Acute Liver Failure and Transaminases (Goljan)

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On page 367 of RR, under heading G (Fulminant Hepatic Failure) it states that transaminases would be DECREASED. This doesn't make sense to me, really, since transaminases INCREASE as they're secreted into the blood from damaged hepatocytes, no?

Or is it perhaps that he's talking about later, after the cells are completely wiped out and there are no more enzymes to leak?

I just want to make sure I'm not crazy here.
 
Not real sure about this one either, but some further evidence that it is correct is that the MELD score (which determines eligibility for liver transplant) uses bilirubin, INR, and serum creatinine (and NOT transaminase levels,) implying that elevated transaminase levels are not necessarily sensitive for end-stage liver disease.
 
Not real sure about this one either, but some further evidence that it is correct is that the MELD score (which determines eligibility for liver transplant) uses bilirubin, INR, and serum creatinine (and NOT transaminase levels,) implying that elevated transaminase levels are not necessarily sensitive for end-stage liver disease.


I recall a graph somewhere in my notes (too lazy to find it at the moment) that had ALT/AST (and LDH, I think, with a smaller peak) all rising and falling in a fairly narrow curvilinear fashion, while bili slowly crept up (reaching its highest point after the transaminases had dropped back down).

But it didn't have any sort of time scale on the X axis, so who knows.
 
Actually busted out my RR for this one. haha. I'm looking at an older edition because that heading is on my page 375, but just below that statement (Decrease in tansaminases) it states "liver parenchyma is destroyed". So I'd guess your assertion that the cells are wiped out and can't make transaminases is correct.
 
Low to normal ALT/AST can mean one of two things - Normal liver or really messed up liver.
Indicators of liver fxnality - PT, bilirubin, albumin
 
LFT's rise until there are no more cells left to produce the enzymes (i.e. they have all died off); at which point, they will begin to decrease. This also correlates with a rise in the PT time (decrease in clotting factor production due to liver cell death).
 
That is correct. Decreasing transaminases + increasing PT = rut roh
 
Yes, if acute....sometimes not so much if chronic or "burned out". Which is why as above, we do not use them to gauge liver function.
 
it's kinda like thyroidits, where at first T3/T4 levels go up due to extravasation in the blood and later go down due to cells function decreasing.
 
First indication of end state liver disease is physical exam. But yes, PT, albumin, electrolyte abnormalities, and signs of hepatorenal syndrome will be things to note.

In fulminant hepatitis I believe that the liver itself shrinks due to parenchymal and connective tissue loss (cirrhotic livers are also small but scarred down) while in acute hepatitis it swells due to inflammation.
 
Remember, coags are your true liver function test, and transaminases are only your liver inflammation test.
 
Increasing AST / ALT = Liver damage "in progress"

Increasing PT, increasing INR, decreasing albumin / clotting factors, etc = Liver losing functionality, "is damaged."

You can have liver failure without a rise of AST / ALT.
Beware the ALK PHOS trap. It isn't specific to the liver.
 
Beware the ALK PHOS trap. It isn't specific to the liver.


Neither is ALT or AST😉

Anyway, thanks for the discussion guys. The more I read/looked into it, obviously the more I realized it wasn't so cut and dried (and don't worry, they made it a big point early on to point out that the transaminases are markers of liver damage, not "LFTs" exactly).

Anyway, we had our GI/Hepatobiliary exam yesterday and I rocked it, and I think just quickly discussing this stuff on here helped me a little in remembering some of the key points.
 
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