Tumor necrosis factor (TNF) inhibitors

Associated with increase frequency of tuberculosis in patients treated for rheumatoid arthritis.

Effective in the treatment of rheumatoid arthritis, and is the first line biologic therapy in its management.

Tumor necrosis factor inhibitors show no significant difference in efficacy in rheumatoid arthritis.

Used to treat ankylosing spondylitis, psoriasis and psoriatic arthritis and inflammatory bowel disease,rheumatoid arthritis, and Crohn’s disease

Increase susceptibility to minor respiratory infections.

Associated with congestive heart failure, demyelinating diseases, and a lupus like syndrome.

Increased risk of opportunistic infections caused by bacteria, mycobacteria, fungus, viruses, Legionella and Listeria.

2011 Cochrane review found biologic users have a 55% increase risk of serious infection among patients with rheumatoid arthritis.

Most patients are screened with tuberculosis skin tests prior to starting such agents.

If patients have a positive tuberculosis skin test anti-tuberculosis drugs are given before or concurrently with anti-TNF-alpha drugs.

Associated with increased frequency of fungal infections.

Controlled studies indicate TNF inhibitors not significantly associated with increased malignancy risk.

Increase in spontaneous lymphoma in children and adolescents.

Increased reports of hepatosplenic T-cell lymphoma primarily in adolescents and young adults being treated with TNF-alpha inhibitors for Crohn’s disease and ulcerative colitis.


In a review of 63 randomized control studies with 29,243 patients with rheumatoid arthritis treated with biological response modifiers, no significant association with increased risk of malignancy was noted compared to other disease- modifying anti rheumatic drugs or placebo (Lopez- Olivo, MA et al).

Met analysis 23 studies:such agents no increased all-cause mortality in RA (Poiroux L et al).

Induction of autoantibody production with development of lupus like syndrome has prevalence of 0.5% to 1% in treated patients (Aringer M).

Adalimumab and infliximab associated with increased risk of herpes zoster infections in patients treated for rheumatoid arthritis, but the receptor fusion protein etanercept is not (Strangfeld).

Use frequently associated with induction of auto antibodies, but the development of lupus like syndrome is uncommon with the prevalence of 0.5-1% in treated patients (Aringer M et al).

In a retrospective study of patients treated with TNF-alpha antagonists for rheumatoid arthritis, inflammatory bowel disease, psoriasis, psoriatic arthritis, or ankylosing spondylitis compared with patients treated with non-biologic agents, and the former was not associated with an increased risk of hospitalization for serious infections(Grijalva CG et al).

In the above analysis infliximab initiated for rheumatoid arthritis was significantly associated with an increased risk of serious infections compared with other TNF-alpha antagonist regimens and non-biologic comparator medications.

A number of meta-analyses demonstrate the use of TNF-alpha antagonists increased the risk of infections, mainly in patients with rheumatoid arthritis.

TNF-alpha antagonists increased the risk of infections by 1.2-2.0 full compared with placebo.

A meta-analysis of trials of TNF-alpha antagonists among patients treated with IBD report no differences in the frequency of serious infections between anti-TNF and placebo-controlled groups (Curtis JR et al).

TNF Inhibitors can improve patients with common Chronic immune mediated inflammatory diseases, however, approximately 20-55% of patients do not respond to these therapies, resulting in reduced quality-of-life and risk of irreversible organ damage and disability.
Lack of response to TNF inhibitors has been attributed to an immune response against the drug, leading to the formation of anti-drug antibodies.
Anti-bodies against TNF Inhibitors reduce serum drug levels and are associated with adverse effects such as infusion reactions.

Infliximab chimeric antibody is more immunogenic than other TNF Inhibitors, and anti-body formation is particularly common during initiation of this drug.

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