Ankylosing spondylitis is a chronic, inflammatory disease that has structure-modifying effects from tumor necrosis factor alpha inhibition. Tumor necrosis factor antagonist therapy may suggest some benefit, at least in the short term.
Before this treatment, ankylosing spondylitis therapy included suppression of inflammatory response usually with nonsteroidal anti-inflammatory drugs to delay disease progression. However, new treatment are based on tumor necrosis factor antagonists suchs as humira, enbrel, and remicade that have all been approved by the US Food and Drug administration for the treatment of ankylosing spondylitis. All of these drugs had studies performed on them, and the results were given in the articles.
Studies were performed for these three treatments, but concerns with the study include the lacking of true placebo groups because NSAID therapy alone may reduce radiographic progression in ankylosing spondylitis. Also, there is no reliable method to predict at an early stage wich ankylosing spondylits patients will develop significant structural damage.
The reason I LOVED this article was because at the end of every study, the authors gave reasons why the study may not be valid. When reading these reports, it is often difficult to understand what is being studied and what the results imply. Even if you do understand this part, it is still difficult to understand if the study was valid or not. This paper gives examples of how to critique and analyze studies.
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If tumor necrosis factor antagonists are being unveiled as a promising therapeutic in AS, then why does it seem that they are not as popular in joint diseases? It seems to me that their application before antioxidant treatment in joint diseases would be beneficial, since the overproduction of TNF-alpha is associated with the inhibition of antioxidant enzymes in joint inflammation. In other words, if we halt TNF-alpha production first, would we then not make antioxidant treatment more effective?
New Therapeutic approaches for spondyloarthritis. Manadan A.M., et al. Curr Opin Rheumatol 19:259-264 (2007)
Does TNF-a inhibit antioxidant systems directly? Or does it increase degredation, reduce steady-state levels, or decrease necessary co-enzyme levels? If the first is true, i.e. that TNF-a physically inhibits these enzymes, then the antagonist alone would be great. Otherwise, you would likely be correct...though antioxident treatment for other diseases has ranged from null effect to mildy useful.
Long has been known the association between certain HLA alleles and disease. A large proportion of patients with AS also have the HLA allele B*27. This is an interesting association, creating a plausible genetic factor in the association of complex disease. It seems that new therapies are also directed at a genotype-specific level. For example, the self-peptide that is presented in the MHC molecules of HLA-B*27 positive individuals could be antagonized using a different ligand than those that are AS+ B*27-. This "tailored" therapy makes things a bit more complicated.
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