of patient performance status, providers in Portland will
prescribe 20 mg on days 1, 2, 8, 9, 15, and 16. They’ll
break up that 40 mg dose and give it that way.
Dr. Chauncey. I don’t know if that strategy is biologically equivalent in terms of antimyeloma activity or less
toxic in terms of myopathy. There’s almost always some
disease marker to track, so that whether you’re using the
serum free-light chain assay or serum protein electrophoresis, you can see if the strategy you’re using is working
in real time.
Dr. Cosgriff. I’ve never known whether it’s been shown
to be more efficacious or if it’s just a way of getting
around some of the adverse effects. However, it does pose
some alternate challenges. With higher doses of steroids,
you’re looking at 2 days where the patient can become
hyperglycemic, if not, a little bit longer.
The other thing with it is that adding on that extra day
of dexamethasone can interfere with some other drugs
and some other therapies. In individuals who have had a
deep vein thrombosis for whatever reason and they’re on
warfarin, now we have an agent that really screws up our
warfarin monitoring. We would have to consider switching them to another agent.
Dr. Mehta. It’s also prothrombotic.
Dr. Chauncey. If you actually ask the patient, independent of the hyperglycemia, independent of the myopathy,
independent of psychosis, but just quality of life, they’ll
typically tell you that the on-and-off of steroids is the
worst part of the regimen. It’s often the roller coaster ride
of short-term hypomania followed by dysphoria.
Dr. Mehta. And the lack of sleep. They describe it as
being out of their skin.
Dr. Chauncey. They are. And as soon as they stop, often
there is a depression.
Dr. Mehta. It is very, very difficult. And some actually develop psychosis.
Dr. Ascensão. We all use some form of acyclovir or
its derivative for the prevention of shingles in patients
exposed to the proteasome inhibitors. We use aspirin,
usually low dose (81 mg), for deep vein thrombosis
prophylaxis. But is anybody using other anticoagulants
or putting everybody prophylactically on proton-pump
inhibitors (PPIs) or just seeing how people do first and
Dr. Chauncey. I typically use conventional dose aspirin,
and if there’s breakthrough thrombosis, the first response
should be that it is not the best regimen for this patient.
Sometimes you have to go back to it, and if someone’s
an anticoagulation candidate, then full anticoagulation is
needed if that’s the best regimen. Usually if there’s a breakthrough thrombosis, it is a deal breaker, and you’re ready
to move on to a nonthrombogenic regimen.
There has been an observation (there is some biological basis to back this up) that if you give bortezomib
with an IMiD, the regimen became less thrombogenic
than with the IMiD and dexamethasone alone.
Dr. Ascensão. On aspirin, even if they’re on an IMiD
plus a proteasome inhibitor, I just don’t know that the
data are good enough for us to avoid it at this point in
time. And I don’t necessarily put people on a PPI unless
they’ve got added gastrointestinal problems and unless
they have associated heartburn or dyspepsia symptoms.
Dr. Mehta. I use low-dose aspirin in every patient. And
if they breakthrough, they go on full anticoagulation
usually with a new oral anticoagulant. I use PPIs only if
needed, although most of them do need it, and, of course,
bisphosphonates so the bone protective aspect. ●