Acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, although presenting less severe forms of the disease in children, seems to play a role in the development of other conditions, including type 1 diabetes mellitus (T1DM). After the beginning of the pandemic, an increase in the number of T1DM pediatric patients was observed in several countries, thus leading to many questions about the complex relationship between SARS-CoV-2 infection and T1DM. Our study aimed to highlight possible correlations between SARS-CoV-2 serology and T1DM onset. Therefore, we performed an observational retrospective cohort study that included 158 children diagnosed with T1DM in the period April 2021–April 2022. The presence or absence of SARS-CoV-2 and T1DM-specific antibodies and other laboratory findings were assessed. In the group of patients with positive SARS-CoV-2 serology, a higher percentage had detectable IA-2A antibodies, more children were positive for all three islet autoantibodies determined (GADA, ICA, and IA-2A), and a higher mean HbA1c value was found. No difference existed between the two groups regarding DKA presence and severity. A lower C-peptide level was found in the patients presenting diabetic ketoacidosis (DKA) at T1DM onset. When compared to a group of patients diagnosed before the pandemic, an increased incidence of both DKA and severe DKA, as well as a higher age at diagnosis and higher levels of HbA1c were present in our study group. These findings have important implications for the ongoing monitoring and management of children with T1DM after the COVID-19 pandemic and highlight the need for further research to better understand the complex relationship between SARS-CoV-2 infection and T1DM.

Representing a pathology frequently encountered in the clinical pediatric practice, non-IgE-mediated food allergy is characterized by delayed immune-mediated adverse reactions to foods. Various genetic and environmental factors play complex and incompletely elucidated roles in the development of this type of allergic pathology. In the present research, we aimed to assess the associations of the TSLP gene single-nucleotide polymorphisms (SNPs) rs3806933 and rs10062929 with the risk of non-IgE-mediated food allergy, as well as with other characteristics of these patients. The study included 87 Romanian patients with non-IgE-mediated food allergy and 115 healthy controls. The two SNPs were genotyped using Real-Time PCR TaqMan Allelic Discrimination Assays. No associations were identified between rs3806933 or rs10062929 and the risk of non-IgE-mediated food allergy. The frequency of the minor allele C of rs3806933 was lower in children with atopic dermatitis (35.4% vs. 46.8%), a positive family history of atopic disease (39.0% vs. 47.8%), and elevated levels of total IgE (39.2% vs. 45.7%), but not statistically significant.

Non-IgE-mediated food allergy is characterized by delayed gastrointestinal manifestations and the absence of reliable non-invasive biomarkers. Increasing evidence suggests that gut microbiota may contribute to this disease pathogenesis. The aim of this study was to characterize the gut microbiome composition in thirty pediatric patients diagnosed with non-IgE-mediated food allergy, in comparison to fifteen healthy controls children, and to investigate its association with fecal calprotectin, eosinophil-derived neurotoxin (EDN) and IgA. Gut microbiota profiling was performed by 16S rRNA gene sequencing targeting the V3–V4 region. Compared with healthy controls, higher mean relative abundances of Bacteroides, Faecalibacterium, Alistipes, Parabacteroides, and Sutterella were observed in patients. Conversely, healthy children showed higher mean relative abundances of Pseudobutyrivibrio, Roseburia, Bifidobacterium, Collinsella, Clostridium, Eubacterium, Streptococcus, and Barnesiella. Several genera (Escherichia–Shigella, Agathobacter, and Enterococcus/Streptococcus) were detected only in the allergy cohort. Shannon diversity was higher in patients compared to controls and in the subgroups of patients with elevated fecal calprotectin (p = 0.028), previous antibiotic exposure (p = 0.015), and atopic dermatitis (p = 0.021). Stratification according to inflammatory biomarkers identified a distinct inflammatory microbiome endotype characterized by increased fecal calprotectin and EDN together with enrichment of Veillonellaceae and depletion of Bifidobacteriaceae and Lachnospiraceae. Correlation analyses further revealed positive associations between Veillonella abundance and both fecal calprotectin and EDN. These findings suggest that pediatric non-IgE-mediated food allergy is characterized by distinct microbiome–inflammation relationships rather than a single dysbiotic signature.