Published online Jun 9, 2026. doi: 10.5409/wjcp.v15.i2.112843
Revised: September 17, 2025
Accepted: January 14, 2026
Published online: June 9, 2026
Processing time: 279 Days and 14.2 Hours
Food protein-induced enterocolitis syndrome (FPIES) is a severe non-IgE-medi
Core Tip: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated hypersensitivity that affects the gastrointestinal tract following ingestion of trigger foods. It typically presents in infancy and is characterized by repetitive, protracted vomiting that begins approximately 1–4 h after ingestion of specific foods. The pathophysiology involves predominantly cell-mediated immune mechanisms. Patients are often misdiagnosed as having sepsis, viral gastroenteritis, or a surgical abdomen. Management includes both acute care during the episodes and long-term dietary modifications and nutritional support. Most children recover from the disease. Multicenter randomized controlled trials are required to build evidence-based guidelines for the diagnosis, acute treatment, and oral immunotherapy. Additionally, awareness of FPIES remains limited among pediatricians and emergency care providers; therefore, more studies focusing on this condition are warranted.
- Citation: Alshehhi K, Abughosh R, Abdelrahman G, Abujouda A, Elghoudi A, Bitar R. Food protein-induced enterocolitis syndrome in children: An updated review on pathogenesis, diagnosis, and management. World J Clin Pediatr 2026; 15(2): 112843
- URL: https://www.wjgnet.com/2219-2808/full/v15/i2/112843.htm
- DOI: https://dx.doi.org/10.5409/wjcp.v15.i2.112843
Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated hypersensitivity affecting the gastrointestinal tract following the ingestion of specific foods. It typically presents in infancy and is characterized by repetitive, protracted vomiting that begins 1–4 hours after ingestion of the culprit foods. Vomiting is often accompanied by lethargy, pallor, and subsequent diarrhea[1]. In more severe cases, FPIES can lead to significant dehydration and metabolic derangements. The clinical phenotype is influenced by several factors, including the age of onset, the presence of associated IgE-mediated food allergy, timing, and duration of symptoms[2].
The identification of FPIES is challenging, especially since there are no specific biomarkers for diagnosis, and the symptoms can mimic those of other diseases, such as sepsis or infectious enteritis[3]. Additionally, the absence of cutaneous and respiratory symptoms makes it unique and different from the usual food-induced anaphylaxis.
FPIES occur after ingestion of certain foods such as cow’s milk, soy, rice, oat, egg, and fish[4]. Despite it being well-characterized clinically, its causes and mechanisms remain poorly understood[5]. The ultimate diagnosis relies on clinical signs and symptoms that resolve upon elimination of the diet, resulting in the disappearance of the symptoms. Additionally, the introduction of trigger foods provokes the symptoms, which helps in confirming the diagnosis.
The management of FPIES includes both acute care and long-term management. Acute management during reactions includes intravenous (IV) hydration, administration of antiemetics, and, occasionally, IV corticosteroids. The long-term management focus is on strict avoidance of trigger foods and nutritional support. Patients can recover from FPIES later in childhood. Therefore, follow-up with food reintroduction under medical supervision is required[6].
In this review, we aim to explore the pathophysiology, clinical presentation, diagnostic criteria, management, and the challenges and recent updates on FPIES. A literature review of the most recent publications and guidelines on FPIES was conducted using the PubMed search engine, and all relevant publications and guidelines were used to help in writing this review. A total of 606 publications were identified. The authors selected the most relevant 29 publications published from 2014 to 2025 for this minireview.
The pathophysiology of PFIES is complex and not yet fully understood; it involves predominantly cell-mediated immune mechanisms that are fundamentally different from those of the classical IgE-mediated food allergies. Therefore, it involves T-cell-mediated responses rather than IgE-mediated mast cell activation[7].
