Tatiana Chisnoiu

Objectives: Intra-abdominal infections (IAIs) requiring surgical intervention represent a significant cause of morbidity in pediatric patients, often leading to prolonged hospitalization and increased antimicrobial exposure. This study aimed to characterize the distribution of pathogenic bacteria, antimicrobial resistance patterns, and clinical associations in pediatric intra-abdominal infections complicated by surgical site involvement. Methods: A retrospective observational study was conducted on children aged 0–16 years, who underwent surgery for intra-abdominal infections with microbiological confirmation. Peritoneal fluid, pus, and other intraoperative or postoperative specimens were analyzed using standard microbiological techniques. Infections were classified as monomicrobial or polymicrobial, and antimicrobial susceptibility was assessed phenotypically. Associations between bacterial pathogens, patient age, underlying diagnosis, surgical procedures, and antibiotic susceptibility patterns were analyzed. Results: 177 pediatric patients were included. Appendicitis was the most common diagnosis (53.53%), followed by intra-abdominal abscesses (32.94%). Gram-negative (GN) bacteria predominated (44.07%), with Escherichia coli being the most frequently isolated pathogen (83.33%). Double and triple GN and GP associations were identified in approximately 25% of cases, particularly in abscesses, complicated appendicitis, and surgical site infections. Our findings revealed that piperacillin–tazobactam and carbapenems were expected to be effective against almost all GN pathogens identified in surgical specimens of pediatric patients. Pathogen distribution and antimicrobial susceptibility varied significantly according to age group and clinical diagnosis. Conclusions: In pediatric patients, intra-abdominal infections requiring surgical management were mainly caused by Gram-negative bacteria and polymicrobial associations. Effective treatment relies on prompt surgical source control and empiric broad-spectrum antimicrobial therapy, followed by culture-guided de-escalation to support antimicrobial stewardship.

Neurodevelopment is a dynamic and multifactorial process, critical in the early stages of life, involving the formation of neural networks, the establishment of synapses, and the maturation of cognitive, social and emotional circuits. In this context, the gut microbiome emerges as an essential regulator of neurodevelopment, exerting influences through multiple biochemical and immunological mechanisms that define the “gut-brain axis”. The microbiota modulates neurodevelopment by regulating neurotransmitters (serotonin, dopamine, GABA), the production of microbial metabolites, including short-chain fatty acids, the modulation of inflammatory cytokines, and vagal signaling to the central nervous system. Recent evidence highlights the role of microbiota in modulating microglia, synaptogenesis, dendritic maturation, and neuronal plasticity, emphasizing how these processes are influenced by microbial activity rather than providing a comprehensive treatise on plasticity itself. Gut microbiota disturbances, or dysbiosis, have been associated with various neuropsychiatric and neurodevelopmental disorders, contributing to cognitive, behavioral, and emotional dysfunctions. This article summarizes, in a narrative manner, the main dysbiosis patterns identified in these disorders and the biological mechanisms by which the microbiome influences neuronal development and function, including immune–neuronal interactions, metabolomic modulation, and neuroendocrine signaling. Finally, emerging directions of intervention aimed at adjusting the microbial profile, such as dietary adjustment, the use of probiotics, prebiotics, symbiotics, and fecal microbiota transplantation, are presented with the aim of positively influencing neurodevelopment and preventing or ameliorating associated dysfunctions. This review emphasizes the need for longitudinal, rigorous, and controlled clinical trials to validate the efficacy of microbiota modulation strategies and to substantiate their integration into individualized pediatric management protocols.

