Vitamin D Effect on Subarachnoid Hemorrhage

Vitamin D Deficiency Clinical Trial

Official title:

Vitamin D Effect on Subarachnoid Hemorrhage

Clinical Trial Details — Status: Active, not recruiting

Administrative data

• NCT number: NCT03482843
• Other study ID #: 142/15
• Status: Active, not recruiting
• First received: March 18, 2018
• Last updated: March 28, 2018
• Start date: February 1, 2017
• Est. completion date: December 31, 2019

Study information

• Verified date: March 2018
• Source: University Clinic Frankfurt
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Active, not recruiting
• Enrollment: 16
• Est. completion date: December 31, 2019
• Est. primary completion date: December 31, 2017
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years and older

Eligibility

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.

Related Conditions & MeSH terms

• Hemorrhage
• Subarachnoid Hemorrhage
• Vitamin D Deficiency

Locations

Country	Name	City	State
Germany	Goethe University Hospital	Frankfurt/Main

Sponsors (2)

Lead Sponsor	Collaborator
University Clinic Frankfurt	Institut für Kardiovaskuläre Physiologie, Vascular Research Center

Country where clinical trial is conducted

Germany, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	clinical outcome at discharge	modified Rankin scale (for measuring the dependence in daily activity. Range 0 (no symptoms) to 6 (dead)	2 to 4 weeks after SAH
Secondary	clinical outcome 6 months after SAH	modified Rankin scale (for measuring the dependence in daily activity. Range 0 (no symptoms) to 6 (dead)	6 months after SAH