La Diabetes Mellitus tipo 2 (DM2) es un problema de salud pública y socioeconómico, tanto por su alta incidencia como por la generación de los costos médicos directos para su tratamiento. Analizar el costo-efectividad de los tratamientos en monoterapia y biterapia en pacientes con DM2. Análisis costo-efectividad, observacional, ambispectivo, transversal y analítico. Análisis de expedientes en una unidad médica de primer nivel. Se ejecutaron los datos en la matriz de costos con el programa Office Excel 2010; se identificó el fármaco más prescrito, se comparó con monoterapia y biterapia. Los costos médicos directos anuales del total de la población fueron: costo del medicamento $118,561.70MN, costo por hospitalización $243,756.00MN, costo por consultas $ 327,414.00MN y costo por estudios clínicos $2416.79MN, obteniendo un total anual de $692,148.58MN. La metformina fue la más indicada en monoterapia (88.4%) y como terapéutica estándar tiene mayor costo-efectividad comparada con la glibenclamida. En biterapia fue metformina/glibenclamida (35.7%) versus las terapéuticas de metformina/insulina NPH, metformina/insulina glargina y metformina/dapagliflozina, las cuales tuvieron un resultando más costo-efectivo, con un costo efectividad incremental de -$1,128,428.50MN, -$34,365.00MN, -$119,848.97MN respectivamente. La metformina presento mejor relación costo efectividad en monoterapia, mientras que en biterapia fue la asociación metformina/Insulina NPH.

Permethrin (PERM) is a synthetic pyrethroid insecticide initially regarded as low risk. However, evidence now indicates that misuse and prolonged exposure can damage multiple physiological systems by disrupting enzymatic functions in subcellular structures. In this study, male Wistar rats were administered PERM (75, 150, or 300 mg/kg/day) for 15 days to assess its effect on hematological and biochemical parameters, including oxidative stress markers in the liver, kidney, and heart. Subacute PERM administration induced significant, dose-dependent toxicological alterations in exposed animals. Hematological analysis revealed impaired hematopoiesis, characterized by increased erythrocytes and platelets alongside decreased hemoglobin, hematocrit, mean corpuscular volume, and red cell distribution width. Biochemical analysis revealed elevated liver enzymes and bilirubin, along with reduced albumin levels, indicating hepatic alterations associated with PERM. The assessment of oxidative stress revealed tissue-specific responses following PERM exposure. While GPx, CAT, and SOD levels remained unchanged, GR activity increased in the heart, and GST activity increased in the liver. Additionally, a substantial decrease in MDA was observed in both the liver and heart. These collective alterations found in PERM-subacute exposed rats suggest the potential for cellular damage with the possible development of chronic pathologies, warranting further investigation.

Background: Amino acid biomarkers have a crucial influence on our understanding of brain injury mechanisms, and their plasma concentrations may indicate neurological damage and recovery patterns. Pediatric mild traumatic brain injury (mTBI) assessment particularly benefits from such molecular indicators, as clinical presentations can be subtle and variable. However, current diagnostic and prognostic tools lack reliable biochemical markers that can track the temporal evolution of injuries and recovery. Methods: We conducted a prospective longitudinal cohort study involving 36 pediatric mTBI patients and 44 controls to characterize the temporal evolution of key amino acids and their derived indices. Blood samples were collected at 3, 6, 12, and 24 h and at 7, 14, and 28 days post-injury, with amino acids quantified using high-performance liquid chromatography. Results: Our analysis revealed significant temporal changes in glutamate, glutamine, and glycine concentrations, with glutamate peaking at day 7 before declining, while glutamine showed steady increases throughout. The GLN/GLU ratio demonstrated an early excitatory imbalance followed by astrocytic compensation, and the GLX ratio indicated progressive recovery. Conclusions: These patterns represent continuous neurochemical processes involving excitotoxicity and glial regulation, suggesting potential utility as biomarkers for mTBI diagnosis and monitoring. While further validation using larger cohorts is needed, these findings provide compelling evidence of the efficacy of using amino acid profiles to track pediatric mTBI progression and recovery.