TNF inhibitor
Overview
Tumor necrosis factor (TNF) promotes the inflammatory response, which in turn causes many of the clinical problems associated with autoimmune disorders such as rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, psoriasis and refractory asthma. These disorders are sometimes treated by using a TNF inhibitor. This inhibition can be achieved with a monoclonal antibody such as infliximab (Remicade) or adalimumab (Humira), or with a circulating receptor fusion protein such as etanercept (Enbrel).
Clinical trials regarding the effectiveness of these drugs on hidradenitis suppurativa are currently ongoing. A fourth anti-TNF biologic, certolizumab pegol, is expected to receive approval for human use in the near future.
In patients with latent Mycobacterium tuberculosis infection, active tuberculosis (TB) may develop soon after the initiation of treatment with infliximab.[1] Before prescribing the drug, physicians should screen patients for latent TB infection or disease. The anti-TNF monoclonal antibody biologics, Infliximab and adalimumab, and the fusion protein etanercept which are all currently Food and Drug Administration (FDA) approved for human use, have label warnings which state that patients should be evaluated for latent TB infection and treatment should be initiated prior to starting therapy with these medications.
TNF or the effects of TNF are also inhibited by a number of natural compounds, including curcumin [2] [3] [4] [5] (a compound present in turmeric) and catechins (in green tea).
References
- ↑ "Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent". N Engl J Med. 345 (15): 1098–104. 2001. PMID 11596589.
- ↑ "The anti-inflammatory effect of curcumin in an experimental model of sepsis is mediated by up-regulation of peroxisome proliferator-activated receptor-gamma". Crit Care Med. 34 (7): 1874–82. 2006. PMID 16715036.
- ↑ "Curcumin protects against radiation-induced acute and chronic cutaneous toxicity in mice and decreases mRNA expression of inflammatory and fibrogenic cytokines". Int J Radiat Oncol Biol Phys. 65 (3): 890–8. 2006. PMID 16751071.
- ↑ "Effects of curcumin on tumour necrosis factor-alpha and interleukin-6 in the late phase of experimental acute pancreatitis". J Vet Med A Physiol Pathol Clin Med. 53 (1): 49–54. 2006. PMID 16411910.
- ↑ "The effect of turmeric extracts on inflammatory mediator production". Phytomedicine. 12 (6–7): 445–52. 2005. PMID 16008121.
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