Richard Adrian Vergara Trujillo

Imaging biomarkers have progressively transformed modern radiology by providing quantitative, functional, and molecular information capable of improving early disease detection, diagnostic precision, therapeutic monitoring, and clinical decision-making in systemic diseases. The present review aimed to analyze the current role of imaging biomarkers in oncology and internal medicine, emphasizing their contribution to precision medicine and multidisciplinary healthcare management. A structured documentary review was conducted using peer-reviewed scientific literature indexed in internationally recognized databases, including PubMed, Scopus, ScienceDirect, and SpringerLink. The analyzed evidence focused on advanced imaging modalities such as computed tomography, magnetic resonance imaging, positron emission tomography, hybrid imaging systems, radiomics, and artificial intelligence-assisted imaging analysis. The reviewed studies demonstrated that imaging biomarkers possess broad applicability in oncology, neurological disorders, cardiovascular diseases, inflammatory conditions, chronic hepatic disease, pulmonary pathology, and metabolic disorders. Functional and molecular imaging techniques showed particular relevance for evaluating metabolism, tissue perfusion, angiogenesis, fibrosis, inflammation, cellular density, and tumor heterogeneity. Radiomics and artificial intelligence were identified as emerging technologies capable of improving predictive analysis, treatment response assessment, and individualized therapeutic planning.

Hypoxia is a complex multisystemic condition characterized by insufficient oxygen availability at the tissue level, producing progressive dysfunction involving the pulmonary, cardiovascular, and neurological systems. Although traditionally associated with respiratory failure, contemporary evidence demonstrates that hypoxia activates interconnected physiological, inflammatory, vascular, metabolic, and neurological pathways capable of generating widespread systemic injury. The objective of this review was to analyze the principal mechanisms through which hypoxia contributes to pulmonary, cardiovascular, and neurological dysfunction, emphasizing the integrated interactions between these systems and their clinical implications in modern medicine. This review was developed using a structured narrative methodology based on scientific literature indexed in international databases including PubMed, Scopus, Google Scholar, Europe PMC, Elsevier, and SpringerLink. The investigation integrated evidence from pulmonology, cardiology, neurology, critical care medicine, and vascular physiology in order to evaluate the systemic consequences of acute, chronic, and intermittent hypoxia. Special attention was given to molecular mechanisms such as hypoxia-inducible factor activation, oxidative stress, endothelial dysfunction, autonomic imbalance, mitochondrial injury, inflammatory cytokine release, and vascular remodeling. The findings demonstrate that pulmonary dysfunction initiates hypoxemia through mechanisms including ventilation-perfusion mismatch, diffusion impairment, hypoventilation, and shunt physiology. Cardiovascular adaptation initially attempts to preserve oxygen delivery through sympathetic activation and pulmonary vasoconstriction; however, prolonged hypoxic exposure contributes to pulmonary hypertension, right ventricular overload, endothelial dysfunction, arrhythmogenic instability, and impaired systemic perfusion. Neurological consequences include neuroinflammation, excitotoxicity, cognitive impairment, cerebral autoregulatory dysfunction, and hypoxic-ischemic injury due to the high metabolic vulnerability of neuronal tissue. Intermittent hypoxia, particularly in obstructive sleep apnea, was associated with substantial cardiovascular and neurocognitive consequences related to oxidative stress and autonomic dysregulation.

Cardiorenal syndrome (CRS) represents a complex bidirectional interaction between the cardiovascular and renal systems in which dysfunction of one organ may induce or worsen dysfunction of the other. The increasing global prevalence of heart failure, chronic kidney disease, hypertension, obesity, and diabetes mellitus has significantly contributed to the growing clinical and epidemiological burden of CRS. This review aimed to analyze the principal pathophysiological mechanisms, diagnostic approaches, and contemporary therapeutic strategies associated with cardiorenal syndrome through an evidence-based analysis of current scientific literature. The study was developed as a narrative and analytical review using scientific evidence obtained from internationally recognized databases, including PubMed, Scopus, Web of Science, and high-impact journals in nephrology, cardiology, and internal medicine. The analysis focused on hemodynamic alterations, neurohormonal activation, venous congestion, inflammatory pathways, endothelial dysfunction, oxidative stress, diagnostic biomarkers, pharmacological therapies, and multidisciplinary management approaches. The reviewed evidence demonstrated that CRS is a multifactorial systemic condition involving complex interactions between cardiac and renal dysfunction. Venous congestion, activation of the renin–angiotensin–aldosterone system, sympathetic nervous system stimulation, chronic inflammation, and endothelial injury were identified as major contributors to disease progression. Biomarkers such as NT-proBNP, cystatin C, NGAL, and KIM-1 showed important diagnostic and prognostic value, although integrated clinical evaluation remains essential. Contemporary therapeutic strategies, particularly sodium-glucose cotransporter-2 inhibitors, demonstrated substantial cardiovascular and renal protective effects. Multidisciplinary care models were also associated with improved patient outcomes and optimization of long-term management. In conclusion, cardiorenal syndrome should be understood as a highly dynamic and multisystemic condition requiring integrated cardiovascular and renal assessment. Early diagnosis, evidence-based therapy, preventive medicine, and multidisciplinary collaboration remain fundamental for improving prognosis and reducing the global burden associated with CRS.

