Impact of Vitamin A on Multiple Sclerosis (MS)

• Expanded Disability Status Scale (EDSS) [ Time Frame: Change from baseline at 12 months ] [ Designated as safety issue: No ]
  Expanded Disability Status Scale (EDSS) as a measure of activity and progression of MS disease
  
  
• Multiple Sclerosis Functional Composite (MSFC) [ Time Frame: Change from baseline at 12 months ] [ Designated as safety issue: No ]
  Multiple Sclerosis Functional Composite (MSFC) as a measure of activity and progression of MS disease
  
  
• fatigue scores [ Time Frame: Change from baseline at 12 months ] [ Designated as safety issue: No ]
  fatigue scores on Multiple Sclerosis Fatigue Impact Scale
  
  
• depression score [ Time Frame: Change from baseline at 12 months ] [ Designated as safety issue: No ]
  depression score on Beck Depression Inventory 2
  
  
• Number of active lesion in magnetic resonance imaging (MRI) number of active lesion in brain MRI [ Time Frame: Change from baseline at 12 months ] [ Designated as safety issue: No ]
  Number of active lesion in magnetic resonance imaging (MRI) as a measure of activity and progression of MS disease
  
  

• number of disease relapses [ Time Frame: Change from baseline at 12 months ] [ Designated as safety issue: No ]
  To measure the effect of vitamin A supplementation on number of disease relapses
  
  

Multiple Sclerosis (MS) is a chronic inflammatory disease where Th1 like responses from myelin-specific CD4+ T cells, as secretion of pro-inflammatory IFNγ, are believed to play a major role in the pathogenesis. The myelin-specific T cells that mediate tissue destruction in MS are believed to become activated outside the central nervous system (CNS) in lymphoid tissue and when they cross the blood brain barrier they will re-encounter their antigen. Immune deviation is the redirection of the immune response from most often Th1 like responses to Th2 like responses, even though the opposite can also occur. Vitamin A or Vitamin A-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(RA) inhibits IL12 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 RA decreases IFNγ and increases IL5, IL10, and IL4 production.