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Doxycycline and Augmentin - why are they contraindicated


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Just curious (cause I'm tired of reading about NP vs PA vs AAPA vs PAFT vs everything), had a pharmacist tell me about it a while ago, but he couldn't explain it. Couldn't find the answer/pharmacologic explanation.

 

Also, is the doxy shortage still going on?

 

you just lazy, doxy decreases effects of augmentin through antagonism rendering the drug ineffective and no antibiotic coverage

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Although my laziness IS very high, my stupidity is even higher. Please explain, preferably with pictures and monosyllable words, why they antagonize each other. Penicillins inhibit cell wall formation (inhibist one of the enzymes involved in cell wall formation, specifically) while tetracyclines target the mRNA-tRNA protein synthesis/translation. Why would they interfere rather than be synergystic?

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I remember that amoxicillin reduce the efficacy of Doxy. Or was it the other way around? It was never explained to me with graphs and charts (prob fell asleep during Pharmacology class on that one) but I remember not to prescribe together. I guess if I really have a gnawing need to know why, I could look it up...so could you. Lol.

 

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clinda covers pretty much everything that combo covers as monotherapy. gets your gram +, anaerobes, mrsa, etc

doesn't cover some of the tropical med indications that doxy does but for those you would not need the augmentin either.

come to think of it, who would need both? a pt with mrsa diverticulitis? augmentin + septra would work for that.

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I remember that amoxicillin reduce the efficacy of Doxy. Or was it the other way around? It was never explained to me with graphs and charts (prob fell asleep during Pharmacology class on that one) but I remember not to prescribe together. I guess if I really have a gnawing need to know why, I could look it up...so could you. Lol.

 

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I've looked before, I haven't found a good answer to be honest.

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I've looked before, I haven't found a good answer to be honest.

 

I figure its one of those "because I said so" things that big daddy medicine throws at us. I'm sure our physician colleagues are in the same boat with this one.

 

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That logic does not really work if you think about it. I.e. If doxy reduces the peptidoglycan synthesis by 90%, the PCN would still work the same on the remaining 10%. The bacteria does not suddenly produce a new type of protein for cell wall synthesis (unless there's a mutation/plasmid transfer/or funky dormant secondary gene).

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  • 2 weeks later...

Taking a shot at this:

Tetracyclines are bacteriostatic while penicillins are bactericidal so they can never be given together because of drug inhibition. As you pointed out, the TCN works by stopping protein synthesis @ the ribosome (30S) while the PCN works at the cell wall. PCN attacks an active bacterium so it needs the bacterium to keep making protein to make the cell wall. If TCN stops the synthesis, there is no cell wall for the PCN to attack. Also, since TCN is bacteriostatic and will only stop new growth, it does not really kill the bacteria and it creates more chances for the bacteria to create efflux pumps contributing to Abx resistance. Because TCN is bacteriostatic, the effects on the ribosome is reversible so the effects are concentration dependent.

This is different from using aminoglycosides with PCN. Although aminoglycosides can either be bactericidal or bacteriostatic and also attacks protein synthesis at the ribosomes, it is an irreversible binding to the ribosome. So if the PCN attacks the cell wall, the AMG gets inside the cell, first at the cell membrane then at the ribosomes resulting in bacterial death.

That's why in H. pylori treatment, TCN + Amox combo does not work while Clarithro + Amox combo does and if you choose the TCN route, it must be for a longer time frame because the actions of the TCN are drug dose dependent.

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Taking a shot at this:

Tetracyclines are bacteriostatic while penicillins are bactericidal so they can never be given together because of drug inhibition. As you pointed out, the TCN works by stopping protein synthesis @ the ribosome (30S) while the PCN works at the cell wall. PCN attacks an active bacterium so it needs the bacterium to keep making protein to make the cell wall. If TCN stops the synthesis, there is no cell wall for the PCN to attack. Also, since TCN is bacteriostatic and will only stop new growth, it does not really kill the bacteria and it creates more chances for the bacteria to create efflux pumps contributing to Abx resistance. Because TCN is bacteriostatic, the effects on the ribosome is reversible so the effects are concentration dependent.

