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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\u00a0h 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\u2019 outcomes were assessed according to the modified Rankin Scale (mRS) and the Barthel\u2019s Index on days 14, 30, and 90. Onehundred fifteen patients were included, of whom 61 were vitamin D deficient (VDD, serum vitamin D\u2009&lt;\u200950 nmol\/L) and 54 were vitamin D sufficient (VDS, serum vitamin D\u2009\u2267\u200950 nmol\/L). The incidence of new ischemic lesions was significantly higher in the VDD group (VDD: 68.63% vs. VDS: 40.74%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.008). 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%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.057). 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%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.011). 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.\n                  <\/jats:p>","DOI":"10.1038\/s41598-026-38728-9","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T19:34:33Z","timestamp":1770233673000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Impact of vitamin D deficiency on clinical outcomes in non-traumatic subarachnoid hemorrhage: A single-center prospective cohort study"],"prefix":"10.1038","volume":"16","author":[{"given":"Dorottya","family":"Sz\u00e1nt\u00f3","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B\u00e9la","family":"F\u00fclesdi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lili","family":"Simon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L\u00e1szl\u00f3","family":"Nov\u00e1k","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J\u00e1nos","family":"Kappelmayer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Csilla","family":"Moln\u00e1r","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,2,4]]},"reference":[{"key":"38728_CR1","doi-asserted-by":"publisher","first-page":"108605","DOI":"10.1016\/j.clineuro.2024.108605.2","volume":"247","author":"S Odensass","year":"2024","unstructured":"Odensass, S. et al. Predictors of survival after aneurysmal subarachnoid hemorrhage: the long-term observational cohort study. Clin. Neurol. Neurosurg. 247, 108605. https:\/\/doi.org\/10.1016\/j.clineuro.2024.108605.2 (2024).","journal-title":"Clin. Neurol. Neurosurg."},{"key":"38728_CR2","doi-asserted-by":"publisher","first-page":"315","DOI":"10.1093\/bja\/aes264.3","volume":"109","author":"MJ Rowland","year":"2012","unstructured":"Rowland, M. J., Hadjipavlou, G., Kelly, M., Westbrook, J. & Pattinson, K. T. Delayed cerebral ischaemia after subarachnoid haemorrhage: looking beyond vasospasm. Br. J. Anaesth. 109, 315\u2013329. https:\/\/doi.org\/10.1093\/bja\/aes264.3 (2012).","journal-title":"Br. J. Anaesth."},{"key":"38728_CR3","doi-asserted-by":"publisher","first-page":"177","DOI":"10.31083\/j.rcm2406177","volume":"24","author":"D Sz\u00e1nt\u00f3","year":"2023","unstructured":"Sz\u00e1nt\u00f3, D. et al. Diagnosis and management of Takotsubo syndrome in acute aneurysmal subarachnoid hemorrhage: A comprehensive review. Rev. Cardiovasc. Med. 24, 177. https:\/\/doi.org\/10.31083\/j.rcm2406177 (2023).","journal-title":"Rev. Cardiovasc. Med."},{"key":"38728_CR4","doi-asserted-by":"publisher","first-page":"213","DOI":"10.1186\/s12974-019-1578-1","volume":"16","author":"SH Ahn","year":"2019","unstructured":"Ahn, S. H. et al. Inflammation in delayed ischemia and functional outcomes after subarachnoid hemorrhage. J. Neuroinflammation. 16, 213. https:\/\/doi.org\/10.1186\/s12974-019-1578-1 (2019).","journal-title":"J. Neuroinflammation"},{"key":"38728_CR5","doi-asserted-by":"publisher","first-page":"61","DOI":"10.1186\/s41232-022-00236-4","volume":"42","author":"H Yamada","year":"2022","unstructured":"Yamada, H. et al. Subarachnoid hemorrhage triggers neuroinflammation of the entire cerebral cortex, leading to neuronal cell death. Inflamm. 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