Glatiramer Acetate for Multiple Sclerosis With Autoimmune Comorbidities
Condition: Relapsing Remitting Multiple Sclerosis
MeSH terms: Multiple Sclerosis; Multiple Sclerosis, Relapsing-Remitting; Sclerosis
Study type: Observational

Summary: 
      The incidence of autoimmune conditions is at least 2-3 times higher in Multiple Sclerosis
      population than in general population. These MS patients category response unfavorably to the
      Interferon. The investigators suggest that autoimmune co morbidity can serve as a biological
      marker predicting good response to GA.
    

Detailed description: 
      Multiple Sclerosis (MS) is an auto-immune neurodegenerative disease that affects more than
      400,000 individuals in the United States, and 2.5 million worldwide
      (www.nationalmssociety.org). The main pathogenic mechanism in MS involves an inflammatory
      condition that damages the myelin of the central nervous system (CNS), resulting in axonal
      damage and neurological impairment, often leading to severe disability. MS is one of the most
      common causes of neurological disability in young and middle-aged adult individuals, and as
      such has a tremendous physical, psychological and social impact on patients' lives. MS is a
      complex disease diagnosed by McDonald criteria with different clinical and pathological
      phenotypes. Several forms of MS have been described: Relapsing-Remitting (RRMS),
      Secondary-Progressive MS (SPMS), Progressive-Relapsing MS (PRMS), and Primary-Progressive MS
      (PPMS).

      Glatiramer Acetate (GA) and Beta-Interferons (β-IFNs) are well established first-line
      immunomodulating treatment options for relapsing remitting multiple sclerosis (RRMS) with
      excellent safety profiles. The mechanisms of action of GA and IFNs are different. It is well
      known that in general Disease-Modifying Treatments (DMTs) reduce relapse rate in more than
      half of the multiple sclerosis (MS) patients who receive DMT, while having little if any
      effect on the rest. It has been speculated that the response to beta-interferons or GA may
      have genetic basis. As Axtell RC et al. indicated the experimental autoimmune
      encephalomyeilits (EAE) in mouse caused by TH1 cells generally respond well to
      interferon-beta, while EAE caused by TH17 cells get worse with interferon-beta.

      Autoimmune disease is an extreme situation where the autoimmune response overshoots and goes
      out of control. The other extreme is a degenerative disorder, where the autoimmune response
      is not strong enough for effective protection, and degeneration therefore continues. GA being
      an immunomodulator may provide both properly regulated immune suppression (in the case of
      autoimmune disease) and properly regulated immune activation (in the case of the
      neurodegenerative disease).

      Autoimmune conditions cluster in families with high risk for multiple sclerosis than in
      general population which suggests that the disease might arise on a background of a
      generalized susceptibility to autoimmunity. Occurrence of psoriasis, autoimmune thyroiditis,
      vasculitis, rheumatoid arthritis, scleroderma, lupus are seen more commonly in MS patients.
      Many of these patients initially get started on beta-IFNs, and usually do not do well on
      them. According to Investigator's and the USC MS Comprehensive Care Center experience,
      autoimmune co-morbidity associated with MS can serve as a biological marker predicting good
      response to GA and unfavorable response to the IFNs.
    

Observational model: Cohort
Time perspective: Prospective
Sampling method: Non-Probability Sample
Study population: 
        All Subjects meeting inclusion/exclusion criteria.
      
Keywords: RRMS; Multiple Sclerosis; Glatiramer Acetate; Autoimmune Comorbidities; Psoriasis; Autoimmune Thyroiditis; Vasculitis; Rheumatoid Arthritis