinophil counts, serum tryptase levels, or atopy status. Interestingly, CRP levels were higher among responders compared with non-responders, which may reflect differences in the underlying inflammatory burden [19]. However, this finding should be interpreted with caution given the limited sample size. In line with ongoing discussions on the identification of biomarkers predictive of therapeutic response in food allergy, our findings raise the possibility that CRP may represent a potential biomarker of response to omalizumab therapy [20].
Evidence on the effects of omalizumab on food-related reactions in adults remains limited and is mainly derived from paediatric studies or trials using omalizumab with oral immunotherapy. The OUTMATCH trial reported reduced reaction severity to multiple foods, primarily in children and adolescents [1]. In line with these findings, a large-scale meta-analysis by Zuberbier et al. demonstrated that omalizumab improves clinical tolerance both as monotherapy and in combination with oral immunotherapy [21].
Given the substantial cost of biologic therapy, expert reviews emphasise that omalizumab use in food allergy should be individualised and reserved for patients at higher risk of severe reactions; although it received the FDA approval for food allergy in 2024, real-world use remains limited due to cost and the need for regular (typically monthly) administration [22].
The severity analysis was limited to patients who were re-exposed to the culprit food after starting omalizumab, which may have reduced recall bias and allowed a more reliable evaluation of clinical change.
Several limitations of this study should be acknowledged. Importantly, given the retrospective design and lack of a control group, causality cannot be definitively established, and the observed reduction in reaction severity may have been influenced by unmeasured confounding factors. Food re-exposure was not standardised and reflected real-life exposures rather than controlled challenge conditions. In addition, selection bias cannot be excluded, as patients who underwent re-exposure may represent a subgroup with different clinical characteristics or risk profiles compared with those who were not re-exposed. Furthermore, the diagnosis of food allergy was based primarily on clinical history, with objective diagnostic testing available only in a subset of patients, which may have affected diagnostic certainty.
Conclusions
Our study suggests that omalizumab treatment may reduce the severity of food-related allergic reactions in adult patients with chronic spontaneous urticaria and concomitant IgE-mediated food allergy. These findings support the growing body of evidence indicating a broader role for omalizumab in food allergy management and highlight the need for prospective, controlled studies focusing on adult populations. From a clinical perspective, these findings suggest that omalizumab may represent a therapeutic option for selected adult patients with CSU and concomitant food allergy who are at high risk of severe reactions or accidental exposure, particularly in cases where conventional management strategies are insufficient.
Funding Statement
Funding No external funding.
Ethical approval
The study was carried out at a tertiary referral centre between 2015 and 2025. The required ethical approval for the study was obtained from the institutional ethics committee (approval number 09.2026.26-0086).
Conflict of interest
The authors declare no conflict of interest.
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