This paper delineates several aspects of cystic fibrosis-related diabetes (CFRD)—a common complication of cystic fibrosis (CF). CFRD exhibits a predilection for older individuals with CF, yet it also extends its influence on children and adolescents. Scientific insights postulate a potential link between CFRD and the aberrant mucus production within the pancreas, thereby culminating in pancreatic insufficiency. This, in turn, perturbs the synthesis of insulin, a pivotal endocrine hormone responsible for the regulation of glycemic levels. Standardized protocols advocate for the systematic screening of CFRD among all individuals with CF, commencing at the age of 10 years using the oral glucose tolerance test (OGTT). Therapeutic modalities encompass insulin therapy, dietary adjustments, and the vigilant monitoring of glycemic parameters. The overarching objective is to maintain blood glucose levels within a targeted range to mitigate the advent of diabetic complications. Untreated or sub-optimally managed CFRD can precipitate a spectrum of deleterious health ramifications, encompassing cardiovascular afflictions, neuropathy, renal dysfunction, and ocular complications.

Introduction: Cystic fibrosis (CF) is a genetic condition affecting several organs and systems, including the pancreas, colon, respiratory system, and reproductive system. The detection of a growing number of CFTR variants and genotypes has contributed to an increase in the CF population which, in turn, has had an impact on the overall statistics regarding the prognosis and outcome of the condition. Given the increase in life expectancy, it is critical to better predict outcomes and prognosticate in CF. Thus, each person’s choice to aggressively treat specific disease components can be more appropriate and tailored, further increasing survival. The objective of our narrative review is to summarize the most recent information concerning the value and significance of clinical parameters in predicting outcomes, such as gender, diabetes, liver and pancreatic status, lung function, radiography, bacteriology, and blood and sputum biomarkers of inflammation and disease, and how variations in these parameters affect prognosis from the prenatal stage to maturity. Materials and methods: A methodological search of the available data was performed with regard to prognostic factors in the evolution of CF in children and young adults. We evaluated articles from the PubMed academic search engine using the following search terms: prognostic factors AND children AND cystic fibrosis OR mucoviscidosis. Results: We found that it is crucial to customize CF patients’ care based on their unique clinical and biological parameters, genetics, and related comorbidities. Conclusions: The predictive significance of more dynamic clinical condition markers provides more realistic future objectives to center treatment and targets for each patient. Over the past ten years, improvements in care, diagnostics, and treatment have impacted the prognosis for CF. Although genotyping offers a way to categorize CF to direct research and treatment, it is crucial to understand that a variety of other factors, such as epigenetics, genetic modifiers, environmental factors, and socioeconomic status, can affect CF outcomes. The long-term management of this complicated multisystem condition has been made easier for patients, their families, and physicians by earlier and more accurate identification techniques, evidence-based research, and centralized expert multidisciplinary care.

Human milk is widely recognised as the optimal source of nutrition for newborns and infants, providing not only an ideal macronutrient composition but also a range of bioactive components that exert important non-nutritional functions, and as such it represents the first functional food consumed in early life. Among these bioactive components, the human milk oligosaccharides (HMOs)—a structurally diverse family of glycans present in human milk at concentrations 100- to 1000-fold higher than in the milk of other mammalian species—have emerged as multifunctional contributors to the establishment of the intestinal microbiome, immune development, anti-infective defence, and epithelial barrier integrity during a developmental window characterised by immune immaturity. The aim of the present narrative review is to synthesise current evidence on the anti-infective properties of HMOs in infancy and to integrate, within a single framework, five interconnected mechanisms through which HMOs protect the infant against infection: glycan-mimicry-based competitive inhibition of pathogen adhesion, direct antimicrobial and antibiofilm activity, selective prebiotic shaping of the gut microbiome, modulation of innate and adaptive immune responses, and reinforcement of mucosal barrier integrity in the gut and lungs. Breastfeeding constitutes a natural strategy for anti-infective protection in early childhood, while infant formulas supplemented with biotechnologically produced HMOs that are structurally identical to those in human milk provide measurable benefits for non-breastfed infants.

