RESEARCH - TNF-alpha antagonists and neuropathy

[Guest guest]

Muscle Nerve. 2008 Mar;37(3):281-92.

Tumor necrosis factor-alpha antagonists and neuropathy.

Stübgen JP.

Department of Neurology and Neuroscience, Cornell University Medical

College, New York Presbyterian Hospital, 525 East 68th Street, New

York, NY 10065-4897, USA.

Tumor necrosis factor (TNF)-alpha plays an important role in many

aspects of immune system development, immune-response regulation, and

T-cell-mediated tissue injury. The evidence that TNF-alpha, released

by autoreactive T cells and macrophages, may contribute to the

pathogenesis of immune-mediated demyelinating neuropathies is

reviewed. TNF-alpha antagonists (infliximab, etanercept, adalimumab)

are indicated for the treatment of advanced inflammatory rheumatic and

bowel disease, but these drugs can induce a range of autoimmune

diseases that also attack the central and peripheral nervous systems.

Case histories and series report on the association between

anti-TNF-alpha treatment and various disorders of peripheral nerve

such as Guillain-Barré syndrome, Fisher syndrome, chronic

inflammatory demyelinating polyneuropathy, multifocal motor neuropathy

with conduction block, mononeuropathy multiplex, and axonal

sensorimotor polyneuropathies. The proposed pathogeneses of

TNF-alpha-associated neuropathies include both a T-cell and humoral

immune attack against peripheral nerve myelin, vasculitis-induced

nerve ischemia, and inhibition of signaling support for axons. Most

neuropathies improve over a period of months by withdrawal of the

TNF-alpha antagonist, with or without additional immune-modulating

treatment. Preliminary observations suggest that TNF-alpha antagonists

may be useful as an antigen-nonspecific treatment approach to

immune-mediated neuropathies in patients with a poor response to, or

intolerance of, standard therapies, but further studies are required.

PMID: 18041052

http://www.ncbi.nlm.nih.gov/pubmed/18041052

--

Not an MD