Advanced chronic kidney disease (CKD) presents a complex hemostatic paradox, characterized by a simultaneous increase in bleeding and thromboembolic risks. This study aimed to evaluate and compare the safety and efficacy of apixaban versus acenocoumarol in a real-world cohort of patients across advanced CKD stages (pre-dialysis and hemodialysis). We conducted a retrospective observational study including 84 adults with CKD stages 4 and 5 (40.5% in stage 4; 59.5% in stage 5, of whom 86.0% were on chronic hemodialysis) receiving oral anticoagulation for at least 3 months. Patients were stratified by CKD stage and anticoagulant type (apixaban vs. acenocoumarol). Clinical outcomes included major and clinically relevant bleeding, anticoagulant overdose, and thromboembolic events. Bleeding events were more frequent in CKD stage 5 than in stage 4 (66.0% vs. 44.1%, p = 0.06), highlighting a pronounced hemorrhagic burden that increases with disease progression. Apixaban was associated with significantly fewer total bleeding events (44.4% vs. 66.7%, p = 0.04) and a lower rate of anticoagulant overdoses (5.6% vs. 18.8%, p = 0.04) compared with acenocoumarol. Thromboembolic event rates did not differ significantly between the two anticoagulant groups (13.9% vs. 16.7%, p = 0.72). Conventional risk scores (CHA₂DS₂-VASc and HAS-BLED) showed limited discriminatory capacity for actual clinical events in this advanced CKD population. In patients with advanced CKD, oral anticoagulation is associated with a high hemorrhagic burden that intensifies as renal function declines. Apixaban demonstrated a more favorable safety profile than acenocoumarol without a loss of thromboembolic protection. These findings suggest that stage-specific biological factors, rather than conventional risk models alone, should guide anticoagulation strategies in this population.

Background/Objectives: Vitamin D has an essential role in immune modulation and inflammatory control, particularly in respiratory infections. Despite widespread supplementation policies, hypovitaminosis D remains common in children and data linking vitamin D status to hospitalization outcomes in pediatric upper respiratory tract infections are limited, especially in Eastern Europe. Methods: We included 400 pediatric patients hospitalized between October 2020 and December 2024 for acute respiratory tract infections (ARTI), and we stratified them into a Normal Vitamin D group (NVD) with sufficient serum 25(OH)D concentrations and a Low Vitamin D group (LVD) with insufficient or deficient levels. Between-group comparisons for continuous variables were performed using non-parametric methods. Results: Children with insufficient or deficient 25(OH)D had a significantly longer duration of hospitalization compared with those with sufficient levels (mean 4.68 ± 2.59 days vs. 2.89 ± 1.81 days). The LVD group showed markedly lower serum vitamin D concentrations (mean 21.63 ± 5.56 ng/mL; median 22.29 ng/mL) compared with the NVD group (mean 47.60 ± 19.59 ng/mL; median 43.70 ng/mL). Markers of disease severity were consistently higher in vitamin D-deficient patients, including higher clinical scores (mean 3.77 ± 2.29 vs. 1.62 ± 1.89), elevated CRP levels (mean 3.50 ± 3.02 mg/L vs. 1.64 ± 1.59 mg/L), and increased O₂ therapy requirement (69.5% vs. 21.0%). Fever was more frequent in the LVD group (61.0% vs. 32.0%). An inverse correlation was observed between serum 25(OH)D concentrations and hospitalization duration, clinical score, and disease severity, with deficiency present across all age strata in the LVD group, while no cases of deficiency were observed in the NVD group. Conclusions: Low serum 25(OH)D concentrations are associated with increased disease severity and prolonged hospitalization.

Pediatric obesity has shown a marked upward trend over the past decade, with a particularly significant impact in certain regions, to the extent that it is increasingly regarded as a global epidemic. The factors involved in its development and progression are highly diverse and complex. From genetic predisposition to the influence of epigenetic mechanisms, environmental exposures, nutritional patterns, psychosomatic factors, and endocrinological status, current evidence highlights multiple interacting pathways contributing to excessive weight gain in children. Although numerous studies have explored specific mechanisms and interventions, there remains a need for a comprehensive synthesis that integrates recent pathophysiological insights with practical clinical implications. This narrative review was undertaken to fill this gap by summarizing and analyzing the current literature on the mechanisms underlying pediatric obesity, emphasizing novel findings and evidence-based approaches. In light of recent advances in the field, this narrative review provides a comprehensive overview of the latest pathophysiological principles associated with childhood obesity, with particular emphasis on clinically relevant aspects. The review focuses on potential strategies to mitigate the impact of modifiable risk factors and highlights current trends in clinical research. The included studies were selected to cover the most relevant evidence on genetic, epigenetic, environmental, and psychosomatic determinants of pediatric obesity, providing a synthesis that informs both research and clinical practice. Its aim is to enhance the dissemination of knowledge regarding the underlying mechanisms involved in the development of pediatric obesity. In parallel, the review addresses evidence-based therapeutic approaches that may contribute to limiting the increasing incidence of the condition and its associated complications. Expanding the scope of scientifically grounded interventions may reduce obesity-related morbidity and substantially improve long-term outcomes in pediatric populations.