Current evidence suggests that FPIES results from an exaggerated antigen-specific T-cell response within the gastrointestinal mucosa. Upon exposure to the offending food protein, T-helper cells, particularly Th17 cells, are activated and secrete pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin (IL)-17, which contribute to increased intestinal permeability and epithelial injury (Figure 1)[8]. These cytokines promote neutrophil recruitment and compromise the integrity of the gut barrier, leading to vomiting, diarrhea, and systemic signs such as pallor and hypotension in severe cases. Furthermore, impaired regulatory mechanisms appear to play a role. Specifically, reduced levels of transforming growth factor-beta, a cytokine responsible for promoting oral tolerance and maintaining intestinal homeostasis, have been observed in individuals with FPIES[8]. Thus, this imbalance between pro-inflammatory and regulatory signals allows food antigens to provoke an abnormal inflammatory response rather than inducing tolerance.
Additionally, during acute FPIES reactions, there is significant recruitment of neutrophils and activation of monocytes and natural killer cells in the gastrointestinal mucosa. This is accompanied by increased expression of innate inflammatory mediators, including IL-8 (CXCL8), which drives neutrophil chemotaxis, and IL-6, a cytokine known to mediate fever and acute-phase responses[8], suggesting that innate immune cells act as early amplifiers of the inflammatory response before the adaptive immune system is fully engaged.
Transcriptomic studies using peripheral blood mononuclear cells during acute FPIES reactions have identified upregulation of innate immune-related genes. For example, S100A8 and S100A9, which encode calprotectin components associated with neutrophilic inflammation, are significantly increased. NLRP3, part of the inflammasome complex, has also been implicated in some studies, suggesting that activation of inflammasome pathways may contribute to epithelial cell damage and systemic symptoms. These gene expression patterns not only provide biomarkers for disease activity but also reinforce the hypothesis that FPIES involves a rapid, antigen-triggered innate immune reaction preceding T cell-driven responses[8]. The European Academy of Allergy and Clinical Immunology (EAACI) further emphasizes that this dual immune activation is likely central to the disorder’s pathophysiology and may help explain the delayed but severe clinical manifestations of FPIES, which are distinct from both classical food allergy and other gastrointestinal inflammatory disorders[9].
FPIES is often not diagnosed until a patient has experienced multiple reactions to the same food. This is attributable to the nonspecific and delayed onset of symptoms following allergen exposure and the broad range of potential food triggers. Initially, clinicians tend to focus on more immediate differential diagnoses based on the most prominent clinical features, usually involving gastrointestinal or infectious conditions. As a result, it is not uncommon for patients to consult multiple specialists before reaching a physician familiar with FPIES, such as an allergist or pediatric gastroenterologist.
Classic FPIES typically emerges in early infancy, although cases in neonates, older children, and adults have also been described. Symptoms usually occur within the first few weeks following the introduction of cow’s milk or soy protein[10]. FPIES triggered by solid foods tends to develop later, generally emerging between 4 and 7 months of age, coinciding with the introduction of these foods[11].
Early-onset neonatal FPIES is a rare variant of FPIES and may have a distinct pathophysiology. Unlike classic FPIES, which typically manifests between 2 and 7 months of age, neonatal FPIES presents within hours or days after birth, often immediately after the initiation of formula feeding. This suggests a potentially unique immunopathological mechanism, influenced by both prenatal sensitization and the immaturity of the neonatal immune system[12].
In addition to pediatric cases, adult-onset FPIES has become increasingly recognized over the past decade, particularly with improved awareness and reporting. Unlike the more common infantile form, which is often triggered by cow’s milk, soy, or grains, adult FPIES most frequently presents with reactions to seafood, especially mollusks and crustaceans[12,13].
FPIES is generally characterized by delayed, protracted gastrointestinal symptoms that occur in the absence of classic IgE-mediated features, such as urticaria, angioedema, and bronchospasm[14]. The clinical presentation varies depending on whether the reaction is acute (following intermittent exposure) or chronic (due to continuous ingestion of the offending food). Patients with FPIES are often misdiagnosed as having sepsis, viral gastroenteritis, or a surgical abdomen owing to the dramatic symptomatology of the disease.
Acute presentation: Acute presentation of FPIES accounts for approximately 90% of all infantile cases. It typically begins with the sudden onset of vomiting, occurring 1–4 h after ingestion of the triggering food. Classical symptoms of acute FPIES usually include repetitive, projectile vomiting, lethargy, and pallor, potentially progressing to hypotension or hypothermia in severe cases. Diarrhea may or may not occur later, typically within 5–10 h of ingestion. Symptoms generally resolve within 24 h, and patients typically remain asymptomatic between episodes[14]. Notably, the child is often completely well before the episode and returns to a baseline state once the reaction resolves, creating a sharp clinical contrast.
