Ignite Creation Date:
2024-05-06 @ 6:58 PM
Last Modification Date:
2024-10-26 @ 2:58 PM
Study NCT ID:
NCT05846373
Status:
RECRUITING
Last Update Posted:
2024-01-17
First Post:
2023-04-26
Brief Title:
Effect of Nicotinic Acid as Add on Therapy in Patients Receiving β Blocker for Prophylaxis of Moderate to Severe Migraine
Sponsor:
Bangabandhu Sheikh Mujib Medical University Dhaka Bangladesh
Organization:
Bangabandhu Sheikh Mujib Medical University Dhaka Bangladesh
Study Overview
Official Title:
Effect of Nicotinic Acid as add-on Therapy in Patients Receiving β Blocker for Prophylaxis of Moderate to Severe Migraine A Randomized Double-blind Placebo-controlled Trial
Status:
RECRUITING
Status Verified Date:
2024-01
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
This is a prospective single center randomized double-blind 3 arm placebo-controlled study in subjects with migraine headache requiring prophylactic treatment The patients will be randomized to receive Nicotinic Acid Extended-release tablet 500 mg or 1000 mg or placebo for 12 weeks The safety and efficacy outcome measures will be assessed at baseline and 12 weeks
Detailed Description:
Migraine is a common episodic neurological disorder with complex pathophysiology that manifests as recurrent attacks of typically throbbing and unilateral often severe headache with certain associated features such as nausea phonophobia and photophobia Worldwide estimated prevalence was 138 to 15 Quality of life of a migraine patient is extremely low and migraine badly hampers ones physical emotional and social efficiency and disrupt familial social and professional relationships Diagnosis is solely clinical depending on characteristics of headache and associated symptoms Neuroimaging can be done only when exclusion of another cause of headache is needed
Exact etiology and pathophysiology of migraine is unknown and multifactorial There are several hypotheses of migraine pain generation Local dilatation of intracranial and extracerebral vessels activate trigeminal nerve surrounding cerebral and meningeal vasculature Migraine pain starts from the activation of trigeminovascular system Afferent fibers innervating cerebral and meningeal vessels project to central nervous system and releases vasoactive peptides and inflammatory mediators Some important mediators like Calcitonin gene related peptide CGRP NO Substance P play role in inflammation and vasodilatation Then sensitization and discharge of thalamic neuron and subsequent projection to sensory cortical neurons occurs Thus pain perception is received in migraine
In studies elevated levels of C reactive protein CRP and Transforming growth factor β TGF-β provides evidence of neuroinflammation In migraine impairment of cerebral mitochondrial energy metabolism and oxidative stress occurs As a result abnormalities in cerebral vasculature results in Cortical Spreading Depression CSD
Niacin which is known as nicotinic acid or Vitamin B3 is the precursor of Nicotinamide Adenine Dinucleotide NAD or Nicotinamide Adenine Dinucleotide Phosphate NADP From dietary tryptophan through kynurenine pathway NAD is produced and rest 1 tryptophan is catabolized to form serotonin 5- hydroxytryptamine 5-HT Migraine is a serotonin deficient condition It has been estimated that dietary intake of Niacin is low in migraine patients
Niacin supplementation provides enough NAD to inhibit Kynurenine pathway and accelerate production of 5-HT from tryptophan Serotonin acting on 5-HT1 receptor causes vasoconstriction It may activate nerve endings in cerebral microcirculation and sensitize them to vasodilatory kinins Serotonin also inhibits synthesis release of NO glutamate Calcitonin gene-related peptide CGRP As a result inhibition of afferent pain transmission and prevention of neuroinflammation occurs Niacin also reduces inflammation evidenced by decrease level of pro inflammatory cytokines like IL-6 IL-1β TNF α high-sensitivity C-reactive protein hs-CRP Increasing level of Niacin also improves brain energy deficiency and has potent antioxidant properties which may be helpful in migraine prevention However more prospective investigations are necessary to validate niacins preventive effect on migraine
Exact etiology and pathophysiology of migraine is unknown and multifactorial There are several hypotheses of migraine pain generation Local dilatation of intracranial and extracerebral vessels activate trigeminal nerve surrounding cerebral and meningeal vasculature Migraine pain starts from the activation of trigeminovascular system Afferent fibers innervating cerebral and meningeal vessels project to central nervous system and releases vasoactive peptides and inflammatory mediators Some important mediators like Calcitonin gene related peptide CGRP NO Substance P play role in inflammation and vasodilatation Then sensitization and discharge of thalamic neuron and subsequent projection to sensory cortical neurons occurs Thus pain perception is received in migraine
In studies elevated levels of C reactive protein CRP and Transforming growth factor β TGF-β provides evidence of neuroinflammation In migraine impairment of cerebral mitochondrial energy metabolism and oxidative stress occurs As a result abnormalities in cerebral vasculature results in Cortical Spreading Depression CSD
Niacin which is known as nicotinic acid or Vitamin B3 is the precursor of Nicotinamide Adenine Dinucleotide NAD or Nicotinamide Adenine Dinucleotide Phosphate NADP From dietary tryptophan through kynurenine pathway NAD is produced and rest 1 tryptophan is catabolized to form serotonin 5- hydroxytryptamine 5-HT Migraine is a serotonin deficient condition It has been estimated that dietary intake of Niacin is low in migraine patients
Niacin supplementation provides enough NAD to inhibit Kynurenine pathway and accelerate production of 5-HT from tryptophan Serotonin acting on 5-HT1 receptor causes vasoconstriction It may activate nerve endings in cerebral microcirculation and sensitize them to vasodilatory kinins Serotonin also inhibits synthesis release of NO glutamate Calcitonin gene-related peptide CGRP As a result inhibition of afferent pain transmission and prevention of neuroinflammation occurs Niacin also reduces inflammation evidenced by decrease level of pro inflammatory cytokines like IL-6 IL-1β TNF α high-sensitivity C-reactive protein hs-CRP Increasing level of Niacin also improves brain energy deficiency and has potent antioxidant properties which may be helpful in migraine prevention However more prospective investigations are necessary to validate niacins preventive effect on migraine
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None