Background/Objectives: Intra-abdominal infections requiring surgical intervention represent a significant cause of morbidity in pediatric patients, often leading to prolonged hospitalization and increased antimicrobial exposure. Pediatric-specific data regarding microbiological profiles and antimicrobial susceptibility are limited, and treatment strategies are frequently extrapolated from adult guidelines. This study aimed to characterize pathogen distribution, antimicrobial resistance patterns, and clinical associations in pediatric intra-abdominal infections complicated by surgical site involvement. Methods: A retrospective observational study was conducted including children aged 0–16 years who underwent surgery for intra-abdominal infections with microbiological confirmation. Peritoneal fluid, pus, and other intraoperative or postoperative specimens were analyzed using standard microbiological techniques. Infections were classified as monomicrobial or polymicrobial, and antimicrobial susceptibility was assessed phenotypically. Associations between pathogens, patient age, underlying diagnosis, surgical procedures, and antibiotic susceptibility patterns were analyzed. Results: A total of 177 pediatric patients were included, predominantly male adolescents. Appendicitis was the most common diagnosis, followed by intra-abdominal abscesses. Gram-negative bacteria predominated, with Escherichia coli being the most frequently isolated pathogen. Polymicrobial infections were identified in approximately one-quarter of cases, particularly in abscesses and complicated appendicitis. The highest susceptibility rates were observed for cephalosporins and combination regimens, whereas penicillins demonstrated limited efficacy. Pathogen distribution and antimicrobial susceptibility varied significantly according to age group and clinical diagnosis. Conclusions: In pediatric patients, intra-abdominal infections requiring surgical management are mainly caused by Gram-negative and polymicrobial pathogens. Effective treatment relies on prompt surgical source control and empiric broad-spectrum antimicrobial therapy, followed by culture-guided de-escalation to support antimicrobial stewardship. Pediatric-specific microbiological data are essential for optimizing therapeutic strategies and improving clinical outcomes.

This systematic review examines chronic kidney disease-associated pruritus (CKD-aP) as a complex clinical manifestation in patients undergoing hemodialysis. Traditionally considered a secondary symptom of end-stage renal disease, emerging evidence now positions CKD-aP as a multidimensional disorder with substantial pathogenic influence on patient outcomes. Using the PRISMA 2020 methodology, we critically evaluated 54 peer-reviewed studies published between 2020 and 2025. Our synthesis highlights a convergence of five mechanistic frameworks underpinning CKD-aP: elevated levels of uremic toxins originating from gut microbial dysbiosis, immune activation driven by IL-31 and other pro-inflammatory cytokines, heightened peripheral and central neural sensitization, dysregulation of endogenous opioid receptor pathways favoring μ-receptor activation, and xerosis-related epidermal barrier dysfunction. These mechanisms contribute to a systemic cycle of microinflammation, pruritogenic signaling, and neural hyperexcitability. We also identified and compared validated assessment tools—including the NRS, VAS, Skindex-10, and the UP-Dial scale—that facilitate standardized quantification of disease burden. While available treatments such as gabapentinoids and phototherapy offer partial relief, targeted therapies—including κ-opioid receptor agonists—represent a major advancement, although long-term effectiveness and accessibility remain under investigation. Growing scientific consensus establishes CKD-aP as a priority therapeutic target in hemodialysis care, underscoring the need for integrated, mechanism-based management strategies to improve quality of life and clinical outcomes. This work represents a narrative systematic review, integrating evidence from mechanistic, translational, and clinical studies to critically examine the biological pathways underlying CKD-associated pruritus.

