More edema after traumatic brain injury if low Vitamin D

The predictive value of serum 25(OH)D, AQP4, and IL-4 levels for edema volume and clinical prognosis after traumatic brain injury

Front. Med. Chinese authors. PDF might be available later in 2026

Objective: This study aims to explore the associations between serum 25-hydroxyvitamin D (25(OH)D), aquaporin 4 (AQP4), and interleukin-4 (IL-4) levels with brain edema volume and outcomes in patients with traumatic brain injury (TBI).

Methods: A cohort of 279 TBI patients, enrolled between January 2023 and December 2024, was analyzed. Serum levels of 25(OH)D, AQP4, and IL-4, as well as brain edema volume, were measured on days 1, 3, and 7 post-admission. Pearson correlation analysis was used to assess relationships between these serum markers and brain edema volume. Based on the 90-day follow-up outcome, patients were classified into a favorable outcome group (n = 215) and a poor outcome group (n = 64). Multivariate logistic regression was employed to identify factors influencing TBI outcomes.

Results: Serum 25(OH)D levels were highest on day 1 post-TBI, followed by day 3 and day 7 (P < 0.05). In contrast, AQP4 and IL-4 levels, along with brain edema volume, were lowest on day 1 and increased significantly by days 3 and 7 (P < 0.05).

Serum 25(OH)D levels were inversely correlated with brain edema volume, while AQP4 and IL-4 levels exhibited a positive correlation (P < 0.05).

On days 1, 3, and 7, the favorable outcome group had higher serum 25(OH)D levels and lower AQP4 and IL-4 levels compared to the poor outcome group (P < 0.05).

Multivariate analysis revealed that serum 25(OH)D on day 1 and the Glasgow Coma Scale (GCS) score were associated with favorable outcomes, whereas IL-4 levels on day 1 independently predicted poor prognosis (P < 0.05). ROC curve analysis demonstrated that all tested biomarkers had prognostic value, with serum 25(OH)D on day 1 showing the highest predictive accuracy.

Conclusion: Serum levels of 25(OH)D, AQP4, and IL-4 are significantly associated with brain edema volume in TBI patients. Among these markers, serum 25(OH)D levels on the first day post-injury serve as the most reliable prognostic indicator of patient outcomes.

Edema After Traumatic Brain Injury - Claude AI April 2026

Edema (brain swelling) is one of the most dangerous secondary complications of TBI, often causing more damage than the initial injury.

Two main types:

  • Vasogenic edema — the blood-brain barrier (BBB) breaks down, allowing fluid to leak from blood vessels into brain tissue. Common around contusions and hemorrhages.
  • Cytotoxic edema — cells swell due to failure of ion pumps (especially Na⁺/K⁺-ATPase) from energy depletion. Occurs in areas of ischemia/hypoxia.

Both types often occur simultaneously after TBI.

Why it's dangerous:

The skull is a rigid box. Swelling raises intracranial pressure (ICP), which reduces cerebral perfusion pressure (CPP), causing further ischemia — a vicious cycle. Severe cases can cause herniation and death.

Timeline: Peaks roughly 24–72 hours post-injury but can persist or worsen over days.

Management approaches:

  • Osmotic therapy (mannitol, hypertonic saline) to draw fluid out of brain tissue
  • Head elevation, controlled ventilation (targeting PaCO₂)
  • Sedation and temperature management to reduce metabolic demand
  • ICP monitoring (ventriculostomy)
  • Decompressive craniectomy in refractory cases

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