Frontiers in neurology · 2026
Association between elevated serum amyloid a levels and clinical outcomes in intracerebral haemorrhage: a retrospective study.
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He Jixin, Xu Tongzhang, Wu Rong, Hu Ying, Zhao Dan, Zhang Wenbo, Wang Fangfang, Cao Jie, Jiang Min, Yin Xiaoping, Wu Moxin
Аннотация
OBJECTIVE: Following an intracerebral haemorrhage (ICH), secondary brain injury (SBI) occurs, triggering an inflammatory response. Serum amyloid A (SAA) levels, an acute-phase response protein, increase during acute inflammation and tissue damage. While SAA is associated with ICH prognosis, systematic studies investigating its dynamic longitudinal progression and its relationship with bleeding severity remain limited.
MATERIALS AND METHODS: In this single-centre, real-world cohort study, we measured SAA levels in 554 ICH patients and 119 healthy controls. Neurological deficit was quantified based on haematoma expansion (HE), the National Institutes of Health Stroke Scale (NIHSS) score, and the Glasgow Coma Scale (GCS) score after ICH. SAA levels were measured within 24 h of admission and on days 3 and 7 after ICH onset in this longitudinal study. Univariate and multivariate logistic regression analyses were performed to determine the independent association between SAA levels and NIHSS and GCS scores. Adjusted logistic regression and receiver operating characteristic (ROC) curves were used to assess the association between HE and SAA levels. Additionally, the role of SAA levels in SBI was evaluated by monitoring their changes within 24 h of admission and on days 3 and 7 after ICH.
RESULTS: SAA levels were significantly higher in patients with ICH than in healthy controls (3.1 vs. 2.4 mg/L, p < 0.001). SAA levels were positively correlated with disease severity (NIHSS: r = 0.106, 95% CI: 0.011-0.200, p = 0.029; GCS: r = -0.128, 95% CI: -0.213 to -0.041, p = 0.003) and were independently associated with a poor prognosis. The AUC for the diagnostic performance of SAA levels in HE was 0.694 (95% CI: 0.630-0.758). Furthermore, SAA levels were significantly elevated on days 3 and 7 compared with the levels at admission (p < 0.001).
CONCLUSION: Patients with ICH exhibit elevated SAA levels that are associated with prognosis. Dynamic monitoring of these levels indicates that day 3 may be a critical time point for observing changes in SAA levels.
MATERIALS AND METHODS: In this single-centre, real-world cohort study, we measured SAA levels in 554 ICH patients and 119 healthy controls. Neurological deficit was quantified based on haematoma expansion (HE), the National Institutes of Health Stroke Scale (NIHSS) score, and the Glasgow Coma Scale (GCS) score after ICH. SAA levels were measured within 24 h of admission and on days 3 and 7 after ICH onset in this longitudinal study. Univariate and multivariate logistic regression analyses were performed to determine the independent association between SAA levels and NIHSS and GCS scores. Adjusted logistic regression and receiver operating characteristic (ROC) curves were used to assess the association between HE and SAA levels. Additionally, the role of SAA levels in SBI was evaluated by monitoring their changes within 24 h of admission and on days 3 and 7 after ICH.
RESULTS: SAA levels were significantly higher in patients with ICH than in healthy controls (3.1 vs. 2.4 mg/L, p < 0.001). SAA levels were positively correlated with disease severity (NIHSS: r = 0.106, 95% CI: 0.011-0.200, p = 0.029; GCS: r = -0.128, 95% CI: -0.213 to -0.041, p = 0.003) and were independently associated with a poor prognosis. The AUC for the diagnostic performance of SAA levels in HE was 0.694 (95% CI: 0.630-0.758). Furthermore, SAA levels were significantly elevated on days 3 and 7 compared with the levels at admission (p < 0.001).
CONCLUSION: Patients with ICH exhibit elevated SAA levels that are associated with prognosis. Dynamic monitoring of these levels indicates that day 3 may be a critical time point for observing changes in SAA levels.