A Rare Case of Systemic Reaction to Carrot Due to PR-10 in a Young Child

Introduction

Pollen-food allergy syndrome (PFAS) is an IgE-mediated allergic condition resulting from cross-reactivity between inhalant pollen allergens and homologous proteins found in plant-derived foods. ¹ This syndrome affects individuals sensitized to pollen allergens such as pathogenesis-related proteins group 10 (PR-10), including Bet v 1, profilins, and gibberellin-regulated proteins, which share structural similarities with certain food proteins. PFAS is the most prevalent food allergy in adults, with an increasing incidence observed in the pediatric population. ²

While PFAS typically presents as oral allergy syndrome (OAS) with mild oral symptoms—such as itching and swelling of the lips, mouth, and throat—in rare cases, it may progress to systemic allergic reactions, including anaphylaxis.

Cofactors like proton pump inhibitors (PPIs), exercise, or fasting can increase allergen absorption and exacerbate reactions. ³ Another factor that can influence the severity of the reaction is the type of allergen involved. For instance, gibberellin-regulated proteins are associated with systemic reactions, despite being technically a PFAS. ⁴ Accurate molecular diagnosis is crucial to identify high-risk patients and prevent severe manifestations.

Case Presentation

We present the clinical case of a 12-year-old male child with a history of allergic rhinitis, sensitized to grass and birch pollen. His medical history included two prior episodes of OAS following the consumption of raw carrot and fennel, which had previously been well tolerated both cooked and raw. The patient was referred to our clinic after developing oral symptoms following the ingestion of a single raw carrot in its natural form, which rapidly progressed to dyspnea, facial edema, and subsequent vomiting within a few minutes. The quantity consumed was no greater than what he had consumed on previous occasions that had resulted only in mild oral symptoms. The systemic reaction occurred during birch pollen season, when the patient usually experienced rhinitis symptoms. Having never experienced systemic reactions before then, the patient had not been prescribed an adrenaline auto-injector. Symptoms improved after administration of antihistamines and oral corticosteroids. The patient had consumed a normal breakfast approximately 2 h before eating the raw carrot. He had not exercised before or after consuming the carrot. At the time of the reaction, he was not taking any drug other than intranasal corticosteroid for managing his rhinitis symptoms. After the reaction, he had avoided raw carrots and fennel. However, he had consumed cooked carrot without developing any symptoms.

Skin prick tests with commercial extracts confirmed sensitization to grass and birch pollen, hazel, and fennel, while prick-by-prick testing with cooked and raw carrot showed positivity only for the raw form (8 mm). The patient’s specific IgE profile showed positivity to PR-10 positivity for carrot, fennel, PR-10 proteins Bet v 1 and Pru p 1 (see Table 1). However, no sensitization to profilins Bet v 2 and Pru p 4 and lipid transfer protein (LTP) Pru p 3 was detected.

The patient was recommended to avoid raw carrot and fennel while continuing to consume them cooked. Education on cofactors and hidden allergens in foods was provided, along with an epinephrine auto-injector for emergency use.

The patient and his parents gave their written informed consent for the publication of this case.

The study was approved by the local Ethics Committee of ASST Fatebenefratelli-Sacco.

Discussion

Sensitization to PR-10 and profilins can lead to immediate “contact” symptoms in the oral cavity, such as itching and swelling, following ingestion of plant-derived foods containing homologous proteins. PR-10 and profilins are thermolabile and gastrolabile proteins; thus, contact with gastric juices or the cooking process leads to their denaturation. However, when they pass intact through the gastric acid barrier and reach the duodenum in a structurally unmodified form, they can trigger systemic symptoms. This occurs particularly in the presence of cofactors that favor labile food allergens to avoid gastric digestion. Such cofactors include the use of PPI, prolonged fasting, consumption of large quantities of the allergen, or ingestion in liquid form. ⁵ The latter scenario is typically observed in systemic reactions to soy-containing beverages, and similar cases have been reported with carrot juice consumption. ⁵

Rarely, systemic reactions can occur in the absence of known cofactors, as in our patient who experienced anaphylaxis (OAS, facial angioedema, dyspnea, and vomiting) after consuming raw carrot without any identified cofactors. Molecular testing revealed isolated PR-10 positivity, thus confirming a PR-10-related PFAS. The patient’s subsequent inadvertent consumption of cooked carrot without symptoms aligns with the known thermal instability of PR-10 allergens. Many reactions to both raw and cooked carrots are due to their status as a hidden allergen and its widespread use as a food dye in industrial applications and as an ingredient in various recipes. ⁶

Systemic PR-10 reactions are uncommon, with anaphylaxis estimated in 1%–2% of PFAS cases. ⁷

The first pediatric case of carrot-induced anaphylaxis due to PR-10 was reported by Balas et al., describing an 11-year-old boy who developed anaphylaxis after drinking raw carrot juice. ⁷

Both cases present similarities. First, the anaphylaxis reactions occurred in early adolescence, when PFAS prevalence increases significantly. ⁸ Second, both of them experienced anaphylaxis during birch pollen season while having active rhinitis symptoms.

The temporal relationship between systemic reactions and birch pollen season suggests that exposure to relevant concentrations of pollens in the air may act as a risk factor for systemic reactions in individuals sensitized to PR-10 proteins.

In addition, our patient exhibited very high Bet v 1 IgE levels, suggesting that all these factors—adolescent age, high Bet v 1 sIgE, pollen season exposure, and concurrent rhinitis—may represent a particularly high-risk phenotype for severe PFAS reactions.

Interestingly, Asero et showed that 44% of systemic reactions to PR-10 occurred without any identifiable cofactors, which aligns with our case. This study also emphasized that tree nuts, Rosaceae fruits, Apiaceae vegetables (including carrots), and soy products were the most common triggers of systemic reactions in PR-10 sensitized individuals. ³

It has also been hypothesized that PFAS could be part of the allergic march, with IgE sensitization to Bet v 1 increasing from 2.2% at age five to 13.9% by age nine, suggesting a developmental progression of the allergic response ⁸ Notably, Bet v 1 sensitization at preschool or school age represented the strongest risk factor for PFAS development in early adolescence. ⁸ This may explain why some children with PR-10 sensitization develop systemic reactions despite previously tolerating allergenic foods.

This case highlights that, although PFAS is typically associated with mild, localized symptoms, it can rarely progress to anaphylaxis—even in the absence of known cofactors. Such severe reactions may occur when labile food allergens, such as PR-10 proteins, escape pepsin digestion—thereby retaining their allergenic potential and triggering systemic responses.

It also points out the importance of molecular diagnostics in the individualized risk assessment and comprehensive patient education, including guidance on trigger avoidance. Epinephrine auto-injectors should be prescribed to sensitized individuals at risk of systemic reactions.

Further research is warranted to elucidate the genetic, immunological, and environmental factors that contribute to the variability in clinical outcomes among PR-10-sensitized patients, which could ultimately enhance risk stratification and management strategies.