Differentiating Acute Food Protein–Induced Enterocolitis Syndrome From Its Mimics: A Comparison of Clinical Features and Routine Laboratory Biomarkers

Lee, Eric; Barnes, Elizabeth H; Mehr, Sam; Campbell, Dianne E.

doi:10.1016/j.jaip.2018.10.020

Cited by 35 publications

(24 citation statements)

References 19 publications

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“…While any solid food can cause FPIES, some overrepresented triggers include grains (rice, oats), vegetables (sweet potato, squash), fruits (banana, avocado), poultry and eggs. Rice is the most commonly reported solid trigger in the United States and Australia, and may be associated with a more severe phenotype [63,[97][98][99]. Furthermore, other geographical variations are evident, such as the high prevalence of soy-induced FPIES in the United States [23,25,26,65,95], and of fish and shellfish reactions in Italy and Spain [20,40,60,76,100,101].…”

Section: Reported Food Triggersmentioning

confidence: 99%

“…Laboratory studies are somewhat helpful in supporting the diagnosis of non-IgE-GI-FA, although the findings are usually nonspecific. In FPIES, blood testing can uncover anemia, hypoalbuminemia, thrombocytosis, and a high white blood cell count with left shift [63,68]. With increased severity, metabolic acidosis and methemoglobinemia may also develop [113].…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…In FPE, iron-deficiency, anemia and hypoproteinemia are frequently present [16,114], while these are uncommon in FPIAP (<15%) [27,85,115,116]. Peripheral eosinophilia can be found in FPIES, FPE and FPIAP, although it is a more prominent feature in the two latter entities [28,58,63,83,85,117]. Lymphocyte transformation tests (LTT) remain experimental, and as such, are not recommended [118].…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…Interestingly, C-reactive protein (CRP), an acute phase reactant produced by the liver in response to the pro-inflammatory cytokine IL-6, has been reported to be marginally elevated following positive OFC in patients with FPIES [72,[135][136][137]. However, while low elevation can be found, a high CRP (>20 mg/dL) should prompt one towards an alternative diagnosis [63]. Platelets, another acute phase reactant, are often elevated in FPIES, with one study reporting a significantly lower mean platelet volume (MVP) than in bacterial sepsis, which may help discriminate between both conditions [63].…”

Section: Other Biomarkersmentioning

confidence: 99%

“…However, while low elevation can be found, a high CRP (>20 mg/dL) should prompt one towards an alternative diagnosis [63]. Platelets, another acute phase reactant, are often elevated in FPIES, with one study reporting a significantly lower mean platelet volume (MVP) than in bacterial sepsis, which may help discriminate between both conditions [63].…”

Section: Other Biomarkersmentioning

confidence: 99%

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Non-IgE-Mediated Gastrointestinal Food Allergies in Children: An Update

2020

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Non-immunoglobulin E-mediated gastrointestinal food allergic disorders (non-IgE-GI-FA) include food protein-induced enterocolitis syndrome (FPIES), food protein-induced enteropathy (FPE) and food protein-induced allergic proctocolitis (FPIAP), which present with symptoms of variable severity, affecting the gastrointestinal tract in response to specific dietary antigens. The diagnosis of non-IgE-GI-FA is made clinically, and relies on a constellation of typical symptoms that improve upon removal of the culprit food. When possible, food reintroduction should be attempted, with the documentation of symptoms relapse to establish a conclusive diagnosis. Management includes dietary avoidance, nutritional counselling, and supportive measures in the case of accidental exposure. The prognosis is generally favorable, with the majority of cases resolved before school age. Serial follow-up to establish whether the acquisition of tolerance has occurred is therefore essential in order to avoid unnecessary food restriction and potential consequent nutritional deficiencies. The purpose of this review is to delineate the distinctive clinical features of non-IgE-mediated food allergies presenting with gastrointestinal symptomatology, to summarize our current understanding of the pathogenesis driving these diseases, to discuss recent findings, and to address currents gaps in the knowledge, to guide future management opportunities.

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