Background/Objectives: An increasing number of studies have reported liver involvement in both children and adults with celiac disease (CD). This often manifests as isolated hypertransaminasemia or hepatic steatosis (HS). The aim of this study was to define the prevalence of hypertransaminasemia and HS in a pediatric population with CD before starting a gluten-free diet (GFD) and to analyze how the introduction of a GFD could modify this condition. We also conducted a state-of-the-art literature review of the association between hypertransaminasemia, metabolic dysfunction-associated steatotic liver disease (MASLD) and CD. Methods: We retrospectively reviewed the clinical charts of pediatric CD patients diagnosed in three different pediatric units of Sicily, analyzing clinical, laboratory, ultrasound, and histology data before and 12 months after the introduction of a GFD. Results: A total of 160 patients (65.0% females, median age 6.4 (0.8–13.2) years) were included; hypertransaminasemia and HS prevalences at diagnosis were 8.1% and 6.1%, respectively. Subjects with hypertransaminasemia were younger (p = 0.01) than those without and had higher frequencies of HS (p = 0.034) and anti-tissue transglutaminase (tTg) immunoglobulin (Ig)G positivity (p = 0.046). Subjects with HS were younger (p = 0.0001) and had a higher frequency of hypertransaminasemia (p = 0.029) compared to non-steatotic ones. After 12 months of a GFD, hypertransaminasemia and HS persisted in 53.8% and 50.0% of patients, respectively. Conclusions: The prevalences of hypertransaminasemia and HS in Sicilian pediatric CD patients seem to be lower than those reported in other geographical areas. A GFD can reverse the trend of liver involvement, although periods of longer than 12 months may be necessary. However, a GFD has been associated with an increased prevalence of HS, and so regular follow-up involving a nutritionist should be recommended to guide physicians in patient management.

Nutritional deficiencies and metabolic alterations are common complications following bariatric surgery, requiring often lifelong monitoring and supplementation. The aim of this retrospective study is to investigate whether a structured follow-up can mitigate micronutrient deficiencies and metabolic changes. This study was conducted at Cannizaro Hospital (Catania, Italy), a national referral center accredited by SICOB (Italian Society for Bariatric and Metabolic Surgery). The cohort included patients who underwent bariatric surgery who completed one year follow-up between October 2022 and May 2024. Medical records such as anthropometric, clinical and laboratory data were collected for each patient at five different timepoints: baseline, 1-, 3-, 6- and 12-months post-surgery. Serum levels of iron, hemoglobin, vitamin D, folate, vitamin B12 and uric acid were analyzed to assess nutritional and metabolic status over time. One-year follow-up adherence of the patient cohort was equal to 97.5%. A significant increase in serum iron, vitamin D and folate levels was observed one year after surgery. Hemoglobin and vitamin B12 levels remained stable over time. Uric acid showed a significant rise at 1 month after surgery, followed by a progressive reduction by 12 months. This study highlights the importance of a structured follow-up program after bariatric surgery, contributing to the prevention of common postoperative complications.

Background/Objectives: Celiac disease (CeD) is a complex autoimmune enteropathy triggered by gluten intake in genetically predisposed individuals. While the bacterial microbiome has been extensively studied in CeD, the role of the gut virome and mycobiome is less well defined. Emerging evidence suggests that viruses and fungi may influence mucosal immunity, intestinal permeability and gluten tolerance, acting as potential environmental cofactors in the onset of this disease. Methods: A narrative review of the literature was conducted to summarize current knowledge of the composition, development and function of the gut virome and mycobiome and to explore their potential involvement in CeD pathogenesis. Results: The gut virome shows high interindividual variability and dynamic maturation early in life. Multiple studies have associated early enterovirus or parechovirus infections with an increased risk of celiac autoimmunity, supporting a virus–gluten “double hit” model. Viral dysbiosis in CeD has been reported to include an enrichment of human polyomavirus 2 (JC polyomavirus) and of specific enterobacterial phages. The mycobiome, although less abundant, also displays disease-associated alterations: cross-sectional mycobiome studies have reported higher relative abundance of Saccharomyces, Candida, and Tricholomataceae and lower relative abundance of Pichia and Pneumocystis taxa in children with CeD. Conclusions: Current evidence, although preliminary, supports associations between selected viral exposures and CeD-related immune alterations, whereas current phageome and mycobiome findings mainly describe cross-sectional compositional differences. These data do not establish temporal direction or causality, and further longitudinal and mechanistic investigations are required before preventive or therapeutic implications can be considered.