Impact of vitamin D deficiency on clinical outcomes in non-traumatic subarachnoid hemorrhage: A single-center prospective cohort study

TL;DR

This study finds that vitamin D deficiency in patients with subarachnoid hemorrhage is linked to worse outcomes, including higher inflammation and more complications.

Contribution

The study is the first to prospectively investigate the impact of vitamin D deficiency on clinical outcomes in non-traumatic subarachnoid hemorrhage patients.

Findings

Vitamin D deficient patients had a significantly higher incidence of new ischemic lesions compared to sufficient patients.

Vitamin D deficiency was associated with higher peaks in inflammatory markers and a tendency for more infections.

Poor clinical outcomes, as measured by the modified Rankin Scale, were more frequent in vitamin D deficient patients.

Abstract

There is growing evidence that neuroinflammation and systemic inflammatory response following SAH have a major effect on patients’ outcomes. We hypothesized that due to the immunomodulating and neuroprotective properties, Vitamin D deficiency may contribute to unfavorable outcome in SAH patients. Consecutive patients admitted with acute non-traumatic SAH were prospectively included. Within 24 h of admission, serum 25(OH)vitamin D levels were measured. During the first 21 days after SAH, inflammatory markers were closely monitored, the development of any infectious complication was noted, and the onset of cerebral vasospasm was evaluated using transcranial color-coded Doppler. New ischemic lesions on follow-up computed tomography imaging were also documented. Patients’ outcomes were assessed according to the modified Rankin Scale (mRS) and the Barthel’s Index on days 14, 30, and 90. Onehundred fifteen patients were included, of whom 61 were vitamin D deficient (VDD, serum vitamin D < 50 nmol/L) and 54 were vitamin D sufficient (VDS, serum vitamin D ≧ 50 nmol/L). The incidence of new ischemic lesions was significantly higher in the VDD group (VDD: 68.63% vs. VDS: 40.74%, p = 0.008). The VDD group also had higher peaks in inflammatory markers and a tendency of higher incidence of infections (VDD: 42.62% vs. VDS: 24.07%, p = 0.057). A poor outcome, as defined by the mRS, was significantly more frequent among VDD patients (on day 90: VDD, 61.02% vs. VDS, 35.19%, p = 0.011). Our findings raise the potential harmful effects of D hypovitaminosis among patients with SAH. Vitamin D deficiency may contribute to greater inflammatory response and increased risk of secondary ischemia, infections, and poor clinical outcomes. Further studies will show whether low vitamin D levels measured at admission are the consequence of SAH severity or whether pre-ictus hypovitaminosis also plays a role in determining the worse prognosis.

The online version contains supplementary material available at 10.1038/s41598-026-38728-9.

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