Measurement of circulating lactate is an essential diagnostic tool in pediatric medicine, playing a crucial role in assessing metabolic status and tissue oxygenation. Initially regarded as a byproduct of anaerobic metabolism, recent research has expanded our understanding of lactate’s roles across various physiological systems, from energy metabolism to immune modulation and neurological health. Elevated lactate levels are widely utilized to monitor critical conditions such as sepsis, trauma, and hypoxic–ischemic injury, offering valuable prognostic information in intensive care settings. Notably, lactate dynamics—particularly trends in serial measurements—are more effective than single readings for predicting clinical outcomes, especially in sepsis and trauma. Measurement of circulating lactate in different body fluids (blood, cerebrospinal fluid, and umbilical blood) provides critical insights into neonatal health and central nervous system involvement. However, challenges remain, including the need for non-invasive and rapid point-of-care testing, particularly in neonatal populations. Our aim was to review and synthesize the current literature on the role and particularities of measurement of circulating lactate in pediatric pathology. Emerging technologies, such as machine learning models and small molecule inhibitors, show promise in advancing lactate regulation and predicting hemodynamic instability. As the role of lactate in pediatric pathology continues to evolve, optimizing measurement protocols and exploring new therapeutic strategies will enhance early detection, intervention, and clinical outcomes for critically ill children.

In the case of SARS-CoV-2 infection, children seem to be less affected than adults, but data regarding epidemiologic characteristics and biochemical values are poor and essentially based on limited case series. The aim of our study is to highlight the predictive value of some biochemical markers at hospitalization, for the correct classification of the patient in the form of disease. Methods: We performed an analytical retrospective study on 82 pediatric patients diagnosed with COVID-19 in the emergency department, with moderate or severe form of disease, and treated in our tertiary hospital. We analyzed the epidemiologic characteristics, symptomatology and biochemical values and compare the data according to the form of disease. Results: The mean age at admission was 4.5 years (median 1 year) and the masculine/feminine ratio was 1.5. Comparing the data between the two groups of patients (42 severe/40 moderate), we observed that the severe form presented with a lower pH at admission (p = 0.02), hyperglycemia (p = 0.01), increased values of transaminases (p = 0.01 and 0.02) and hypoproteinemia (p = 0.01). Also, the severe form was statistically significantly associated with comorbidities, acute respiratory distress, rising of the inflammatory markers during hospitalization. Hyperlactatemia (Lactate > 1.5 mmol/L) was significantly associated with the age under one year (p < 0.001). Mortality rate was 9.75% and the median age at death was 3 months. Univariate logistic regression model shows that the presence of anemia increased the probability of death 88 times, comorbidities 23.3 times and ketoacidosis 16.4 times. Conclusions: Metabolic acidosis, hyperlactatemia, hyperglycemia, modified hepatic values and hypoproteinemia are biochemical markers associated with the severe form of disease in SARS-CoV-2 infection in children. Presence of anemia, comorbidities and ketoacidosis are important risk factors for death of pediatric patients with SARS-CoV-2 infection.

Background/Objectives: Hepatoblastoma, the most common pediatric primary liver cancer, is no longer regarded as a conventional malignancy but rather as a tumor emerging from disrupted hepatic developmental processes. Although improvements in chemotherapy, surgical techniques, and liver transplantation have markedly enhanced survival, therapeutic decision-making is still primarily guided by anatomical criteria and insufficiently reflects the biological heterogeneity that contributes to variable treatment response and disease recurrence. This narrative review integrates recent advances in molecular biology, tumor stemness, microenvironmental interactions, and translational research models in pediatric hepatoblastoma. We critically examine how developmental signaling pathways, cellular plasticity, and immune–vascular context shape tumor behavior and therapeutic vulnerability, with a focus on emerging targeted, anti-angiogenic, immune, and epigenetic strategies. Results: Hepatoblastoma is characterized by aberrant activation of key developmental pathways, including Wnt/β-catenin, Hippo–YAP, IGF, and mTOR signaling, which cooperate to sustain proliferation, stem-like phenotypes, and treatment resistance. Tumor heterogeneity is further reinforced by cancer stem cell populations and a predominantly immune-cold microenvironment. While innovative therapeutic approaches show promise, their clinical impact has been limited by biological complexity and insufficient integration into current treatment algorithms. Liquid biopsy biomarkers, advanced translational models, and multi-omics approaches offer new opportunities for biologically informed risk stratification and therapy adaptation. Conclusions: Future progress in pediatric hepatoblastoma will require a paradigm shift from purely clinicopathological management toward an integrated molecular and surgical framework. Incorporating biological stratification into therapeutic decision-making may enable personalized treatment, rational therapy de-escalation, and improved outcomes for high-risk disease. This review highlights the foundations and future directions for precision medicine in hepatoblastoma.

