Although there is still not enough
evidence to determine a causal relationship between the associate of GBS and anti-TNF-?
therapy. Physicians should still monitor patients who are receiving anti-TNF-?
therapy for neurologic signs and symptoms of demyelinating diseases and should
rule out other causes especially GBS presented as a paraneoplastic syndrome. If
indeed their neurological disorder was associated with the use of an anti-TNF-alpha
agent like infliximab, clinician shoulder considers stopped the agent or switching
to a different TNF-? antagonist or different class of medications.
Anti-TNF-? medications have been reported to be
associated with multiple disorders including the central and the peripheral
nerves systems 2-3. Over the years, infliximab, one of earliest anti-TNF
alpha antagonists agent for treating inflammatory
arthrtitis and complicated Crohn’s
disease with fistula hashave
been report to have rare association with severe demyelinating diseaseDKH2 MZ3 3.
GBS is defined as an acute autoimmune polyradiculoneuropathy that has rapid
evolvement within hours to days of ascending muscle weakness and sensory loss
with areflexia especially in lower extremities 3. The disease may progress to
involve the respiratory muscles causing patients to have respiratory distress
needing intubation. Diagnostic criteria for GBS include the above mentioned
physical findings with characteristic CSF findings of albuminocytologic