Reactions recur with re-exposure to the trigger food. In moderate to severe cases, affected children may present with poor perfusion; prolonged capillary refill time; metabolic acidosis; and elevated white blood cell counts, thrombocytosis, methemoglobinemia, and neutrophilia, which may sometimes require emergency care or hospitalization[1,15].
Chronic presentation: Chronic FPIES is observed in approximately 10% of cases, and occurs when a trigger food is consumed regularly (e.g., daily formula feeding with cow’s milk or soy), typically in young infants under 4 months of age. It is characterized by a more insidious onset, including intermittent emesis, watery diarrhea, and irritability. As a result, affected children usually have poor weight gain and/or failure to thrive. The presentation may resemble malabsorption syndromes, gastroenteritis, or feeding intolerance. Symptoms generally improve rapidly within days following the elimination of the offending food and recur upon reintroduction. Chronic FPIES can be reflected in laboratory workup with findings of anemia, low albumin, and total protein[7].
FPIES reactions are typically isolated to the gastrointestinal tract, and IgE-mediated symptoms are absent. However, a small proportion of children with FPIES may eventually develop IgE sensitization to the same food over time, known as “atypical FPIES.” This is observed in around 25% of patients with FPIES, in whom a positive skin prick test and/or detectable serum IgE specific to the triggering food is identified. The diagnosis of atypical FPIES requires both evidence of food-specific IgE and a clinical presentation consistent with FPIES. Approximately one-third of these individuals may go on to develop an IgE-mediated food allergy, which can cause immediate and potentially severe reactions such as anaphylaxis, particularly in those with cow’s milk allergy.
Although the precise mechanisms are unclear, it is hypothesized that these individuals may have a mixed immune response involving both T cells and IgE-producing B cells. Studies suggest that children with atypical FPIES may have a more persistent course, a higher risk of transitioning to IgE-mediated allergy (e.g., immediate-type anaphylaxis), and may take longer to develop oral tolerance[7]. Clinically, these patients may require more cautious reintroduction protocols and closer monitoring over time. Immunologically, the dual expression of IgE and T cell pathways in these patients warrants further investigation, particularly in identifying biomarkers that may predict this progression.
While most individuals with FPIES develop tolerance during early childhood, some may continue to exhibit symptoms into adolescence or even adulthood[7]. Additionally, there have been cases where individuals who were asymptomatic during childhood developed FPIES symptoms for the first time as adults[16]. Atypical FPIES tends to follow a more prolonged course, with delayed resolution of symptoms[17].
FPIES can occur after ingestion of certain foods such as cow’s milk, soy, rice, oat, egg, and fish[4]. A systematic review of FPIES by Prattico et al[10], which evaluated 45 studies over the past 10 years, demonstrated that the prevalence of common FPIES triggers differed across countries and regions; however, cow’s milk, fish, eggs, and grains were con
The current diagnostic approach is based on the international consensus guidelines on the diagnosis and management of FPIES, published in 2017[1]. The diagnosis of FPIES requires the presence of one major criterion along with at least three minor criteria (Table 1). The major criterion is the onset of delayed symptoms, typically 1–4 h after consuming the sus
| Category | Diagnostic criteria |
| Major criterion | Vomiting within 1–4 h after ingestion of the suspected food, in the absence of classic IgE-mediated allergic skin or respiratory symptoms |
| Minor criteria | ≥ 2 episodes of repetitive vomiting after eating the same suspected food |
| Repetitive vomiting episode 1–4 h after ingestion of a different food | |
| Extreme lethargy with any suspected reaction | |
| Marked pallor with any suspected reaction | |
| Need for emergency department evaluation following a suspected reaction | |
| Need for intravenous fluid support during a suspected reaction | |
| Diarrhea within 24 h (usually 5–10 h) after ingestion | |
| Hypotension or hypothermia |
Owing to the potential for severe reactions, OFCs in FPIES are considered high-risk procedures. Patients with a history of severe episodes should undergo testing in settings equipped with intravenous access, rapid fluid resuscitation, and extended observation, ideally in an inpatient facility.
