Considering the fact that even today in the 21st century, diet is the basis of the treatment in phenylketonuria (PKU), this review aims to provide a comprehensive analysis of existing current data from the last 15 years on dietary treatment and its impact on nutritional status and quality of life to identify gaps in knowledge and offer insights into future directions for optimizing nutritional care in PKU. Dietary treatment for PKU has evolved over the years, and in order to optimize and standardize the care, European PKU experts developed guidelines useful for both professionals and patients and their parents. The current literature underscores the essential role of diet in both managing PKU and preventing obesity, but malnutrition in these children is a complex issue that necessitates a multifaceted approach. The literature emphasizes the crucial role of dietary adherence in managing PKU. Advancements in therapy offer the potential to reduce the challenges associated with dietary phenylalanine (Phe) restrictions. Maintaining adequate levels of essential nutrients in children with PKU and monitoring trace element intake and micronutrient levels are vital for preventing deficiencies and ensuring optimal growth and development. Overall, the literature highlights the importance of personalized treatment strategies. Conclusions. Effective management of PKU necessitates strict dietary control and personalized treatment to maintain optimal blood Phe levels. Continuous monito-ring, nutritional education, and adherence to dietary recommendations are critical components in achieving the best patient outcomes. Future studies should also explore innovative therapeutic modalities, including gene therapy and novel dietary strategies that consider the gut–brain axis, to enhance the quality of life and mental health for individuals with PKU.

Pesticide poisoning in pediatric patients is still an important reason for presenting to the emergency department in Romania. In this context, the present study aims to raise awareness of the toxicological impact of pesticides on human health in pediatrics. For this purpose, the demographic characteristics, clinical assessment, and outcome of pediatric patients with acute pesticide poisoning admitted to the toxicology department of “Saint Mary” Emergency Children’s Hospital from Iasi, were analyzed. This retrospective study focused on the clinical and laboratory data of patients aged under 18 years diagnosed with acute pesticide poisoning between 2010–2020. The statistical analysis was performed using the Statistica 10 package. A total of 49 patients presented with manifestations of acute pesticide poisoning, and the most common pesticide involved was diazinon. The most frequent exposure route was accidentally ingesting pesticide products (95%). The primary clinical manifestations were toxic encephalopathy, coma, depressive disorder, gastric disorders, and respiratory failure. Changes in the glycemic status, liver, and kidney damage were also present. Treatment included decontamination, administration of antidote, supportive care, and recommendations to be closely monitored to avoid a new incident. These results highlight the toxic potential of pesticides on human health and their biological consequences, which require an increase in consciousness of the precautions imposed on their use, especially when children are nearby.

Central precocious puberty (CPP) may be influenced by gut microbiota through changes in short-chain fatty acids (SCFAs), β-glucuronidase activity, and enterohepatic estrogen recycling. This narrative review integrates current evidence from human and animal studies exploring microbial contributions to pubertal timing. Across multiple cohorts, CPP is associated with loss of SCFA-producing commensals, such as Bacteroides, and increased abundance of taxa like Alistipes, Ruminococcus, and Lachnoclostridium. These microbial shifts are linked to altered SCFA profiles, diminished anti-inflammatory and neuroendocrine modulation, and enhanced reabsorption of estrogens via microbial β-glucuronidase activity. Experimental models support a causal connection: gut dysbiosis accelerates pubertal onset, whereas microbiota-targeted interventions can restore hormonal balance and delay activation of the HPG axis. While some overlap with obesity-associated microbiota exists, the endocrine-specific microbial changes observed in CPP suggest partially distinct mechanisms. Overall, the gut microbiota emerges as both a modulator and potential biomarker of early pubertal onset. Its integration into pediatric endocrine frameworks could improve early risk assessment and guide future interventions, though further validation through standardized, longitudinal, and diverse population studies is still required.

Obesity, the current pandemic, is associated with alarming rises among children and adolescents, and the forecasts for the near future are worrying. The present paper aims to draw attention to the short-term effects of the excess adipose tissue in the presence of a viral infection, which can be life-threatening for pediatric patients, given that the course of viral infections is often severe, if not critical. The COVID-19 pandemic has been the basis of these statements, which opened the door to the study of the repercussions of obesity in the presence of a viral infection. Since 2003, with the discovery of SARS-CoV-1, interest in the study of coronaviruses has steadily increased, with a peak during the pandemic. Thus, obesity has been identified as an independent risk factor for COVID-19 infection and is correlated with a heightened risk of severe outcomes in pediatric patients. We sought to determine the main mechanisms through which obesity is responsible for the unfavorable evolution in the presence of a viral infection, with emphasis on the disease caused by SARS-CoV-2, in the hope that future studies will further elucidate this aspect, enabling prompt and effective intervention in obese patients with viral infections, whose clinical progression is likely to be favorable.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most common chronic liver disorder in the pediatric population, closely paralleling the global rise in childhood obesity. Increasing evidence highlights the gut–liver axis as a key contributor to MASLD pathogenesis, with gut microbiota dysbiosis influencing hepatic steatosis through multiple interconnected mechanisms, including increased intestinal permeability, endotoxemia, altered bile acid metabolism, and modulation of host energy homeostasis. In children, the characterization of microbiota signatures associated with MASLD remains challenging due to heterogeneity across studies, age-related microbial dynamics, and methodological variability. This review synthesizes current evidence regarding the role of the gut microbiota in pediatric MASLD, focusing on pathogenetic pathways, reported microbial patterns, and microbiota-targeted therapeutic strategies, while incorporating relevant mechanistic evidence from adult studies where pediatric data remain limited. Although several taxa have been repeatedly associated with pediatric MASLD, findings are not yet sufficiently consistent for clinical application. Interventions such as probiotics, prebiotics, and dietary modulation show promising but still preliminary results, with limited high-quality pediatric trials available. A deeper mechanistic understanding and standardized study designs are needed to clarify causality and to support microbiota-based precision approaches in pediatric MASLD management.