Background and Clinical Significance: In the clinical management of major pediatric traumatic injuries and other hypoxic conditions, lactate is widely recognized as a key indicator of tissue hypoxia and potential necrosis. However, its prognostic value remains uncertain. Several factors influence post-surgical outcomes, including the time between amputation and replantation, transport conditions, asepsis, the extent of tissue necrosis, hemorrhagic shock, coagulation disorders, and the heightened risk of contamination. Case presentation: We present this case to emphasize the utility of systemic lactate versus lactate levels in the replanted limb for monitoring post-transplantation outcomes in a pediatric patient with traumatic limb amputation. Significant fluctuations in lactate levels within the replanted limb were observed at the onset of unfavorable evolution, specifically on the seventh postoperative day, coinciding with the identification of Aspergillus spp. infection. This necessitated the use of synthetic saphenous vein grafts and Amphotericin B administration. Despite these interventions, disease progression ultimately led to limb amputation. Conclusions: Lactate levels in the replanted limb may serve as an early biomarker for assessing post-surgical evolution. However, further case reports are required to confirm its predictive value.

Background: Skeletal muscle ischemia–reperfusion (I/R) induces metabolic, inflammatory, and oxidative disturbances that may persist after restoration of blood flow. This study evaluated circulating lactate kinetics together with tissue lactate, inflammatory, cellular injury, and oxidative markers following experimental skeletal muscle I/R. Methods: Animals subjected to skeletal muscle I/R were compared with vascular I/R, bone fracture, sham, and control groups. Circulating lactate, PO₂, glucose, hematocrit, and calculated oxygen saturation were assessed immediately after ischemia, approximately 15 min after reperfusion, and approximately 2 h after reperfusion. Tissue and plasma lactate, lactate dehydrogenase (LDH), interleukin-6 (IL-6), malondialdehyde (MDA), and superoxide dismutase (SOD) were also evaluated. Results: In the skeletal muscle I/R group, circulating lactate decreased from 2.19 ± 0.67 mmol/L immediately after ischemia to 1.44 ± 0.84 mmol/L during early reperfusion, before rising to 3.33 ± 1.15 mmol/L at approximately 2 h (Friedman p < 0.001), resulting in a negative lactate clearance. This biphasic pattern contrasted with the progressive decline in lactate observed in the vascular I/R and bone fracture groups. Tissue lactate was markedly elevated (11.96 ± 1.27 mmol/L) and showed positive correlations with MDA (ρ = 0.802), IL-6 (ρ = 0.741), and LDH (ρ = 0.671), all p < 0.001. Conclusions: Skeletal muscle I/R was characterized by a late increase in circulating lactate together with elevated tissue lactate and biochemical evidence of inflammatory activation, cellular injury, and oxidative stress. Serial lactate assessment may provide complementary information on post-ischemic metabolic recovery, although further validation is required.

Background/Objectives: Gonadal germ cell tumors (GCTs) arise in the testis and ovary from primordial germ cells. Despite shared origins, they display distinct molecular and genetic features. Understanding these differences is essential for clarifying tumor pathogenesis and improving diagnostic and therapeutic strategies. This review aims to compare these features and to better define the biological differences between testicular and ovarian GCTs. Methods: We reviewed cytogenetic alterations, epigenetic modifications, and somatic mutations reported in testicular and ovarian GCTs. Comparative analysis was performed to identify common and site-specific mechanisms. Results: Isochromosome 12p is a hallmark of testicular GCTs, while ovarian GCTs show diverse chromosomal changes. DNA methylation and other epigenetic marks differ by tumor subtype and gonadal origin. Somatic mutations affect pathways regulating cell cycle, pluripotency, and differentiation, with overlapping and unique patterns between testicular and ovarian tumors. Collectively, these findings define a molecular framework that explains both shared biology and gonadal-specific divergence in GCTs. Conclusions: Understanding molecular similarities and differences across gonadal GCTs can refine classification, guide biomarker discovery, and inform translational research. This comparative perspective highlights core pathogenetic mechanisms and gonadal-specific features relevant to clinical and experimental oncology.