249from corticosteroid therapy [ 70 ]. Autoantibodies, particularly ANA, tend to decrease
or disappear after corticosteroid therapy [ 70 , 71 ].
Although there is limited data to guide management, corticosteroid therapy is
generally indicated if there is no improvement in liver enzymes within 2 months
after withdrawal from the offending agent [ 71 ]. There is currently no standard dos-
ing or duration of corticosteroid therapy for treatment of anti-TNF-associated hepa-
totoxicity. However, an attempt to withdraw corticosteroid should be considered
once liver enzymes normalize.
Rechallenging with another anti-TNF therapy may be considered, particularly in
case where alternate therapy is not available. In the rheumatology literature, patients
who had hepatotoxicity attributed to infliximab or adalimumab subsequently toler-
ated etanercept [ 72 – 75 , 77 ]. In the study by Bjornsson et al., one patient previously
treated with infliximab for treatment of CD developed adalimumab-associated hep-
atotoxicity; the patient was later able to tolerate restarting infliximab without recur-
rence of hepatotoxicity [ 71 ]. More data is needed in guidance on management of
anti-TNF-associated hepatotoxicity, particularly in the IBD population.
Demyelinating Diseases
Clinical Manifestation
Demyelinating disease associated with anti-TNF therapy is rare, with prevalence
ranging between 0.05 and 0.2% for infliximab, etanercept, and adalimumab [ 78 ]. In
comparison, the incidence of multiple sclerosis (MS) in the general population is
Fig. 14.4 Liver biopsy
showing mild mixed
inflammation with
scattered plasma cells.
There is mild interface
hepatitis and focal
hepatocellular loss (arrow).
Image was provided by
William Twaddell, MD
14 Noninfectious and Nonmalignant Complications of Anti-TNF Therapy