Neuroinflammation has emerged as a fundamental pathophysiological mechanism linking neurological disorders with systemic inflammatory diseases. Increasing evidence demonstrates that chronic immune activation contributes significantly to neuronal dysfunction, cognitive impairment, neurodegeneration, and multisystem clinical manifestations through complex interactions involving microglial activation, cytokine signaling, oxidative stress, endothelial dysfunction, mitochondrial injury, and blood–brain barrier disruption. The objective of this review was to analyze the role of neuroinflammation as an interdisciplinary bridge between neurology, immunology, and internal medicine while evaluating its clinical, molecular, and translational implications. A narrative review methodology based on the Scientific Method and Process-Based Methodology was employed. Scientific literature indexed in international databases including PubMed, Scopus, ScienceDirect, SpringerLink, and Frontiers was analyzed. The review prioritized peer-reviewed studies published primarily between 2020 and 2025 addressing neuroimmune communication, neurodegeneration, metabolic disorders, autoimmune diseases, infectious syndromes, and gut–brain axis interactions. The analyzed evidence demonstrated that neuroinflammatory mechanisms are strongly associated with metabolic diseases such as obesity and type 2 diabetes mellitus, autoimmune disorders including systemic lupus erythematosus, infectious conditions such as sepsis and long COVID syndrome, and neurodegenerative diseases. Persistent inflammatory activation was consistently related to cognitive impairment, chronic fatigue, depression, autonomic dysfunction, chronic pain, and progressive neuronal injury. Furthermore, the gut–brain axis emerged as a major regulator of neuroimmune communication, reinforcing the systemic nature of neuroinflammation.

Emergency medicine requires rapid and accurate clinical decision-making in environments characterized by uncertainty, cognitive overload, overcrowding, and limited time availability. The present review analyzes the principal factors influencing decision-making under time pressure in emergency departments, with emphasis on neurological and internal medicine emergencies. The study explores the relationship between diagnostic reasoning, cognitive biases, treatment delay, risk stratification, organizational stressors, and patient outcomes. A narrative review methodology based on the Scientific Method and evidence-based analysis was employed. Scientific literature was obtained from internationally recognized databases including PubMed, Scopus, NCBI, and peer-reviewed medical journals. The review incorporated studies related to emergency medicine, cognitive psychology, patient safety, neurological emergencies, internal medicine emergencies, triage systems, and healthcare management. The analysis included evidence from international healthcare systems with special consideration of emergency care realities in Mexico, Colombia, and Ecuador. The findings demonstrate that increasing time pressure is associated with reduced diagnostic accuracy and greater vulnerability to cognitive biases such as anchoring bias, premature closure, confirmation bias, and availability bias. Overcrowding was identified as one of the principal systemic factors negatively affecting emergency department workflow, contributing to diagnostic delay, treatment postponement, prolonged length of stay, and increased physician workload. Acute ischemic stroke, sepsis, and acute coronary syndrome showed the strongest association between delayed intervention and adverse patient outcomes.

The kidney has traditionally been recognized as an organ responsible for filtration and homeostasis; however, recent evidence highlights its role as a sensitive sensor capable of detecting early systemic alterations. This review analyzes the function of the kidney as a sensor organ through the evaluation of renal biomarkers, with a particular focus on pediatric populations and their interaction with gastrointestinal diseases. A structured narrative review methodology was applied, integrating evidence from nephrology, internal medicine, pediatrics, and gastroenterology. Emerging biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and cystatin C demonstrate greater sensitivity for early detection of renal and systemic alterations compared to traditional markers such as serum creatinine. These biomarkers reflect different pathophysiological mechanisms, including tubular injury, inflammation, and glomerular dysfunction, allowing for a multidimensional assessment of disease processes. The findings also emphasize the relevance of the gut–kidney axis, where gastrointestinal conditions such as dehydration, inflammatory bowel disease, liver dysfunction, and dysbiosis can induce early renal responses. This relationship is particularly significant in pediatric patients, where systemic disturbances may progress rapidly and remain clinically silent in early stages.

