Among the dozens of thousands of studies on Crohn’s disease, all effective treatments, from the different small molecules to biologics, are related to immune suppression, which would be a straight indication that CD is associated with an enhanced immune reaction.
We already have a detailed discussion on this early (see post #164). I would like to repost some of that post here.
"I also felt the notion that the high efficacy of the immune suppression agents like inflixmab and 6-MP is largely due to their [wiki2="Bactericidal"]bactericidal[/wiki2] activity on MAP a fascinating idea, but I just wonder how this miracle occurred. A study (Greenstein RJ, et al. On the action of methotrexate and 6-mercaptopurine on M. avium subspecies paratuberculosis. PLoS One. 2007 Jan 24;2(1):e161) showed that although 6-MP have some inhibition on the growth of MAP, its activity is still much lower than some antibiotics like clarithromycin (4 ug/ml 6-MP versus 0.5 ug/ml clarithromycin to cause 80% growth inhibition of the bacteria). For the treatment of IBD, 6-MP is usually used in a dose below 100 mg/day and lasted for several weeks. However, in the study by Selby W, et al. (Antibiotics in Crohn's Disease Study Group. Two-year combination antibiotic therapy with clarithromycin, rifabutin, and clofazimine for Crohn's disease. Gastroenterology. 2007 Jun;132(7):2313-9), even clarithromycin used at 750 mg/day, along with 450 mg/day rifabutin and 50 mg/day clofazimine to treat the patients with Crohn’s disease for up to two years failed to show evidence of sustained benefit. I just cannot image how 6-MP, with much less bactericidal capability and used at a much lower dose and in such a short period can achieve the effective treatment for Crohn’s disease through the claimed killing of MAP".
Again, what is your explanation for the close relationship between the epidemiological distribution of UC and CD in the world?
