A likely explanation is that fewer chronic comorbidities (malnutrition/inflammation) in younger individuals mean that acute LDH/ALB shifts more specifically reflect the current inflammatory–ischemic insult, improving the signal-to-noise ratio for LAR; conversely, in older or large-hematoma patients, multiple concurrent pathways (hemodynamic instability, multiorgan ischemia) may dilute LAR's incremental value (“risk saturation”). The gene discussed is ALB; the disease is hematoma.