I received a call from a physician who may be doing a case report on a patient I once saw, so I won't spoil the discussion here. Needless to say the event raises some interesting discussion on how we treat our patients. It turns out I once cared for a patient who had a heparin induced thrombocytopenia (HIT) positive antibody, confirmed with a positive SRA, who developed an impressive acute thrombocytopenia that resolved after discontinuation of Arixtra and placement on Argatroban. Confirmation was made as to the lack of exposure to any heparin or Lovenox over a prior six month period. What does this mean? Is this a case of Arixtra induced HIT? Is it all coincidence? If true, it could have significant implications in how we treat our patients.
I won't get into the details of HIT antibody syndrome, except to say it can be nasty a thing to have. Patients receiving heparin or Lovenox can develop antibody complexes against these medications that promotes clot formation resulting in potentially life threatening deep venous thrombosis or pulmonary embolism. These are very effective blood thinners, but if you get HIT from their use, you are at very high risk of developing blood clots.
The treatment of HIT with clot requires the use of Argatroban, another horribly expensive anticoagulant. Some folks use Arixtra to treat HIT antibody positivity without documented clot. I'm not aware if this use has received an FDA indication or not. You can understand the dilemma this causes. Would we want to treat a HIT patient with a drug that could potentially contribute to the antibody process? Does this change everything?
At Happy's hospital, we have hospital safety protocols, government approved of course, in place to monitor for HIT as part of our anticoagulation safety initiatives. Part of that protocol involves monitoring platelet counts every other day on patients being given heparin or Lovenox for the sole purpose of discovering patients who may develop HIT antibody syndrome in the hospital. This protocol excludes platelet monitoring with Arixtra because Arixtra is not thought to be associated with HIT syndrome.
Now, the question is, does this change everything? I use Arixtra, often, as medical VTE prophylaxis (off label but no reason to suspect ineffective) so I don't have to have my patients stuck every other day for platelet checks.
As far as I know, there is only one prior case report of Arixtra associated with HIT syndrome.
What now?
What now?
