Acute ischemic stroke (AIS) triggers systemic inflammation and metabolic stress and post-stroke malnutrition is common and strongly associated with poor outcomes. There is increasing evidence that inflammation and malnutrition interact in a bidirectional, self-reinforcing manner, particularly in disease-related, inflammation-associated malnutrition, rather than in purely starvation-driven states. The objective of this study was to synthesize the current evidence regarding the inflammation-malnutrition axis in AIS, including (1) inflammation as a contributor to AIS risk and severity, (2) AIS-induced neuroinflammation and systemic immune dysregulation, (3) inflammatory mechanisms promoting malnutrition, (4) malnutrition as a modifier of inflammatory responses, and (5) the combined impact on clinical outcomes and management. Inflammation contributes to AIS risk through atherosclerosis progression and plaque instability, endothelial dysfunction, and thromboinflammatory pathways. After AIS, local and systemic inflammatory cascades (eg, cytokine release, leukocyte activation, blood-brain barrier disruption, stress-axis activation) can lead to anorexia, hypermetabolism, muscle catabolism, hepatic acute-phase protein reprioritization, and gastrointestinal barrier dysfunction. These processes can worsen nutritional status. Malnutrition, in turn, impairs immune competence and may amplify inflammatory dysregulation, increasing susceptibility to complications such as infections and delirium, as well as contributing to poorer functional recovery and higher mortality risk. Because albumin is strongly influenced by the acute-phase response, it should not be interpreted as a standalone nutritional biomarker. However, composite indexes integrating inflammation and nutritional reserve (eg, the ratio of C-reactive protein to albumin, Prognostic Nutritional Index, Controlling Nutritional Status, Geriatric Nutritional Risk Index), and related scores, retain prognostic value in AIS cohorts. The inflammation-malnutrition interaction is a clinically relevant factor in AIS, supporting early, integrated assessment and targeted management strategies. Practical implications include systematic screening within 24-48 hours of admission. Future research should prioritize longitudinal designs and combined interventions targeting both inflammatory and nutritional pathways to improve AIS outcomes.
Golenia et al. (Thu,) studied this question.