While protocols vary across centers, several key principles are generally followed[19]. Testing for food-specific IgE, via skin prick testing or serum assays, is used to assess the risk of IgE-mediated reactions, especially with foods such as cow’s milk or egg. Patients should ingest an age-appropriate portion of the suspected food, either all at once or divided into smaller doses. A minimum observation period of 4–6 h after ingestion is standard. IV access should be readily available. Ondansetron (administered orally, intravenously, or intramuscularly) may help reduce symptom severity, while the benefit of corticosteroids remains uncertain.
An alternative protocol involves administering one-third of a typical age-appropriate serving during the initial supervised challenge, followed by a 4-h observation period. If tolerated, intake is gradually increased at home every 3 days over 9–12 days until a full serving is achieved. In a cohort of 169 OFCs conducted using this protocol, 18% (30 cases) yielded positive results, with 17 reactions occurring during the initial supervised challenge and 13 during the at-home dosing phase. Most reactions during the initial phase required IV fluids, although hypotension was rare. The home reactions, occurring later the same day or within a few days of the initial challenge, typically involved delayed diarrhea, with some cases of vomiting. Only one patient sought emergency care and recovered without further treatment. This protocol demonstrates that supervised OFCs followed by home titration can be a safe and effective method for confirming FPIES[20].
The absence of a standardized protocol for FPIES OFC for confirming/ruling out the diagnosis, combined with the requirement for extended monitoring and the risk of severe reactions requiring intravenous fluid resuscitation, has led to clinician hesitation and limited access to centers equipped to perform these OFCs[21].
The management of FPIES encompasses acute care during symptomatic episodes, long-term strategies focused on dietary modifications and nutritional support, followed by a trial of reintroduction of the trigger food at a later stage to assess whether the child has outgrown FPIES.
Acute episodes require prompt recognition and medical intervention owing to the risk of significant fluid loss and hemodynamic instability. Intravenous fluid resuscitation is the mainstay of treatment in children who present with dehydration or hypotension, helping to restore circulatory volume and correct any electrolyte imbalances. Additionally, the administration of ondansetron, a serotonin 5-HT3 receptor antagonist, has been shown to significantly reduce vomiting and shorten the duration of acute reactions. Its use is supported by both clinical reports and consensus guidelines, highlighting its role as a well-tolerated, effective antiemetic in FPIES episodes[1,8]. In more severe or prolonged episodes, systemic corticosteroids such as methylprednisolone may be considered to attenuate the inflammatory response. Although robust data from randomized trials are lacking, corticosteroids are frequently used in clinical practice to reduce gut inflammation and promote quicker resolution of symptoms. It is important to note that epinephrine, the first-line treatment in IgE-mediated anaphylaxis, is not indicated in typical FPIES reactions, as the underlying pathophysiology does not involve mast cell degranulation or histamine release. However, if an individual exhibits overlapping IgE-mediated symptoms or progresses to anaphylaxis, epinephrine may be administered[7,22].
Long-term treatment of FPIES is centered on the strict avoidance of the identified trigger food. This requires individualized dietary planning and regular follow-up with an allergist and nutritionist, especially for infants and toddlers who are dependent on formula feeding. For infants with cow’s milk or soy-induced FPIES, extensively hydrolyzed formulas are the first-line alternatives. These formulas contain broken-down proteins into smaller peptides, thus reducing their immunogenic potential. If symptoms persist despite the use of hydrolyzed formulas, amino acid-based formulas are recommended to ensure complete tolerance and adequate nutrition[1,23]. Additionally, parents and caregivers should receive comprehensive education and support to read food labels and prevent accidental exposures.
Dietary exclusion must be introduced while avoiding nutritional deficiencies, particularly when common foods such as rice, oats, or dairy are excluded. Follow-up evaluations are crucial for monitoring the child’s growth, developmental milestones, and nutritional status. Therefore, in children with limited food repertoires, dietary supplementation and additional testing may be required to manage macro- and micronutrient deficiencies.
