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Liver Metabolized Antibiotics/Orals

I just started a course of Azithromycin for what appears to be a sinus infection at 500/250/250/250/250 mg

It is known to be somewhat liver/hepa toxic, and has caused jaundice in a few rare cases.

I asked my doctor and pharmacist, my doctor thought its liver toxicity was almost insignificant, they don’t even put a warning about alcohol and such on the label.

My pharmacist proceeded to tell me it was metabolized in the liver and was therefor not hepatoxic…which does not make sense in the slightest.

Needless to say I think my pharmacist is not very trustworthy. As I have apprently read more case studies on a VERY commonly used antibiotic than she has.

Im a little hesitant to run my orals with the azithromycin in my system.

Does anyone have experience with this ?

I could just skip the orals for a few days until the Azithro course is finished.

[quote]Westclock wrote:
My pharmacist proceeded to tell me it was metabolized in the liver and was therefor not hepatotoxic…which does not make sense in the slightest.

Needless to say I think my pharmacist is not very trustworthy.
[/quote]
Exactly how does it not make sense that simply the fact a substance is metabolized in the liver does not mean it is hepatotoxic?

Almost everything is metabolized in the liver (excluding those things that need no metabolism to be excreted.)

Do you think they are all hepatotoxic?

What a lousy way for the liver to work that would be.

Azithromycin is widely administered and is hardly destroying livers right and left.

Your doctor and pharmacist’s statements that the effect is minimal have a lot more weight and correctness than your theory on the consequences of being metabolized by the liver.

Additionally, if you have not been abusing 17-alkylateds to this point – that is to say, you haven’t been using them for an excessive duration of time nor at an extreme dose – then their adverse effect on the liver is pretty minimal as well. I would not be concerned about the combination for a period of a few days. Only if a person were on the edge of a serious liver problem already would such a thing possibly push them over the edge. If you’re in that position, then stopping the orals for just a few days, as per your plan, isn’t the right plan as you would need to stop them period for quite some time. Or if you’re not in that position, then again your plan of stopping the orals for a few days would not offer advantages.

[quote]Bill Roberts wrote:
Westclock wrote:
My pharmacist proceeded to tell me it was metabolized in the liver and was therefor not hepatotoxic…which does not make sense in the slightest.

Needless to say I think my pharmacist is not very trustworthy.

Exactly how does it not make sense that simply the fact a substance is metabolized in the liver does not mean it is hepatotoxic?

Almost everything is metabolized in the liver (excluding those things that need no metabolism to be excreted.)

Do you think they are all hepatotoxic?

What a lousy way for the liver to work that would be.

Azithromycin is widely administered and is hardly destroying livers right and left.

Your doctor and pharmacist’s statements that the effect is minimal have a lot more weight and correctness than your theory on the consequences of being metabolized by the liver.

Additionally, if you have not been abusing 17-alkylateds to this point – that is to say, you haven’t been using them for an excessive duration of time nor at an extreme dose – then their adverse effect on the liver is pretty minimal as well. I would not be concerned about the combination for a period of a few days. Only if a person were on the edge of a serious liver problem already would such a thing possibly push them over the edge. If you’re in that position, then stopping the orals for just a few days, as per your plan, isn’t the right plan as you would need to stop them period for quite some time. Or if you’re not in that position, then again your plan of stopping the orals for a few days would not offer advantages. [/quote]

Azithro specifically is hepatotoxic according to what I have read.

Then again so is tylenol, hence my question on how toxic it might be.

I have not been abusing 17aa, but I do run them for the normal length of time, my liver values were good as of the beginning of my run.

If you dont see any obvious problems with it then that makes me feel significantly better.

Thank you for the response Bill.

I really don’t see any problems with it (with the above potential exception, namely if already on the edge of liver problems, which doesn’t sound like it applies to you) and understand your pharmacist and doctor to be correct that the hepatotoxicity is low and ordinarily just not a matter of concern.

Combining a substantial number of things that all had low but non-zero hepatotoxicity and doing so for extended time would be a bad idea, but combining two things of low hepatotoxicity for a few days is no big deal.

it was my understanding that what makes a substance toxic to the liver is the liver’s inability to break it down…17aa is used so the steroid survives the first pass through the liver right? I thought it was the inability to process the compound that made it toxic…

No. In fact the compounds are metabolized by the liver. Inability to be metabolized is not so far as I know ever a cause of hepatotoxicity.

In the case of 17-alkylated steroids, the exact mechanism of the problem was unknown as of the last time I looked into it, but the general cause was suggested in the literature to be impaired excretion of bile,

probably from competitive interference with transcanalicular transport, this being dependent on the exact structural feature of having the 17-alkylation and reliably being present for those steroids having it, and not being the case for those not having that substitution.

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No, if for no reason other than the methyl (or ethyl, or any other alkyl) group is never removed from these molecules. Can’t be – not without any enzyme, and there isn’t any, that would hydroxylate it which could enable the process.

A methyl or ethyl can’t break off of a carbon skeleton in that manner (as an unchanged alkyl.)

By the way, I had a similar sort of hypothesis, but which I don’t find reasonable evidence to be right. Namely, that the 17-alkylation yielding a tertiary alcohol whereas a non-alkylated androgen is only a secondary alcohol, the tertiary alcohol would be much more stable as a free radical, and thus have much more actual existence, and perhaps this was the cause of damage.

However, there is no proof out there of that whatsoever, and if it were true there ought to be more of a general phenomenon of tertiary alcohols being liver toxic than is the case. So I don’t think that is it. Just fair to mention that I had an “oops” sort of theory along those lines as well! :slight_smile: