Vitamin D Effect on Subarachnoid Hemorrhage
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|ClinicalTrials.gov Identifier: NCT03482843|
Recruitment Status : Unknown
Verified March 2018 by Juergen Konczalla, University Clinic Frankfurt.
Recruitment status was: Active, not recruiting
First Posted : March 29, 2018
Last Update Posted : March 29, 2018
|Condition or disease|
|Vitamin D Deficiency|
Subarachnoid hemorrhage (SAH) as a worldwide significant cause for morbidity and mortality, especially affecting young population, accounts for 4%-10% of all strokes. About 25% of SAH patients die and 50% left with significant disability, which according to the relative youth of the affected individuals means that this event is responsible for a quarter of all years of life lost as a result of stroke. Cerebral vasospasm, as the most feared complication after SAH leading mostly into ischemia, associated with delayed deterioration, continues to be both a difficult entity to treat and a leading cause of morbidity in patients. A high number of investigators focused on vasospasm research to develop effective therapy strategies to treat this entity, however, results of experimental studies and clinical trials about calcium channel blocker nicardipine and the endothelin-1 antagonist clazosentan as sources of hope in vasospasm treatment did not reveal an improvement in patient outcomes. Recently, there is a renewed interest in looking for other potentially targets for therapy.
Vitamin D, especially the aktive hormone 1,25-dihydroxycholecalciferol (1,25VitD3), has been suggested to limit inflammation, cancer, development of heart failure and myocardial infarction through the nuclear vitamin D receptor (VDR) by balancing the gene expression. Thus, vitamin D deficiency is linked to increased risk in many clinical settings including cardiovascular disease, stroke and critically ill patients. Furthermore, low vitamin D status has been associated with autoimmune disorders such as multiple sclerosis or neoplastic diseases, increased rates of infections and increased mortality. In case of ischemic stroke, a higher rate of vitamin D insufficiency has been suggested in patients associated with poorer outcomes. Nevertheless, these observations still remain controversial.
However, current data attracted considerable attention in neurovascular research to study the effects of this hormone on SAH. Recently, a few experimental and clinical studies have already worked on this topic. A rat model of SAH confirmed that vitamin D pretreatment attenuates cerebral artery remodeling and vasospasm as well as blood-brain barrier (BBB) disruption mainly through endogenous upregulation of osteopontin. Clinical data proved the fact that there is an increased incidence of hypovitaminosis D among patients requiring treatment for cerebral aneurysms and a high prevalence of vitamin D insufficiency among SAH patients. Contrary to expectations, an association between vitamin D deficiency and outcomes in SAH patients could not be detected. However, in view of recent limited research data on this topic a final statement could not yet be made. Therefore, the investigators aimed to determine the effect of vitamin D on vasospasm discussing mechanistic evaluations of inflammation in SAH based on a translational study design including patient data to underline our experimental findings.
|Study Type :||Observational|
|Actual Enrollment :||16 participants|
|Official Title:||Vitamin D Effect on Subarachnoid Hemorrhage|
|Actual Study Start Date :||February 1, 2017|
|Actual Primary Completion Date :||December 31, 2017|
|Estimated Study Completion Date :||December 31, 2019|
Vitamin D Deficiency
25-Vitamin D level <25 ng/ml
Sufficient Vitamin D Level
25-Vitamin D Level >=25-70 ng/ml
- clinical outcome at discharge [ Time Frame: 2 to 4 weeks after SAH ]modified Rankin scale (for measuring the dependence in daily activity. Range 0 (no symptoms) to 6 (dead)
- clinical outcome 6 months after SAH [ Time Frame: 6 months after SAH ]modified Rankin scale (for measuring the dependence in daily activity. Range 0 (no symptoms) to 6 (dead)
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Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03482843
|Goethe University Hospital|
|Principal Investigator:||Juergen Konczalla, Prof.||Goethe University Hospital|