Impact of Vitamin A on Gene Expression, in Multiple Sclerosis Patient

Relapsing Remitting Multiple Sclerosis Clinical Trial

— MS  

Official title:

The Impact of Vitamin A Supplementation on Gene Expression of Cytokine Secreted by CD4+ T Lymphocyte in Multiple Sclerosis Patients

Clinical Trial Details — Status: Enrolling by invitation

Administrative data

• NCT number: NCT01407211
• Other study ID #: 89/8/18-10033
• Status: Enrolling by invitation
• Phase: Phase 4
• First received: February 14, 2011
• Last updated: July 17, 2012
• Start date: April 2011
• Est. completion date: September 2013

Study information

• Verified date: July 2012
• Source: Tehran University of Medical Sciences
• Contact: n/a
• Is FDA regulated: No
• Health authority: Iran: Ministry of Health
• Study type: Interventional

Clinical Trial Summary

The aim of this study is the comparison between the effects of supplementation with vitamin A (retinyl palmitate) or placebo for 6 months on gene expression of T CD4+ lymphocyte in multiple sclerotic patient.

Description:

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS).The most important reason for the limited success obtained in the treatment and prevention so far is most likely related to the limited knowledge about its cause and pathogenesis of MS.One of the recent proposed mechanism for autoimmunity base of MS is Th1/Th2 implance of as well as other inflammatory and anti-inflammatory T cell such as Th17 and Treg and their releasing cytokines. Therefore the control of cytokine production may become potential therapeutic targets and modulation of the Th1/Th2 balance may provide a new pharmacological tool to treat this disease. Vitamin A (VA) or VA-like analogs known as retinoids, are potent hormonal modifiers of type 1 or type 2 responses but a definitive description of their mechanism(s) of action is lacking. high level dietary vitamin A enhances Th2 cytokine production and IgA responses, and is likely to decrease Th1 cytokine production. Retinoic acid inhibits IL 12 production in activated macrophages, and RA pretreatment of macrophages reduces IFNγ production and increases IL4 production in antigen primed CD4 T cells. Supplemental treatment with vitamin A or retinoic acid (RA) decreases IFNγ and increases IL5, IL10, and IL4 production. Thus, vitamin A deficiency biases the immune response in a Th1 direction, whereas high level dietary vitamin A may bias the response in a Th2 direction.

Recruitment information / eligibility

• Status: Enrolling by invitation
• Enrollment: 30
• Est. completion date: September 2013
• Est. primary completion date: April 2013
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 20 Years to 45 Years

Eligibility

Inclusion Criteria:

Patients who have used interferon beta in last 3 months. Patients with 1-5 EDSS

Exclusion Criteria:

• Patients who have diseases which affect on Th1/Th2 balance such as asthma, active viral infections, and autoimmune diseases, OR

• Patients who have allergy to vitamin A compounds, OR

• Patients who have used vitamin supplements in last 3 months. -

Study Design

Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Treatment

Related Conditions & MeSH terms

• Multiple Sclerosis
• Multiple Sclerosis, Relapsing-Remitting
• Relapsing Remitting Multiple Sclerosis
• Sclerosis

Intervention

Dietary Supplement:
• vitamin A
25000 IU/day vitamin A 6 months 1 Cap/Day 1 cap placebo/day for 6 month

Locations

Country	Name	City	State
Iran, Islamic Republic of	Tehran University of Medical Sciences, School of Public Health	Tehran

Sponsors (1)

Lead Sponsor	Collaborator
Tehran University of Medical Sciences

Country where clinical trial is conducted

Iran, Islamic Republic of, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	serum Total cholesterol		Change from baseline at 6 months	No
Primary	serum HDL cholesterol		Change from baseline at 6 months	No
Primary	serum triglycerides level		Change from baseline at 6 months	No
Primary	RBP/ TTR ratio		Change from baseline at 6 months	No
Primary	PBMC's prolifration(BrdU colorimetric)		Change from baseline at 6 months	No
Primary	complete blood count (CBC)		Change from baseline at 6 months	No
Primary	serum SGOT concentration		Change from baseline at 6 months	No
Primary	serum SGPT concentration		Change from baseline at 6 months	No
Secondary	gene expression of T-bet, INF-gamma, IL-4, GATA3, IL-17, RORc, IL-10, FOXP3 (Relative quantification)		Change from baseline at 6 months	No