
"Statin" metabolism: Cytochrome P450
For recurrent major depression, I take Prozac (fluoxetine) 40mg/day,
along with Wellbutrin (bupropion) 150mg/day. These meds are managed by a
board-certified psychiatrists. During the past 15 years, I've taken
many different anti-depressants, alone and in combination. The
Prozac-Wellbutrin regimen works great. In addition, I take Lipitor
(atorvastatin) 10mg/day. My lipid profile is terrific, and my liver
enzymes have always been normal.
Effective 1-1-1999, my HMO (Aetna US Healthcare) is adopting a formulary
that excludes Lipitor. They identify other HMG-CoA reductace inhibitors
as being similarly efficacious and more "cost effective". (Their equal
efficacy is questionable, but that's not why I'm writing!) If I can
demonstrate "medical necessity" for staying on Lipitor, the HMO will
continue to pay for the drug.
As I understand it, Prozac depends on cytochrome P-450 for its
metabolism (particularly CYP2D6). Additionally, Prozac is a potent
inhibitor of CYP2C19, although it is not metabolized by it.
Are certain "statins" less dependant than others on cytochrome P-450
enzymes for their metabolism? I don't want to{*filter*}up the balance of
meds I now enjoy. If changing from Lipitor to another statin means
potential toxicity from the new statin (because of P450), I'd like to
know that. The Prozac cannot be discontinued in favor of another
anti-depressant with a different metabolic profile. Do you think
remaining on Lipitor is medically justified?
Many thanks!
Stuart Caplan