Asthma prevalence in school-age children varies widely by geography, from below 5% in some regions to above 20% in others, averaging 10–12% across industrialized countries, but genetic factors account for less than 40% of disease liability. Gut microbiota is increasingly recognized as a critical intermediary between early-life dietary exposure and immunological trajectories that determine asthma susceptibility. Through the production of short-chain fatty acids (SCFAs), particularly butyrate, propionate, and acetate, commensal bacteria regulate dendritic cell function, promote T-regulatory (Treg) cell differentiation, and attenuate Th2-polarized airway inflammation via the gut–lung axis. Epidemiological cohorts including CHILD, WHEALS, and PASTURE associate early-life dysbiosis and reduced Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii with increased asthma risk, while dietary patterns rich in fermentable fibre, omega-3 polyunsaturated fatty acids, and diverse plant-based foods are associated with preserved microbial diversity and, in preclinical models, attenuated type-2 inflammatory signalling. This narrative review synthesizes mechanistic and epidemiological evidence on how nutritional exposures shape gut microbiota composition and influences asthma onset and severity in paediatric populations, including the distinct obesity-related asthma phenotype. Critical gaps, insufficient dietary intervention trials with microbiome endpoints, methodological heterogeneity across cohorts, and the paucity of data from non-Western populations are discussed, with implications for preventive nutritional counselling in paediatric allergology practice.

Background/Objectives: Maternal nutrition is an important exogenous factor which, together with other factors, may play a fundamental role in ensuring the well-being of the pregnant woman and in the development of the offspring, with long-term effects on health. Therefore, this narrative review aims to synthesize current evidence on how maternal dietary patterns and nutrient intake during pregnancy affect maternal well-being, pregnancy outcomes, fetal growth, and the short- and long-term health of the child, while addressing research gaps, and implications for antenatal nutrition guidance. Literature Search Strategy and Study Selection: A comprehensive literature search was performed using the electronic databases PubMed and Google Scholar. The selection and curation of articles were guided by the central research question: “How does maternal diet during pregnancy influence maternal health and offspring outcomes?” Results: The analysis of the literature reveals that the overall maternal dietary pattern is more important than the isolated intake of nutrients in determining the course of pregnancy and the long-term health of the offspring. Conclusions: The present review pointed out that maternal nutrition is not merely energy support for pregnancy, but a factor in fetal programming with a long-term impact on the child, in line with the Developmental Origins of Health and Disease (DOHaD) concept, and may act as an epigenetic and metabolic influence with potential transgenerational effects. Optimizing the diet in the periconceptional period and during pregnancy represents an accessible and effective form of preventive intervention, but it requires personalized recommendations and structured nutritional education begun as early as the preconception period.

Globally, chronic kidney disease (CKD) affects over 800 million individuals and is characterized by significant genetic complexity. More than 600 genes are associated with hereditary kidney disease, which may manifest as isolated kidney issues or as part of a syndrome that also includes extrarenal manifestations. The aim of this study was to identify genetic variants in a group of ten patients who presented with clinical signs suggestive of genetic syndromes associated with CKD, or who were asymptomatic but had a positive family history of CKD. Extensive genetic testing (targeted gene panels and whole-exome sequencing—WES) identified a mutation in the PKD1 gene in 3 out of 10 cases. In one patient, a known mutation in the PKD2 gene was identified. Another four patients were diagnosed with Alport syndrome: three of these presented with de novo missense mutations in the COL4A5 gene, and one patient had a mutation in the COL4A3 gene. One patient was diagnosed with MODY5, caused by a known mutation in the HNF1B gene, and one patient was diagnosed with Bartter syndrome type 1, resulting from a known mutation in the SLC12A1 gene. We present genotype–phenotype correlations, highlighting the particularities of each patient within their family context. Our findings emphasize the importance of genotype–phenotype correlations in refining diagnosis, personalizing therapeutic management, and providing essential genetic counseling for at-risk relatives.