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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
Sponsor:
Collaborator:
Institut für Kardiovaskuläre Physiologie, Vascular Research Center
Information provided by (Responsible Party):
Juergen Konczalla, University Clinic Frankfurt

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.

Condition or disease
Vitamin D Deficiency

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.

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Study Type : Observational
Actual Enrollment : 16 participants
Observational Model: Cohort
Time Perspective: Prospective
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

Resource links provided by the National Library of Medicine

Drug Information available for: Vitamin D

Group/Cohort
Vitamin D Deficiency
25-Vitamin D level <25 ng/ml
Sufficient Vitamin D Level
25-Vitamin D Level >=25-70 ng/ml



Primary Outcome Measures :
  1. 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)


Secondary Outcome Measures :
  1. 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)



Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years and older   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population
All admitted SAH patients over 18 years of age.
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.

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03482843


Locations
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Germany
Goethe University Hospital
Frankfurt/Main, Germany
Sponsors and Collaborators
University Clinic Frankfurt
Institut für Kardiovaskuläre Physiologie, Vascular Research Center
Investigators
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Principal Investigator: Juergen Konczalla, Prof. Goethe University Hospital

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Responsible Party: Juergen Konczalla, Prof. Dr., University Clinic Frankfurt
ClinicalTrials.gov Identifier: NCT03482843    
Other Study ID Numbers: 142/15
First Posted: March 29, 2018    Key Record Dates
Last Update Posted: March 29, 2018
Last Verified: March 2018

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Studies a U.S. FDA-regulated Drug Product: No
Studies a U.S. FDA-regulated Device Product: No
Additional relevant MeSH terms:
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Subarachnoid Hemorrhage
Vitamin D Deficiency
Hemorrhage
Pathologic Processes
Avitaminosis
Deficiency Diseases
Malnutrition
Nutrition Disorders
Intracranial Hemorrhages
Cerebrovascular Disorders
Brain Diseases
Central Nervous System Diseases
Nervous System Diseases
Vascular Diseases
Cardiovascular Diseases
Vitamin D
Ergocalciferols
Vitamins
Micronutrients
Nutrients
Growth Substances
Physiological Effects of Drugs
Bone Density Conservation Agents
Calcium-Regulating Hormones and Agents