The panel of experts review the monitoring parameters for determining efficacy of DOACs.
Jessica Kerr, PharmD, CDE: Dr. Dobesh, talk to us a little about proper monitoring for DOACs. When we’re looking at the monitoring, are there certain considerations we need to view when we’re looking at the severely obese patient population? I guess greater than 190 kg.
Paul Dobesh, PharmD, FCCP, BCPS: When we talk about monitoring of DOACs, most people can monitor an anti-Xa level. If you ask for an anti-Xa at my hospital, and my guess is if you asked for it at Matt’s hospital, you’d probably get 1 that’s titrated to either unfractionated heparin or low-molecular-weight heparin. What you get back is basically qualitative. It basically tells you that there’s drug in the system, but it doesn’t correlate to how much. This is where clinicians can get confused. Because if someone comes back with an anti-Xa level of 0.4 IU/mL and someone comes back and their anti-Xa level is 1.4 IU/mL, that doesn’t mean the patient who’s got the 1.4 IU/mL has more anticoagulation or is more likely to bleed than the other patient. The lab doesn’t allow you to make that determination. Basically, you can’t make an estimation on what’s going on between the drug; it’s yes or no. There’s drug in the system or there isn’t. That’s all it allows you to do. That’s probably the best way to do it. Don’t use a prothrombin time. Definitely don’t use an INR. At most places, when you get a PT, you get an INR. I feel like Yoda sometimes because it’s as if you must unlearn what you have learned. Why do we use an INR with warfarin? Because the prothrombin time has a lot of variability, and the INR lowers that variability. With direct Xa inhibitor specifically, there is variability with the prothrombin time, but the variability actually goes up with an INR. If you have a patient who is on a DOAC, and they have an INR of 6, people freak out. But it doesn’t mean anything, so prothrombin times are better. Once again, it’s yes or no. It’s elevated or it’s not, and the INR will reflect that. There is anticoagulation in the system; that’s all those tell you. There is no FDA-approved qualitative test, which basically tells you how much drug is in the system. But you can get them for research purposes. A number of hospitals have gotten them and used them that way. They have the appropriate calibrators and controls for rivaroxaban and for apixaban. That’s the only way you could do that. Most of us don’t have that. We don’t have it at the University of Nebraska Medical Center. If you’re going to use laboratory monitoring, remember what the number tells you. Just because the number is high, that doesn’t mean the patient is at risk of bleeding, started holding doses of the drug, things like that.
We start looking at these very heavy patients. As you said, at 190 kg, that’s a question we still are going to get. What about the patients over 190 kg? I don’t know, and neither does anybody else. We are having a hard time getting studies of patients over a 120 kg. In those patients, if you did a test—if you give them the drug, monitor anti-Xa—and get a positive result, there’s drug in the system.
That’s what you know. You don’t know how much, but you know there’s drug in the system. If you want to monitor that at peak, which is about 4 hours after they take any of these DOACs, that seems reasonable. Is it necessary? Nobody really knows right now. Matt, how are you are approaching this in Lincoln, Nebraska?
Matthew Johnson, MD: Very similarly. We don’t have any of the research assays that we would do any of those levels. Clinically we’re just doing what we would starting at agents. Especially with this, we have training last year to use fewer DOACs in the extreme over there. Now we’re seeing more utilization, especially in the last 6 months, in that patient subgroup. That’s going to continue to go up as we get more data.