Guest guest Posted May 14, 2005 Report Share Posted May 14, 2005 The fluoroquinolones have a lot of attractive features (especially the newer ones with the C8-methoxyl group) but the damage they can cause to tendons is not uncommon. Lots of people on LymeNet have testified to the damage they've experienced. And there's good data on PubMed showing just how toxic these antibiotics are to chondrocytes, tenocytes, etc. If you do use them, here are some things to consider. The basis of the toxicity is still being worked out, but some of it appears to relate to magnesium deficiency: http://tinyurl.com/82hgt PMID: 12019086 http://tinyurl.com/dpcyl PMID: 11280370 http://tinyurl.com/bm26v PMID: 10639347 But this article: http://tinyurl.com/8dfjh PMID: 15546943 suggests that magnesium (and other minerals) should not be taken at the exact same time as the fluoroquinolone dose, but the two should instead be staggered. But magnesium is not the whole story. It turns out that fluoroquinolones may damage tendons in part due to the generation of ROS, reduction of glutathione, etc.: This paper: http://tinyurl.com/9azzh PMID: 15478945 notes glutathione problems and that vitamin E and allopurinol seem to provide some protection against fluoroquinolone toxicity. This paper: http://tinyurl.com/9sqbu PMID: 14569066 also discusses the role that these inflammatory signaling molecules play, saying, " A likely hypothesis is that the glutathione content falls rapidly so that the intracellular antioxidant enzymes lose their ability to modulate the overproduction of ROS. " Perhaps, then, glutathione and/or other anti-inflammatory agents, along with staggered magnesium supplementation, may, to some extent, protect against tendinopathy in patients using fluoroquinolones. However, if memory serves fluoroquinolones can cause seizures and NSAIDs significantly enhance this risk. Something about their respective influence on GABA receptors, I think. Verify this if it matters to you. I should say that I've taken only a cursory look into glutathione and am not informed enough to comment on it more than I did above. I am also not endorsing a model that traces chronic illness back to anything that might be called, by the commonly held meaning of the word, " stress " . That may be relevant for some people, but it has nothing to do with my disease. My interest here is related strictly to the possibility of reducing fluoroquinolone toxicity. Matt Quote Link to comment Share on other sites More sharing options...
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