Food protein-induced enterocolitis syndrome (FPIES) is an allergic disorder that manifests as reproducible gastrointestinal symptoms within hours of ingestion of the causative food, which can progress to dehydration and hypotension. Historically, FPIES has been recognized as a disease affecting the pediatric population but it can also develop de novo in adults. The pathophysiology is not well understood; however, the local adaptive immune system and gene expression linked to innate immune activation are implicated. Adult-onset FPIES has some differences with pediatric FPIES. Vomiting may be absent, while abdominal pain is the most common manifestation. A clear predominance in women occurs, being seafood the most common trigger, although many other foods have also been implicated. Diagnosis of adult-onset FPIES is based on a thorough clinical history but in many cases, it should be followed by an oral food challenge (OFC), due to the absence of vomiting in some patients and the lack of confirmatory diagnostic test. The first-line treatment for acute FPIES reactions is fluid replacement, by the oral route in mild to moderate reactions or via the intravenous route in severe reactions. Ondansetron may be effective in shortening the duration of emesis. Management of patients after diagnosis includes dietary advice and follow-up with supervised OFC at regular intervals to monitor for resolution. Tolerance to the trigger food in children is commonly achieved, a finding not so common in adult-onset FPIES. The aim of this article is to review the most important current concepts in epidemiology, pathophysiology, diagnosis, and management of FPIES.

Seaweed, a rich source of bioactive compounds, has gained increasing attention for its potential therapeutic applications in allergy and inflammation. This review examines the current scientific literature investigating the effects of seaweed derived food and diet factors on allergic and inflammatory conditions. Seaweed is abundant in polysaccharides, peptides, polyphenols, and fatty acids, which possess anti-inflammatory, antioxidant, and immunomodulatory properties. These bioactive compounds have the capacity to modulate immune responses and mitigate allergic reactions, rendering seaweed a promising candidate for the development of functional foods and dietary interventions targeting allergy and inflammation. Explorations into the effects of seaweed consumption on allergic conditions such as allergic rhinitis, asthma, and atopic dermatitis have shown encouraging results. Factors found in seaweed have the potential to alleviate symptoms, reduce inflammation, and boost immune function in allergy sufferers. Furthermore, inquiries into the effectiveness of diets incorporating seaweed in preventing and managing chronic inflammatory conditions like inflammatory bowel disease and rheumatoid arthritis have been undertaken. The mechanisms underlying the therapeutic effects of seaweed derived compounds are being unraveled, revealing their ability to modulate immune cell activity, regulate cytokine production, inhibit inflammatory mediators, and promote gut microbiota balance. Understanding these molecular mechanisms is crucial for targeted interventions and the identification of specific bioactive compounds responsible for the observed therapeutic effects. Seaweed derived food and diet factors hold significant promise as natural interventions for the prevention and management of allergic and inflammatory conditions. However, further research is required to establish the optimal dosage, formulation, and long-term effects of seaweed-based interventions. Additionally, clinical trials are necessary to validate their efficacy and safety in diverse patient populations. This review emphasizes the therapeutic potential of seaweed derived compounds and underscores the importance of incorporating seaweed into dietary strategies to combat allergy and inflammation.

Nutritional therapy through exclusive enteral nutrition (EEN) is successful with Crohn’s disease (CD), but most patients relapse when returning to a normal diet. Personalized and sustainable diets over time have not been tried. This pioneering case report shows the successful response to the use of a skin prick test (SPT) with a 0.5 mm cutoff and a combination of parameters to guide the diet of a child with CD, ensuring continued remission and a regular diet over a follow-up period of 3 years. The 5-year-old patient had a history of chronic diarrhea. Laboratory showed anemia, hypoalbuminemia, high erythrocyte sedimentation rate (ESR), and fecal calprotectin (FCP) > 2,100 µg/g. Endoscopies revealed duodenal ulcer scar and ulcerative pancolitis. Simple endoscopic score for CD score (SES-CD) = 16 (severe). Pathology showed CD. EEN started with a polymeric formula, later moving to an elemental formula due to a suboptimal response. Medication included prednisolone, mesalazine, azathioprine, and methotrexate. Foods were introduced guided by the SPT and included 54 protein extracts from food tested every 3–4 months. The patient has clinical and histological remission despite having lamb, turkey, eggs, cereals (including wheat), and fish in his diet. FCP has been measured with every change in diet and maintained at < 100 µg/g with the reintroduction of food, with the exception of fish and eggs which, despite a negative SPT, gave mild symptoms and raised FCP to 223 µg/g. Both eggs and fish were successfully reintroduced (FCP < 100 µg/g) after 7 and 11 months respectively from failed reintroduction. This innovative approach based on SPT and strict clinical and follow-up inflammatory markers can potentially ensure remission, reintroducing foods with objective parameters, and improving the patient’s quality of life.

Food allergy is characterized by an abnormal immune reaction that occurs reproducibly upon exposure to a specific food. This immune response can lead to a variety of symptoms, the prevalence of food allergies has increased in recent decades, most likely due to environmental factors that likely play a role in the expression of genetic susceptibility. Recent understanding of the immunopathogenesis of allergic diseases has suggested that these atopic diseases may be due to monogenic mutations associated with inborn errors of immunity (IEI). Aspects to be assessed in suspected IEI involve the onset of atopic disease within the initial months of life, the progression of the condition, and the response to conventional therapy. A prospective study was conducted on 385 patients admitted to the clinic with suspected immunodeficiency. Most children were referred for recurrent respiratory infections, but almost half had concurrent atopy (44%), atopy and autoimmunity (3%), autoimmunity (6%) and malignancy (1%). The results of the study underline the importance of the allergic phenotype and suggest that children with more severe allergic diseases should be screened for possible underlying inborn defects of immunity. If a congenital disorder of immunity is suspected, comprehensive immunologic testing is required, and genetic testing is essential to identify the specific genetic abnormalities. Molecular diagnosis provides a comprehensive understanding of congenital immune disorders, allowing tailored interventions and personalized surveillance strategies.

Desensitization (DSZ) or oral tolerance induction is increasingly used in children who do not outgrow their food allergies. Off-label omalizumab (OMZ) is used as adjuvant therapy for those with severe reactions, but there is little information on outcomes when OMZ is withdrawn. The long-term outcome in a group of children with severe milk or egg allergy who had undergone an OMZ-assisted DSZ procedure is here described. Clinical data from 21 children from the time they started DSZ until database closure were retrospectively collected, to assess the appearance of symptoms and response to clinical decisions under real-life conditions. Patients received OMZ before, during, and after the DSZ procedure itself and OMZ was subsequently discontinued. The scheduled treatment protocol had to be changed in almost all patients due to reactions or individual needs. Three of 21 patients had to prematurely abandon the procedure due to DSZ failure. The other 18 patients were able to tolerate the target dose of food, but nine of them developed symptoms when eating the food 1.5 to 6 months after stopping OMZ. These patients underwent a second course of OMZ-assisted DSZ, which was successful in six, but three had a second relapse 3 to 8 months after stopping OMZ and decided to quit. OMZ-assisted DSZ failed in almost a third of patients with severe allergy even after a second course of OMZ, almost 40% had a successful outcome with one course of OMZ, while almost a third required a second course. Relapses of symptoms occurred up to six months after stopping OMZ.