Serum TNF‐α Modulation and Serum TNF‐α Modulation and Functional Recovery Following Taurine Supplementation in Acute Spinal Cord Injury: A Prospective Observational Cohort Study With Healthy Controls

Background Acute spinal cord injury (SCI) is associated with persistent inflammation and impaired functional recovery. We investigated longitudinal changes in serum tumour necrosis factor‐α (TNF‐α), their association with functional independence, and the relationship of taurine supplementation with inflammatory and functional outcomes after acute traumatic SCI. Methods In this prospective observational cohort study, 70 adults with acute traumatic SCI and 70 age‐ and sex‐matched healthy controls were studied at King George’s Medical University, Lucknow, India. Patients received standard management, with 36 receiving oral taurine (3 g/day) and 34 receiving conventional treatment for 6 months; allocation was nonrandomised. Serum TNF‐α was measured at baseline and 6 months, and functional independence was assessed using the Spinal Cord Independence Measure (SCIM). Longitudinal associations were examined using correlation and repeated‐measures correlation analyses, with false discovery rate adjustment. Receiver operating characteristic (ROC) analysis assessed the diagnostic discrimination of baseline TNF‐α, and multivariable linear regression identified independent predictors. Findings Serum TNF‐α decreased from 0.7636 (SD 0.5433) pg/mL at baseline to 0.4913 (0.4942) pg/mL at 6 months in the overall SCI cohort ( p < 0.0001). The decrease was greater in the taurine group (0.7002 [0.5059]–0.2109 [0.0883] pg/mL) than in the conventional‐treatment group (0.8308 [0.5803]–0.7883 [0.5708] pg/mL). At 6 months, TNF‐α in the taurine group was comparable with healthy controls ( p = 0.2553), whereas concentrations remained elevated in the conventional‐treatment group ( p < 0.0001). Baseline TNF‐α discriminated SCI from healthy controls with an AUC of 0.892 (95% CI 0.829–0.946; p < 0.0001). At 6 months, total SCIM was higher in the taurine group than in the conventional‐treatment group (71.14 [9.78] vs. 34.53 [4.76]; p < 0.001), with higher scores across all SCIM domains. Higher TNF‐α was consistently associated with lower functional independence; repeated‐measures correlations were −0.673 for total SCIM, −0.684 for self‐care, −0.642 for respiration and sphincter management and −0.681 for mobility (all FDR‐adjusted p < 0.001). However, no significant TNF‐α × time × treatment interaction was observed for total SCIM or any SCIM domain. In multivariable analysis, baseline TNF‐α independently predicted 6‐month TNF‐α ( β = 0.582, 95% CI 0.409–0.756; standardised β = 0.640; FDR‐adjusted p < 0.001; R 2 = 0.494). Interpretation Lower TNF‐α concentrations were associated with greater functional independence over 6 months after acute traumatic SCI. Taurine supplementation was associated with greater TNF‐α reduction and higher functional scores, but nonrandomised treatment allocation and the absence of a significant longitudinal treatment interaction preclude causal inference. These findings support TNF‐α as a candidate inflammatory biomarker and justify adequately powered randomised trials to determine the therapeutic efficacy of taurine after SCI. Trial Registration: Clinical Trial Registry of India: CTRI/2022/11/047262