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

This study is enrolling participants by invitation only.
Sponsor:
Information provided by (Responsible Party):
Tehran University of Medical Sciences
ClinicalTrials.gov Identifier:
NCT01407211
First received: February 14, 2011
Last updated: July 17, 2012
Last verified: July 2012
  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

Resource links provided by NLM:


Further study details as provided by Tehran University of Medical Sciences:

Primary Outcome Measures:
  • 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 ]

Secondary Outcome Measures:
  • 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
Criteria

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
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01407211

Locations
Iran, Islamic Republic of
Tehran University of Medical Sciences, School of Public Health
Tehran, Iran, Islamic Republic of
Sponsors and Collaborators
Tehran University of Medical Sciences
  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
Multiple Sclerosis, Relapsing-Remitting
Sclerosis
Autoimmune Diseases
Autoimmune Diseases of the Nervous System
Demyelinating Autoimmune Diseases, CNS
Demyelinating Diseases
Immune System Diseases
Nervous System Diseases
Pathologic Processes
Retinol palmitate
Vitamin A
Vitamins
Anticarcinogenic Agents
Antineoplastic Agents
Antioxidants
Growth Substances
Micronutrients
Molecular Mechanisms of Pharmacological Action
Pharmacologic Actions
Physiological Effects of Drugs
Protective Agents
Therapeutic Uses

ClinicalTrials.gov processed this record on October 23, 2014