kageyd
12-04-2009, 09:53 AM
I have been fortunate in having at my side over the years throughout many illnesses a trained physiologist spouse who knows how to read the science articles about current research. He has, as always, been searching Google Scholar and other sources, and he explained some things to me about antibiotics and RA, a topic that has been addressed here. I asked him to write a little summary for the folks who post here on this Forum. Like so many things in medicine, the issues are very, very complex, and RA is one of those diseases that is poorly understood. No quick answers. I hope some of you find his summary informative.
Quote:
Over the past ten years, an increasing number of labs have documented some causative role for mycoplasmas in RA (and in other autoimmune diseases as well, e.g., fibromyalgia). There is a good bit of current research, especially in the U.S. and Japan, on just how the mycoplasma organisms actually damage the tissues in joints. There is considerable discussion in the literature of how some level of antibiotic treatment can reduce mycoplasma populations, and thus reduce the damage to tissues that is seen in RA. However, and this is a big however, repetitive use of antibiotics to reduce mycoplasma provides an environment throughout the body in which other pathogenic organisms may develop resistance to the antibiotics; this growth of antibiotic-resistant organisms in the body can lead to serious pathology in lung and other tissue. So while antibiotics like doxycycline and minocycline have clearly been shown to alleviate RA symptoms in some people in good clinical trials, this is not yet an acceptable clinical treatment because of the potential long-term side effects. There seems to be a sense in the rheumatology community that intensive use of antibiotics for RA should at this time be limited to severe cases. As usual , though, the definition of “intensive” and of “severe” is left to the individual rheumatologist, and certainly there are some rheumatologists who are prescribing heavy antibiotic doses for even mild RA cases.
Much of the research today is focused on the cellular mechanisms of action by which the mycoplasma triggers the events that result in damage in the joints. In other words, the more effective answer to addressing the mycoplasma population is not just in destroying it by antibiotics, but lies in “inactivating” the chemical mechanisms in the series of events by which the mycoplasmas cause their damage. This will eventually bring about a different set of chemical treatments that get at the cause of RA, rather than alleviate its symptoms. Unfortunately, no one has a projected timetable, however.
Quote:
Over the past ten years, an increasing number of labs have documented some causative role for mycoplasmas in RA (and in other autoimmune diseases as well, e.g., fibromyalgia). There is a good bit of current research, especially in the U.S. and Japan, on just how the mycoplasma organisms actually damage the tissues in joints. There is considerable discussion in the literature of how some level of antibiotic treatment can reduce mycoplasma populations, and thus reduce the damage to tissues that is seen in RA. However, and this is a big however, repetitive use of antibiotics to reduce mycoplasma provides an environment throughout the body in which other pathogenic organisms may develop resistance to the antibiotics; this growth of antibiotic-resistant organisms in the body can lead to serious pathology in lung and other tissue. So while antibiotics like doxycycline and minocycline have clearly been shown to alleviate RA symptoms in some people in good clinical trials, this is not yet an acceptable clinical treatment because of the potential long-term side effects. There seems to be a sense in the rheumatology community that intensive use of antibiotics for RA should at this time be limited to severe cases. As usual , though, the definition of “intensive” and of “severe” is left to the individual rheumatologist, and certainly there are some rheumatologists who are prescribing heavy antibiotic doses for even mild RA cases.
Much of the research today is focused on the cellular mechanisms of action by which the mycoplasma triggers the events that result in damage in the joints. In other words, the more effective answer to addressing the mycoplasma population is not just in destroying it by antibiotics, but lies in “inactivating” the chemical mechanisms in the series of events by which the mycoplasmas cause their damage. This will eventually bring about a different set of chemical treatments that get at the cause of RA, rather than alleviate its symptoms. Unfortunately, no one has a projected timetable, however.