Allergies

Pediatric food allergies are an escalating public health concern, with nut allergies representing a primary cause of persistent hypersensitivity and anaphylaxis. New data suggests that pediatric populations with multiple nut allergies (MNA) may be at higher anaphylaxis risk than their counterparts with single nut allergies. Despite this, there is an absence of literature posing multiple nut allergies against singular nut allergy cases. The majority of the research in this topic is directed towards singular nut allergy, without any differentiation between children with one versus multiple sensitivities. Epidemiological evidence indicates that multiple nut allergies are associated with lifelong sensitization, high cross-reactivity potential and increased risk and severity of reactions. Compounding clinical risk factors reinforce the already high risk associated with MNA and indicate that these children require careful monitoring and individual management. Diagnostic tools, including component-resolved diagnostics and oral food challenges, enable differentiation between true multi-nut sensitization and cross-reactivity, guiding targeted interventions. Management strategies must therefore be multifaceted, encompassing selective allergen avoidance, emergency preparedness with epinephrine auto-injectors, asthma control, nutritional support, and psychosocial care. Recognizing MNA as a distinct, high-risk phenotype highlights the necessity of precision-based, biomarker-driven clinical approaches to optimize safety, reduce morbidity, and improve quality of life for affected pediatric populations.

Alpha-gal syndrome (AGS) is an emerging, relatively newly recognized allergic disorder with clinical manifestations that occur as a result of hypersensitivity reactions to oligosaccharide galactose-α-1,3-galactose (α-gal), a carbohydrate present in lower-mammalian meat, dairy products, and some biopharmaceutical products. These reactions are delayed with oral ingestion of the antigen but can be immediate with intravascular or other parenteral antigenic exposure. Over the past 15 years, many revelations have occurred in the realm of AGS. However, there is still a huge unmet need related to its pathophysiology, diagnostics, timely recognition, and management. This article is geared towards providing a review of AGS for healthcare providers (HCPs) from all realms of medicine. It is a universal challenge, with cases being recognized from various parts of the world. Hence, it is critically important for HCPs planet-wide to pay heed to the prompt recognition of AGS and educate their patients. This can prevent morbidity as well as potentially fatal complications like severe anaphylaxis. It is a narrative clinical review. The PubMed database was searched from 2009 to 2025. Alpha-gal syndrome and related topics were included in the search engine.

Background: Pruritus is burdensome across dermatoses. Beyond Staphylococcus, broader components of the cutaneous microbiome—bacteria, fungi, and viruses—and their products shape itch via barrier disruption, immune polarization, and direct neurosensory activation. Methods: We conducted a narrative review of human and translational studies. PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to 27 August 2025 using terms for itch, skin microbiome, bacteriotherapy, proteases, PAR, TRP channels, IL-31, Malassezia, and AHR ligands. English and Italian records were screened; randomized trials, systematic reviews, and mechanistic studies were prioritized; and unsupported single case reports were excluded. Results: Beyond Staphylococcus aureus, microbial drivers include secreted proteases activating PAR-2/4; pore-forming peptides and toxins engaging MRGPRs and sensitizing TRPV1/TRPA1; and metabolites, especially tryptophan-derived AHR ligands, that recalibrate barrier and neuro-immune circuits. Commensal taxa can restore epidermal lipids, tight junctions, and antimicrobial peptides. Early studies of topical live biotherapeutics—Roseomonas mucosa and Staphylococcus hominis A9—report reductions in disease severity and itch. Fungal communities, particularly Malassezia, contribute via lipases and bioactive metabolites with context-dependent effects. Across studies, heterogeneous itch metrics, small samples, and short follow-up limit certainty. Conclusions: The cutaneous microbiome actively contributes to itch and is targetable. Future studies should prioritize standardized itch endpoints, responder stratification, and robust safety for live biotherapeutics.