Cancer-Related Fatigue and Circulating Biomarkers in Breast Cancer Survivors

Abstract

El estudio de García-González et al. (2023) analiza la relación entre la fatiga relacionada con el cáncer (FRC) y diversos biomarcadores sanguíneos en mujeres supervivientes de cáncer de mama. En una muestra de 91 participantes, se evaluaron marcadores de inflamación, disfunción del eje hipotálamo-hipófisis-adrenal (HPA), estrés oxidativo, resistencia a la insulina y hormonas sexuales. Los resultados mostraron una asociación significativa entre la FRC y dos biomarcadores: la relación neutrófilo-linfocito (NLR), positivamente correlacionada con la fatiga, y el cortisol, inversamente correlacionado. No se hallaron asociaciones relevantes con otros marcadores. El estudio concluye que la inflamación y la disfunción del eje HPA son factores clave en la fisiopatología de la FRC, aunque se necesitan investigaciones longitudinales para confirmar su papel causal. Los hallazgos ofrecen nuevas perspectivas para el manejo clínico de la fatiga postcáncer y la mejora de la calidad de vida en mujeres supervivientes.

Purpose: Cancer-related fatigue (CRF) is the most common and disruptive symptom experienced by cancer survivors and because of its frequency and severity is especially worrisome in breast cancer survivors (BCS). Despite a great deal of research, the mechanisms underlying CRF have not been determined. The present study aims to describe associations between CRF in BCS and different blood biomarkers. Methods: A descriptive and cross-sectional study was conducted. A set of biomarkers assessing inflammation were measured in BCS: C-reactive protein (CRP), neutrophil-lymphocyte ratio (NLR), IL-1β, IL-6, IL-8, IL-10, tumor necrosis factor (TNF); HPA axis dysfunction (cortisol), autonomic dysfunction (noradrenaline); oxidative stress (8- OH deoxyguanosine); insulin resistance markers (insulin, IGF-I, IGFBP3) and sexual hormones (estrogens, progesterone, testosterone). Results: NLR (p = .00) and cortisol (p = .02) were positive and negatively associated with CRF, respectively. The rest of the blood markers were not associated with CRF. Conclusion: Our results increase the evidence on pathophysiological mechanisms driving CRF in BCS. However, longitudinal studies are needed to explore the role of these factors as potential causal mechanisms