This is different from using aminoglycosides with PCN. Although aminoglycosides can either be bactericidal or bacteriostatic and also attacks protein synthesis at the ribosomes, it is an irreversible binding to the ribosome. So if the PCN attacks the cell wall, the AMG gets inside the cell, first at the cell membrane then at the ribosomes resulting in bacterial death.

That's why in H. pylori treatment, TCN + Amox combo does not work while Clarithro + Amox combo does and if you choose the TCN route, it must be for a longer time frame because the actions of the TCN are drug dose dependent.

 

This is correct.

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  • 3 years later...

Taking a shot at this:

Tetracyclines are bacteriostatic while penicillins are bactericidal so they can never be given together because of drug inhibition. As you pointed out, the TCN works by stopping protein synthesis @ the ribosome (30S) while the PCN works at the cell wall. PCN attacks an active bacterium so it needs the bacterium to keep making protein to make the cell wall. If TCN stops the synthesis, there is no cell wall for the PCN to attack. Also, since TCN is bacteriostatic and will only stop new growth, it does not really kill the bacteria and it creates more chances for the bacteria to create efflux pumps contributing to Abx resistance. Because TCN is bacteriostatic, the effects on the ribosome is reversible so the effects are concentration dependent.

This is different from using aminoglycosides with PCN. Although aminoglycosides can either be bactericidal or bacteriostatic and also attacks protein synthesis at the ribosomes, it is an irreversible binding to the ribosome. So if the PCN attacks the cell wall, the AMG gets inside the cell, first at the cell membrane then at the ribosomes resulting in bacterial death.

That's why in H. pylori treatment, TCN + Amox combo does not work while Clarithro + Amox combo does and if you choose the TCN route, it must be for a longer time frame because the actions of the TCN are drug dose dependent.

I was thinking about this (and decided to revive this thread lol) if the reason that Doxycycline and PCN are CI is TCN inhibits protein synthesis which reduces cell wall production, wouldn't Macrolide do the same thing since macrolide disrupts protein synthesis as well? (the post states aminoglycosides but cites clarithro as the example which is a macrolide) ????

 

Don't ask me why I remembered this 3 yr old post but I was reviewing for PANRE and thought of this post when I saw Doxycycline as a TX for CAP... Weird huh? Lol

 

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Caution Advised

 

amoxicillin + doxycycline

caution advised if bactericidal action necessary: combo may decr. amoxicillin efficacy (tetracycline bacteriostatic effects may decr. penicillin bactericidal action)

 

 

strangely enough this is only a "caution advised" from epocrates.....

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Caution Advised

 

 

 

 

amoxicillin + doxycycline

 

 

caution advised if bactericidal action necessary: combo may decr. amoxicillin efficacy (tetracycline bacteriostatic effects may decr. penicillin bactericidal action)

strangely enough this is only a "caution advised" from epocrates.....
In Medscape both Doxy and Macrolide have a warning due to pharmacodynamic antagonistic action but Doxy has an "avoid" warning but macrolides have a "minor/significance unknown" warning.

 

My question is why is macrolide less of a CI than Doxycycline when, if the above description is correct, they both inhibit protein synthesis. Is macrolide's inhibition of protein synthesis more selective in that it does not involve the cell wall allowing PCN to bind? Or is it like the explanation about the aminoglycosides as explained above? ????(the post cites clarithromycin as the example of why Aminoglycosides and PCN work together but clarithro is a mac and aminoglycosides also inhibit protein synthesis at 30s like TCN so more confusion)

 

I asked my SP and he looked at me like "whuuuut?" lol

 

Or am I just brain fried from reviewing? Lol

 

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I feel 76% dumber after reading some of your responses. :-O How does anyone remember all these mechanism of actions? Looks like I have reading to do...

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