The enteric nervous system (ENS), commonly referred to as the “second brain,” has emerged as a key integrative network in clinical medicine. This review analyzes its role beyond gastrointestinal physiology, emphasizing its involvement in neurological, nephrological, and urological conditions through interconnected mechanisms such as the gut–brain, gut–kidney, and gut–bladder axes. A structured analysis of current scientific literature was conducted to identify the main pathways linking ENS dysfunction with multisystem disease, including microbiota dysbiosis, neuroimmune activation, autonomic imbalance, epithelial barrier disruption, and visceral hypersensitivity. The findings demonstrate that while gastrointestinal manifestations remain predominant, ENS-related alterations are strongly associated with systemic inflammation, neurological symptoms, and urinary dysfunction. Additionally, emerging therapeutic strategies highlight the importance of integrative approaches, including dietary interventions, microbiota modulation, neuromodulation, and anti-inflammatory treatments. These results support the concept of the ENS as a central regulator in multisystem physiology and reinforce the need for interdisciplinary clinical reasoning. Understanding the ENS from a systems-based perspective provides valuable insights for improving diagnosis, treatment, and medical education in the context of complex and chronic diseases.

Workplace health systems have emerged as a strategic intersection between occupational medicine, public health, and healthcare management, particularly in response to the growing burden of chronic diseases and the need for sustainable health interventions. This study aimed to analyze the integration of these disciplines within workplace settings and to identify key factors influencing their effectiveness at the population level. A structured narrative review was conducted using a scientific method-based approach, incorporating evidence from international sources with a particular focus on Latin American contexts, including Mexico, Colombia, and Ecuador. The findings indicate that integrated workplace health systems significantly contribute to improved health outcomes, including better chronic disease control, reduced absenteeism, enhanced mental health, and increased organizational productivity. The results also highlight critical barriers such as limited funding, system fragmentation, and lack of trained personnel, as well as facilitating factors including leadership commitment, intersectoral collaboration, and policy support. Comparative analysis revealed variability in implementation across the selected countries, reflecting differences in health system structures and resource allocation.

Cardiovascular disease remains the leading cause of mortality worldwide, and traditional risk stratification models based on static variables are often insufficient to explain the complexity of cardiometabolic disorders. In this context, metabolic flexibility—defined as the ability of the organism to adapt substrate utilization according to physiological demands—has emerged as a relevant integrative concept linking endocrinology and cardiovascular disease. This review analyzes metabolic flexibility as a central mechanism in cardiovascular risk, exploring its physiological basis, its relationship with insulin resistance and metabolic disorders, and its implications in cardiovascular pathology. Evidence shows that impaired metabolic flexibility is associated with altered substrate utilization, mitochondrial dysfunction, systemic inflammation, and increased cardiovascular risk. These alterations contribute to inefficient myocardial energy metabolism, vascular dysfunction, and disease progression. Additionally, current therapeutic strategies that improve metabolic regulation have demonstrated significant cardiovascular benefits, supporting the relevance of metabolic pathways in disease prevention and management. The analysis also highlights the importance of considering metabolic flexibility in populations with a high burden of cardiometabolic disease, particularly in Latin American countries such as Mexico, Colombia, and Ecuador.

Neuromodulation has emerged as an innovative therapeutic approach that extends neurosurgical indications beyond structural disease toward the dynamic regulation of neural networks and brain–body interactions. This review analyzes the current and potential role of neuromodulation in emergency neurology, focusing on its capacity to influence key physiological mechanisms such as thalamocortical connectivity, autonomic regulation, neuroinflammation, and neuroplasticity. A structured narrative review was conducted using scientific databases including PubMed, Scopus, and Web of Science, selecting peer-reviewed studies relevant to neuromodulation techniques such as deep brain stimulation, vagus nerve stimulation, and transcranial magnetic stimulation. The findings indicate that neuromodulation demonstrates significant applicability in conditions such as refractory epilepsy, traumatic brain injury, stroke, and disorders of consciousness, particularly when conventional therapies are insufficient. Non-invasive techniques show advantages in feasibility and safety, while invasive approaches provide targeted and sustained modulation in selected cases. Additionally, the analysis highlights disparities in implementation across international contexts, including Mexico, Colombia, and Ecuador, where access to advanced technologies varies. Overall, neuromodulation represents a promising and evolving strategy in emergency neurology, with the potential to improve outcomes through the modulation of complex neural and systemic processes.