The Effect of Vitamin A on Atherosclerosis

This study is enrolling participants by invitation only.
Sponsor:
Information provided by:
Tehran University of Medical Sciences
ClinicalTrials.gov Identifier:
NCT01414972
First received: February 14, 2011
Last updated: August 10, 2011
Last verified: August 2011
  Purpose

The aim of this study is the comparison between the effects of supplementation with 25000 IU preformed vitamin A (retinyl palmitate) or placebo for 4 months on gene expression of T CD4+ lymphocyte in atherosclerotic patients(documented with angiography).


Condition Intervention Phase
Atherosclerosis
Drug: Vitamin A
Drug: placebo
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: Prevention
Official Title: The Effect of Vitamin A Supplementation on Gene Expression of Cytokine Secreted by T CD4+ Lymphocyte in Atherosclerotic 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 4 months ] [ Designated as safety issue: No ]
  • serum HDL cholesterol [ Time Frame: Change from baseline at 4 months ] [ Designated as safety issue: No ]
  • serum triglycerides level [ Time Frame: Change from baseline at 4 months ] [ Designated as safety issue: No ]
  • RBP/ TTR ratio [ Time Frame: Change from baseline at 4 months ] [ Designated as safety issue: No ]
  • PBMC's proliferation (BrdU colorimetric) [ Time Frame: Change from baseline at 4 months ] [ Designated as safety issue: No ]
  • complete blood count (CBC) [ Time Frame: Change from baseline at 4 months ] [ Designated as safety issue: No ]
  • SGOT [ Time Frame: Change from baseline at 4 months ] [ Designated as safety issue: No ]
  • SGPT [ Time Frame: Change from baseline at 4 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 4 months ] [ Designated as safety issue: No ]

Enrollment: 45
Study Start Date: May 2010
Estimated Study Completion Date: November 2011
Primary Completion Date: January 2011 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Active Comparator: patients with atherosclerosis/ vitamin A
patients with angiographically confirmed CAD (defined as luminal stenosis ≥50% in at least one major coronary artery branch)who receive 25000 IU/day vitamin A
Drug: Vitamin A
1 cap vitamin A 25000 IU/day for 3 month
Placebo Comparator: patients with atherosclerosis/ placebo
patients with angiographically confirmed CAD (defined as luminal stenosis ≥50% in at least one major coronary artery branch)who receive placebo
Drug: placebo
1 cap placebo/day for 3 month
Active Comparator: people without athrosclerosis/ vitamin a
people in whom significant (e.g. stenosis ≥ 50%) CAD is ruled out by coronary angiography, who receive 2500 Iu/day vitamin A
Drug: Vitamin A
1 cap vitamin A 25000 IU/day for 3 month

Detailed Description:

Atherosclerosis, the leading cause of death and disability in the world, is considered an inflammatory disease with a complex etiology. The immune system has a prominent role in the formation, development and destabilization of atherosclerotic plaques. A whole range of identified cytokines have been shown to play a part in atherogenesis, some with proatherogenic properties while others having antiatherogenic properties. With increasing evidence for the significant role of inflammation and the cytokines involved together with the Th1/Th2 imbalance in atherosclerosis and its progression to Coronary artery diseases (CADs), 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:   35 Years to 70 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

• The criteria for enrollment of the patients and control subjects is consecutive patients of both sexes referred to the Division of Cardiology of the one of the Hospitals of Tehran University of Medical Sciences for coronary angiography for investigation of chest pain and/or suspected CAD.

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
Please refer to this study by its ClinicalTrials.gov identifier: NCT01414972

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
Investigators
Study Chair: Ali Akbar saboor Yaraghi, PhD Tehran University of Medical Sciences
Principal Investigator: Azadeh Mottaghi, PhD student Tehran University of Medical Siences
  More Information

No publications provided

Responsible Party: Ali Akbar Saboor Yaraghi /Assistant Professor, Tehran University of Medical Sciences
ClinicalTrials.gov Identifier: NCT01414972     History of Changes
Other Study ID Numbers: 89-01-27-10471
Study First Received: February 14, 2011
Last Updated: August 10, 2011
Health Authority: Iran: Ministry of Health

Keywords provided by Tehran University of Medical Sciences:
Atherosclerosis
Coronary Artery Disease
Vitamin A
CD4-Positive T-Lymphocytes
gene expression

Additional relevant MeSH terms:
Atherosclerosis
Arteriosclerosis
Arterial Occlusive Diseases
Vascular Diseases
Cardiovascular Diseases
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 April 14, 2014