Background/Objectives: Fetal growth restriction (FGR) describes the situation of a fetus that fails to reach its genetic growth potential. Postnatal catch-up growth represents a central adaptive process, yet its timing and magnitude vary widely and may influence one individual’s state of health and later metabolic risk. This study aimed to characterize longitudinal growth trajectories from birth to 10 years in children born at term, affected antenatally by growth restriction, with a particular focus on the influence of sex and FGR severity on catch-up growth. Methods: We conducted a retrospective observational study including 170 term-born children with documented FGR, admitted to a tertiary pediatric center between 2019 and 2023. Anthropometric data (weight, length/height, BMI) at birth, 1, 2, 5, and 10 years were converted to World Health Organization (WHO) age- and sex-adjusted z-scores. Catch-up growth was defined as an increase of >0.67 SD. Participants were stratified by sex and FGR severity (moderate: 10th–3rd percentile; severe: p < 0.01). By 5 and 10 years, growth trajectories converged between severity groups, with no differences in BMI at any age. Sex influenced absolute anthropometric values but not the probability of achieving catch-up growth. Conclusions: Among term-born FGR infants, severity—but not sex—shapes early postnatal growth. Despite early deficits, most children achieved substantial catch-up, underscoring the need for careful monitoring to support healthy, proportionate growth and mitigate subsequent metabolic risk.

Vitamin D deficiency (VDD) is highly prevalent in pediatric patients, and it has been implicated in the pathogenesis and clinical severity of acute respiratory infections (ARI). To evaluate the prevalence of VDD and its association with ARI disease severity and clinical outcomes in hospitalized pediatric patients. A 4-year prospective case-control study, conducted between 2021 and 2024, in two Romanian pediatric hospitals, included 400 inpatients, aged 0-18 years, admitted for ARI. Patients were stratified into cases with a low level of vitamin D (n=200) and controls with a normal vitamin D (n=200). Clinical severity of ARI, inflammatory biomarkers, presence of fever, need for supplemental oxygen, and length of hospital stay were recorded and analyzed in both cases and controls. Low serum vitamin D levels were significantly associated with severe ARI (26.5% vs. 5.5%), fever at admission (61.0% vs. 32.0%), and increased requirement for oxygen therapy (69.5% vs. 21.0%). Cases also exhibited higher C-reactive protein levels (3.50 vs. 1.64mg/L), higher clinical severity scores (3.77 vs. 1.62), and longer hospital length of stay (4.68 vs. 2.89 days). Vitamin D deficiency was strongly associated with increased disease severity and adverse clinical outcomes in pediatric inpatients with ARI.

Background: Anticoagulation in patients with advanced chronic kidney disease (CKD) and atrial fibrillation (AF) remains challenging due to the concurrent risks of thrombosis and bleeding driven by endothelial dysfunction, uremic inflammation, and impaired hemostasis. Evidence comparing vitamin K antagonists (VKAs) with direct oral anticoagulants (NOACs) in this high-risk population, particularly in dialysis, is still limited. Methods: We conducted a single-center, retrospective observational study including 93 patients with CKD stages 4–5 and AF treated between January 2021 and February 2025. Fifty patients received apixaban (2.5–5 mg twice daily), and forty-three received acenocoumarol with a target INR of 2.0–3.0. Thirty-eight patients (41%) were on maintenance hemodialysis. Demographics, comorbidities, and risk scores (CHA₂DS₂-VASc and HAS-BLED) were analyzed. Bleeding events were classified per ISTH criteria. Statistical comparisons used t-tests and χ² tests, with p < 0.05 considered significant. Results: The mean age was 67.8 ± 9.1 years, and 51.6% were male. Major bleeding occurred in 9.7%, minor in 15.8%, and overdose-related bleeding in 10.0% of patients. The overall bleeding rate was significantly lower in the apixaban group (16.0%) than in the acenocoumarol group (53.5%; p = 0.01). No thromboembolic events were observed in either group. Dialysis patients had higher bleeding rates overall (13.2% vs. 7.4%), mainly among those on VKAs. The HAS-BLED score moderately correlated with bleeding incidence (r = 0.43, p < 0.01). Conclusions: Apixaban provided comparable thromboembolic protection with significantly fewer bleeding events than acenocoumarol, including in patients on dialysis. These findings support apixaban as a safer and more practical anticoagulant option in advanced CKD, consistent with its limited renal clearance and reduced influence on the inflammation–coagulation axis. Further multicenter prospective studies are warranted to validate these real-world results.