Impact of Vitamin A on Gene Expression, in Multiple Sclerosis Patient (MS)
- Full Text View
- Tabular View
- No Study Results Posted
- Disclaimer
- How to Read a Study Record
Purpose
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.
| Condition | Intervention | Phase |
|---|---|---|
|
Relapsing Remitting Multiple Sclerosis |
Dietary Supplement: vitamin A |
Phase 4 |
| Study Type: | Interventional |
| Study Design: | Allocation: Randomized Endpoint Classification: Efficacy Study Intervention Model: Parallel Assignment Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor) Primary Purpose: Treatment |
| Official Title: | The Impact of Vitamin A Supplementation on Gene Expression of Cytokine Secreted by CD4+ T Lymphocyte in Multiple Sclerosis Patients |
- serum Total cholesterol [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- serum HDL cholesterol [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- serum triglycerides level [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- RBP/ TTR ratio [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- PBMC's prolifration(BrdU colorimetric) [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- complete blood count (CBC) [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- serum SGOT concentration [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- serum SGPT concentration [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
- gene expression of T-bet, INF-gamma, IL-4, GATA3, IL-17, RORc, IL-10, FOXP3 (Relative quantification) [ Time Frame: Change from baseline at 6 months ] [ Designated as safety issue: No ]
| Estimated Enrollment: | 30 |
| Study Start Date: | April 2011 |
| Estimated Study Completion Date: | September 2013 |
| Estimated Primary Completion Date: | April 2013 (Final data collection date for primary outcome measure) |
| Arms | Assigned Interventions |
|---|---|
|
Active Comparator: with Multiple Sclerosis/ vitamin A
Patients with Multiple Sclerosis confirmed Relapsing Remitting Type who receive 25000 IU/day vitamin A
|
Dietary Supplement: vitamin A
25000 IU/day vitamin A 6 months 1 Cap/Day 1 cap placebo/day for 6 month |
|
Placebo Comparator: with Multiple Sclerosis/ placebo
Patients with Multiple Sclerosis confirmed Relapsing Remitting Type who receive 1 cap of placebo/day
|
Dietary Supplement: vitamin A
25000 IU/day vitamin A 6 months 1 Cap/Day 1 cap placebo/day for 6 month |
Detailed 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.
Eligibility| Ages Eligible for Study: | 20 Years to 45 Years |
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | No |
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. -
Contacts and Locations More Information
No publications provided
| Responsible Party: | Tehran University of Medical Sciences |
| ClinicalTrials.gov Identifier: | NCT01407211 History of Changes |
| Other Study ID Numbers: | 89/8/18-10033 |
| Study First Received: | February 14, 2011 |
| Last Updated: | July 17, 2012 |
| Health Authority: | Iran: Ministry of Health |
Keywords provided by Tehran University of Medical Sciences:
|
multiple sclerosis Myelin Oligodendrocyte Glycoprotein(MOG) Vitamin A CD4-Positive T-Lymphocytes |
gene expression Th1 Cells Th2 Cells |
Additional relevant MeSH terms:
|
Multiple Sclerosis Sclerosis Multiple Sclerosis, Relapsing-Remitting Demyelinating Autoimmune Diseases, CNS Autoimmune Diseases of the Nervous System Nervous System Diseases Demyelinating Diseases Autoimmune Diseases Immune System Diseases Pathologic Processes Vitamin A Vitamins |
Retinol palmitate Micronutrients Growth Substances Physiological Effects of Drugs Pharmacologic Actions Antioxidants Molecular Mechanisms of Pharmacological Action Protective Agents Anticarcinogenic Agents Antineoplastic Agents Therapeutic Uses |
ClinicalTrials.gov processed this record on June 17, 2013