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Step I D-Dimer vs. Fibrin degradation products
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D-dimer is a degradation fragment of the amount of fibrin degraded. It is very specific for DIC. It is not normally detected in plasma and when present it tells you how well plasmin is working or overworking on clots.
FDP is similar(also a degradation product), but more sensitive in detecting DIC, so that is why they order them together. At least that is how I understand it.
I guess I don't get WHY it's so specific. Is it because FDP's are just from the breakdown of random fibrinogen floating around? Whereas D-dimers occur after fibrinogen has been turned into fibrin (and then degraded)?
a D-dimer IS a FBP,,, is that why you are confused? I don't think you need to concern yourself with the differences.. plasmin splits fibrin up into degradation products, one of which is d-dimers and then some other stuff..
The only thing that makes a D-dimer special is that we have a test for it
this pic from wikipedia may make it clearer:
The only thing that makes a D-dimer special is that we have a test for it
this pic from wikipedia may make it clearer:
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Exactly. Plasmin breaks down fibrinogen into a bunch of different products. Fragment X, Y, D, E and maybe some others. Theoretically these can all be present but none of them tell you that a clot has formed. The d-dimer is the degradation product of cross-linked fibrin so ipso facto there must have been a clot first.
dude, an elevated D-dimer level is anything BUT specific for DIC. Tell that to an attending and they'll laugh their asses off at you!
Now, an elevated d-dimer is specific for the degradation of cross-linked fibrin. You know, like after factor XIII has gone to work on it. FDPs, on the other hand, are just that, various peptides derived from the breakdown of fibrinognen. They are not specific for cross-linked fibrin, and hence are not specific for the action of plasmin on a stable thrombus.
If you still don't get it, look up it up online--there should be a diagram showing the structures of d-dimers.
Now, an elevated d-dimer is specific for the degradation of cross-linked fibrin. You know, like after factor XIII has gone to work on it. FDPs, on the other hand, are just that, various peptides derived from the breakdown of fibrinognen. They are not specific for cross-linked fibrin, and hence are not specific for the action of plasmin on a stable thrombus.
If you still don't get it, look up it up online--there should be a diagram showing the structures of d-dimers.
anyone in the hospital for a few days has elevated d-dimer. not that great of a test
What exactly is the mechanism by which thrombosis leads to an increase in D-dimers? Does thrombosis naturally lead to increased fibrin degradation?
Came here looking for the answer....thought I would put what I've decided.
As stated, FDP only indicates active plasmin without active factor XIII. d-dimer indicated plasmin acting on cross linked clots. Examples:
FDP only:
- Open heart surgery decreasing alpha-2-antiplasmin and increasing tPA
- radical prostatectomy increasing release of urokinase
- liver dz decreasing alpha-2-antiplasmin production
Both increases:
- monitoring fibrinolytic therapy for CA thrombus
- screening test for PE
- screening test for DIC
here's the salient point. Plasmin is part of the normal clotting cascade. If there is a thrombus somewhere, d-dimer is elevated. Plasmin can also be activated elsewhere (or its inhibition decreased) without there being a clot, and therefore only FDP increases.
Godspeed,
And may your COX be blocked
As stated, FDP only indicates active plasmin without active factor XIII. d-dimer indicated plasmin acting on cross linked clots. Examples:
FDP only:
- Open heart surgery decreasing alpha-2-antiplasmin and increasing tPA
- radical prostatectomy increasing release of urokinase
- liver dz decreasing alpha-2-antiplasmin production
Both increases:
- monitoring fibrinolytic therapy for CA thrombus
- screening test for PE
- screening test for DIC
here's the salient point. Plasmin is part of the normal clotting cascade. If there is a thrombus somewhere, d-dimer is elevated. Plasmin can also be activated elsewhere (or its inhibition decreased) without there being a clot, and therefore only FDP increases.
Godspeed,
And may your COX be blocked
if you have a thrombosis (a blood clot), why would your body be breaking down a fibrin clot (as explained by elevated D-dimer levels)
wouldnt the breakdown of a fibrin clot make you less likely for thrombosis?
can someone offer a conceptual model to answer these questions.
wouldnt the breakdown of a fibrin clot make you less likely for thrombosis?
can someone offer a conceptual model to answer these questions.
It’s ok, I’ve been an attending Dermatologist for >2 years now, I think i’ve got things figured out.
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