Q. In liver cirrhosis, why is the PTT not elevated? In all of my review books, it says the PT is used as one of the ways to evaluate liver function. But it seems like the PTT should also be elevated!

A. Both the PT and the PTT can be prolonged in liver failure. The liver makes most of the coagulation factors – including the factors in both the intrinsic and extrinsic pathways. So both the PT (which assesses the extrinsic pathway) and the PTT (which assesses the intrinsic pathway) will be prolonged if the liver is not making coagulation factors like it should.

When you’re using coagulation tests to monitor liver failure, the PT may be a better test than the PTT. The PT assesses factor VII, which is the coagulation factor with the shortest half-life. So the first test to become abnormal if you stop making coagulation factors is the PT; then later, as the other coagulation factors start to become noticeably less abundant, the PTT becomes prolonged too. Perhaps that’s why board review books focus more on the PT (rather than the PTT) in this context.

The same principle holds for people on coumadin. Coumadin affects all the vitamin K dependant coagulation factors (II, VII, IX, X), so eventually, if you’re on a big enough dose, you’ll end up with both a prolonged PT and a prolonged PTT. Usually, though, you use the PT to follow someone as you’re adjusting their coumadin dose, because it’s more sensitive (it will become prolonged before the PTT). That’s important, because when someone is on coumadin, you want to anticoagulate them a little, but not too much. If you only used the PTT, you wouldn’t see an abnormality until factors IX and X dropped below normal levels – and by then the patient would be severely anticoagulated.

Bottom line: you are absolutely correct – both PT and PTT can be prolonged in liver failure.

The image of a cirrhotic liver above is from Wikimedia commons (http://commons.wikimedia.org/wiki/File:Cirrhosis_high_mag.jpg).