Vitamin D Effect on Subarachnoid Hemorrhage

NCT ID: NCT03482843

Last Updated: 2018-03-29

Basic Information

• Recruitment Status: UNKNOWN
• Total Enrollment: 16 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2017-02-01
• Study Completion Date: 2019-12-31

Brief Summary

Vitamin D has been promoted to vascular regeneration in non-cerebral arteries because of its anti-inflammatory properties. Cerebral vasospasm (CVS) as the most feared complication after subarachnoid hemorrhage (SAH), correlated with higher mortality and poor outcome, is the result of a multifactorial mechanism with inflammation as one of the main role players. The investigators therefore hypothesized that vitamin D attenuates cerebral vasospasm and increases the chance for favorable outcome after SAH.

Detailed Description

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.

Conditions

Vitamin D Deficiency

Study Design

• Observational Model Type: COHORT
• Study Time Perspective: PROSPECTIVE

Study Groups

Vitamin D Deficiency

25-Vitamin D level \<25 ng/ml

No interventions assigned to this group

Sufficient Vitamin D Level

25-Vitamin D Level \>=25-70 ng/ml

No interventions assigned to this group

Eligibility Criteria

Inclusion Criteria

• Admitted patients suffering from SAH over 18 years of age with consent form.

Exclusion Criteria

• Admitted patients suffering from SAH younger than 18 years of age.
• SAH patients without consent form.

• Minimum Eligible Age: 18 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

Institut für Kardiovaskuläre Physiologie, Vascular Research Center

UNKNOWN

Sponsor Role: collaborator

University Clinic Frankfurt

OTHER

Sponsor Role: lead

Responsible Party

Juergen Konczalla

Prof. Dr.

Responsibility Role: PRINCIPAL_INVESTIGATOR

Principal Investigators

Juergen Konczalla, Prof.

Role: PRINCIPAL_INVESTIGATOR

Goethe University Hospital

Locations

Goethe University Hospital

Frankfurt am Main, , Germany

Countries

Germany

Other Identifiers

142/15

Identifier Type: -

Identifier Source: org_study_id