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For people with ALS, from the start, prescribe Rilutek

Information on Amyotrophic Lateral Sclerosis

What is ALS?

  • ALS, or amyotrophic lateral sclerosis, is a chronic progressive disease characterized by selective degeneration of motor neurons that control voluntary muscle movement1,2
    • Amyotrophic means “without muscle nourishment” and refers to the loss of signals these neurons normally send to the muscles
    • Lateral refers to the location of damage to the spinal cord.
    • Sclerosis, or “hardened,” characterizes the nature of the spinal cord in advanced ALS2
  • The incidence of ALS is 2 per 100,000 people,3,4 and it is estimated that as many as 30,000 Americans have the disease at any given time.3
  • Although it can affect anyone, ALS is most common in the 40- to 70-year age range.4
  • About 20% of people with ALS live 5 years or more from the time of diagnosis, and up to 10% will survive more than 10 years.4
  • In the US, ALS is also known as Lou Gehrig’s disease, after the New York Yankee and National Baseball Hall of Fame first baseman, who was one of the first famous people to become ill with ALS in the early 1940s.2

Forms of ALS

Three classifications of ALS have been described:4

  • Sporadic is the most common form in the US, comprising 90% to 95% of cases.
  • Familial accounts for 5% to 10% of all cases.
  • Guamanian, named for an extremely high incidence of ALS observed in Guam and the Trust Territories of the US in the 1950s.

Causes of ALS

Although the cause of ALS is not completely understood, recent research suggests that glutamate, the excitatory amino acid neurotransmitter, may be involved in the pathophysiology of the disease.1

  • Elevated plasma glutamate levels have been observed in patients with Early stage ALS.5
  • Glutamate has neurotoxic properties and can produce lesions resembling human neurodegenerative disorders.5
  • Abnormally enhanced glutamatergic neurotransmission may cause excitotoxic cell damage and lead to neuronal death.6,7

Clinical Progression of ALS

Muscle weakness is a hallmark initial sign in ALS, occurring in about 60% of patients. The course of the disease may include the following:4

  • Muscle weakness in the hands, arms, and/or legs, or the muscles of speech, swallowing, and/or breathing.
  • Twitching and cramping of muscles, especially in hands and feet.
  • Impairment of use of arms and legs.
  • “Thick speech” and difficulty in projecting voice.
  • Shortness of breath, difficulty in breathing and swallowing in more advanced stages.
 
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Important Treatment Considerations

  • Evaluate serum ALT levels every month during the first 3 months of treatment, and every 3 months during the remainder of the first year. Thereafter, serum ALT levels should be periodically evaluated more frequently in patients who develop elevations. Rilutek should be discontinued if ALT levels increase to 5 times ULN or if clinical jaundice develops.
  • Advise patients about the potential for dizziness, vertigo, or somnolence and not to drive or operate machinery until they have sufficient experience on Rilutek.
  • Advise patients to report any febrile illness; measure WBCs.
  • Use Rilutek with caution in patients with concomitant liver insufficiency; caution should be exercised when prescribing Rilutek to patients taking drugs that are potentially hepatotoxic or highly protein bound:
    • Interactions may also occur when riluzole is given concurrently with agents that affect hepatic CYP 1A2 activity.*
*CYP 1A2 is the principal isoenzyme involved in the initial oxidative metabolism of riluzole. CYP 1A2 inhibitors, such as amitriptyline, caffeine, phenacetin, theophylline, or quinolones, may potentially decrease the rate of riluzole elimination. CYP 1A2 inducers, such as cigarette smoke, charcoal-broiled food, rifampicin, or omeprazole, may potentially increase the rate of elimination.
 
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References

  1. Rothstein JD, Martin LJ, Kuncl RW. Decreased glutamate transport by the brain and spinal cord in amyotrophic lateral sclerosis. N Engl J Med. 1992;326:1464-1468.
  2. Facts About Amyotrophic Lateral Sclerosis (ALS). Muscular Dystrophy Association, ALS Division website. Available at http://als-mda.org/publications/fa-als.html. Accessed May 11, 2007.
  3. Bromberg M. Accelerating the diagnosis of amyotrophic lateral sclerosis. The Neurologist. 1999;5:63-74.
  4. Facts you should know about ALS. The ALS Association website. Available at http://www.alsa.org/als/what.cfm?CFID=3664013&CFTOKEN=28694482. Accessed May 11, 2007.
  5. Plaitakis A, Caroscio JT. Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann Neurol. 1987;22:575-579.
  6. Choi DW. Amyotrophic lateral sclerosis and glutamate—too much of a good thing? N Engl J Med. 1992;326:1493-1495.
  7. Greenamyre JT. The role of glutamate in neurotransmission and in neurologic disease. Arch Neurol. 1986;43:1058-1063.
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US.RIL.07.07.001 Last Update: May 2007