As there is currently no reliable in vitro biomarker to confirm the resolution of FPIES, OFC remains the gold standard for assessing whether a child has outgrown the condition. The challenges are generally considered 12–18 months after the last symptomatic episode, although the timing may vary based on several factors[1]. The EAACI emphasizes that individual factors, including age at diagnosis and comorbid allergic diseases, may influence outcomes and should be considered when developing reintroduction plans[9].
The OFC typically begins with small incremental doses of the previously offending food, administered under physician supervision with access to IV fluids, ondansetron, and resuscitative equipment. If tolerated without delayed symptoms (especially vomiting within 1–4 h), the food may be cautiously reintroduced into the diet. However, in atypical FPIES, where specific IgE to the trigger food is present, additional precautions are warranted. Therefore, measuring serum-specific IgE levels before food reintroduction is recommended, as these patients may be at risk of transitioning to an IgE-mediated allergy, including immediate anaphylaxis[7,10]. If food-specific IgE is detected or shows an increasing trend, clinicians may delay the challenge or adjust the protocol to align more closely with those used for traditional IgE-mediated allergy testing.
Therefore, a stepwise OFC approach that includes pre-challenge IgE testing, especially for triggers such as cow’s milk, soy, or egg, which have a higher overlap in sensitization with individualized reintroduction plans to prevent adverse outcomes in children exhibiting evolving allergic profiles, is recommended[24]. Ultimately, shared decision-making with families, regular reassessment of food-specific IgE when indicated, and coordination with dietitians and allergists are key components of a successful food reintroduction process.
With the establishment of the first International Consensus Guideline for the diagnosis and management of FPIES in 2017 by the American Academy of Allergy, Asthma, and Immunology and the International FPIES Association[1,22], we now have better pathways for the diagnosis and management of FPIES. However, there have been further advances in the understanding of FPIES; a recent addition in managing FPIES was the recognition of peanut and egg as new triggers, evolving alongside the traditional list of foods, including cow’s milk, oat, and rice[24]. Additionally, exploring home reintroduction of trigger foods has potentially reduced the need for hospital admission in some cases[25]. However, modified OFC protocols are still evolving and are being studied for safer introduction of culprit foods[25]. Therefore, one future aspiration involves establishing uniform, safer, and age-specific OFC protocols for children with FPIES[26]. New insights related to the serotonin and purine pathway have been identified, suggesting that serotonin and purine serve as neuromodulators and metabolic drivers of emesis and lethargy[27]. Moreover, neonatal FPIES is emerging as a distinct phenotype characterized by Th2-skewed immunity, necessitating unique diagnostic considerations.
While no reliable biomarkers exist for FPIES, gastric juice analysis demonstrating more than 10 leukocytes per high-power field 3 h post-challenge has been explored as a potential diagnostic tool[28]. Therefore, the lack of specific biomarkers and the reliance on clinical history and OFCs pose considerable diagnostic challenges for clinicians. Additionally, post-challenge fecal samples have shown elevated levels of tumor necrosis factor-α and eosinophil-derived products, suggesting localized intestinal inflammation. Further investigation of the gut microbiome, the gut-brain-immune axis, and cytokine signaling pathways could help uncover therapeutic targets and deepen the understanding of the mechanisms underlying FPIES symptoms[28].
FPIES is a non-IgE-mediated hypersensitivity that affects the gastrointestinal tract following ingestion of specific foods. It typically presents in infancy and is characterized by repetitive, protracted vomiting that begins approximately 1–4 h after ingestion of specific foods. Management includes both acute care during the episodes and long-term dietary modifications and nutritional support. Most children recover from the disease by 3–5 years of age and can tolerate reintroduction of the trigger food.
Despite its potential severity, awareness of FPIES remains limited among pediatricians and emergency care providers, highlighting the need for targeted educational efforts aimed at increasing awareness amongst first-line healthcare professionals. Current evidence on FPIES is limited, and large, multicenter randomized controlled trials are required to establish robust, evidence-based guidelines for the diagnosis, acute treatment, and oral immunotherapy. Future research should also prioritize the identification of specific blood or stool biomarkers to reduce reliance on OFCs, as well as the development and evaluation of oral immunotherapy strategies for infants and children affected by the disease.
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