Tropical Myeloneuropathies Medication

  • Author: Eliad Culcea, MD; Chief Editor: Karen L Roos, MD   more...
 
Updated: Jan 14, 2011
 

Medication Summary

HAM/TSP

A multicenter, randomized, double-blind study in 48 patients indicated that treatment with subcutaneous interferon alfa (Roferon) 3 million U (MU) twice a week was effective in more than 66.7%.[11] In another study, 32 patients were treated with interferon alfa; 20 patients showed a fair-to-excellent response in motor function. The effect was sustained, however, for only 1-3 months after the last injection.[9]

An open-label study showed that pentoxifylline 300 mg PO once a day induced clinical improvement in 14 of 15 patients. The authors postulated that the effect probably was due to TNF-alpha suppression.[12] In a recent open-label trial, 12 patients with HAM/TSP were treated with doses of interferon beta-1a of up to 60 µg twice weekly. During the trial, the therapy reduced the HTLV-1 tax messenger RNA load, but the HTLV-1 proviral DNA load remained unchanged. Some measures of motor function were improved, and no significant clinical progression occurred during therapy.[13]

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Interferons

Class Summary

These agents are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions.

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Interferon alfa 2a (Roferon-A)

 

Highly purified protein containing 165 amino acids, has approximate molecular weight of 19,000 Daltons. Mechanism of action not clearly understood; however, modulation of host immune response may play important role.

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Interferon beta-1a (Avonex, Rebif)

 

For treatment of relapsing remitting MS. Avonex has also gained approval for treating patients with a first MS attack if brain MRI shows abnormalities characteristic of MS. Believed to act via ability to counteract cell surface expression of proinflammatory or pro-adhesion molecules on immune cells, among other effects. More studies needed to fully understand mechanisms of action. Only differs from interferon beta-1b in that it has amino acid sequence identical to that of natural compound and is glycosylated. Presence of glycosylation may lead to structural stability and presumably to higher biological potency.

Interferons act through common receptor that activates Jak/Stat pathway of signal transduction molecules, which, in turn, lead to activation of interferon-responsive genes. Interferon beta may decrease expression of B7-1 (a proinflammatory molecule) on surface of immune cells and increase levels of TGF-beta (anti-inflammatory) in circulation of MS patients. Interferon beta-1a is most convenient ABC drug to administer due to weekly schedule.

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Blood viscosity reducer agents

Class Summary

These agents decrease the viscosity of blood.

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Pentoxifylline (Trental)

 

May alter rheology of red blood cells, which, in turn, reduces blood viscosity

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Contributor Information and Disclosures
Author

Eliad Culcea, MD  Consulting Staff, Department of Neurology, Great Falls Clinic

Eliad Culcea, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Friedhelm Sandbrink, MD  Assistant Professor of Neurology, Georgetown University School of Medicine; Assistant Clinical Professor of Neurology, George Washington University School of Medicine and Health Sciences; Director, EMG Laboratory and Chief, Chronic Pain Clinic, Department of Neurology, Washington Veterans Affairs Medical Center

Friedhelm Sandbrink, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Specialty Editor Board

Carmel Armon, MD, MSc, MHS  Professor of Neurology, Tufts University School of Medicine; Chief, Division of Neurology, Baystate Medical Center

Carmel Armon, MD, MSc, MHS is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American College of Physicians, American Epilepsy Society, American Medical Association, American Neurological Association, American Stroke Association, Massachusetts Medical Society, Movement Disorders Society, and Sigma Xi

Disclosure: Avanir Pharmaceuticals Consulting fee Consulting

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed  Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

Disclosure: Nothing to disclose.

Chief Editor

Karen L Roos, MD  John and Nancy Nelson Professor of Neurology, Professor of Neurological Surgery, Department of Neurology, Indiana University School of Medicine

Karen L Roos, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association

Disclosure: Nothing to disclose.

References

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Light microscopy of thoracic spinal cord of 2 patients with HTLV-1–associated myelopathy (Klüver-Barrera staining). (Source: Aye et al, 2000, Fig. 1.)
Light microscopy of perivascular inflammatory infiltration in the spinal cord (A, C) and in the brain (B, D) (A, B H&E; C, D Elastica Van Gieson; A, C x400; B, D x200). (Source: Aye et al, 2000, Fig. 2.)
Light microscopy of the middle thoracic spinal cord (A, C, E) and subcortical white matter of the brain (B, D, F). Fibrotic changes are seen even in the capillaries (arrows) (A, B, F H&E; C-E Elastica van Gieson; A, C, D, F x400; B x300; E x100). (Source: Aye et al, 2000, Fig. 3.)
Immunostaining of the infiltrating cells in the thoracic spinal cord (A, C, E) and subcortical white matter of the brain (B, D, F) (A, B UCHL-1 [antibody to CD45RO]; C, D CD8; E, F OPD-4; A-F x150). (Source: Aye et al, 2000, Fig. 4.)
Immunostaining of the infiltrating cells in the thoracic spinal cord (A, C) and subcortical white matter of brain (B, D) (A, B UCHL-1[antibody to CD45RO]; C, D CD8; A-D x160). (Source: Aye et al, 2000, Fig. 5.)
 
 
 
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