I’m passionate about medicine. I love practicing it, teaching it, learning it…everything about it. It’s also damned scary sometimes. Knowledge changes; patients don’t walk in with textbook diseases; and you have to be able to doubt yourself without drowning in indecision. Every time a patient brings me an article or monograph that looks relevant to their care, and it’s new to me, I have to go through it and see if there really is something to it.
For example, there has been some data recently about popular medications for acid reflux (called PPIs, including such medications as Prilosec) and possible interactions with a potent anti-platelet agent called clopidogrel (Plavix). What does this mean for me and my patients?
This is not a trivial conundrum. Here’s a fairly typical scenario: a patient comes in with a heart attack, and the cardiologist performs an intervention to save her. Knowing the data, the cardiologist decides to deploy a drug-eluding stent in the patient’s blocked artery. Without the procedure, the patient is likely to be disabled or dead. In order to prevent the stent from re-occluding, leading to another heart attack, she must stay on clopidogrel for a long time (probably a year).
Then, a few months into the treatment, the patient develops rectal bleeding. Endoscopy reveals a bleeding ulcer, which the doctor cauterizes. In order to prevent further bleeding, the patient needs to be on proton pump inhibitor such as omeprazole (Prilosec). We can’t just stop the clopidogrel, or the patient may have a heart attack. We also can’t let the patient bleed to death.
The whole clopidogrel/omeprazole thing is pretty interesting. It turns out that clopidogrel is really a pro-drug, and must be metabolized in the liver by the cytochrome P450 (CYP) system into its active metabolite. Some people are naturally deficient in the necessary functional CYP, and continue to clot even on the drug. In the future, we may even be able to do genetic testing to see what patients may need a higher dose of the drug or a different approach altogether. Prilosec is available over the counter, and a patient may take it without my knowledge (and without needing it) complicating things further.
It turns out that omeprazole inhibits the same CYP enzyme that is needed by clopidogrel. Lots of patients are on ompeprazole (and other similar drugs called PPIs), so in clinical settings, we don’t know if patients who get more blood clots on clopidogrel do so because of their genetics, because of a PPI, for other reasons, or just by chance. If the patient asks me what to do next, how do I give a reasonable answer?
This kind of thinking is going on continuously. Do I give this patient with a sinus infection antibiotics? If so, will there me a medication interaction? Is the patient at high risk for side effects, such as C. difficile colitis? And how can I relieve their symptoms without raising their blood pressure?
My decisions have real consequences. This is the reason that I get really, really angry when people who don’t know what they are talking about spend a few minutes at Google U. and all of a sudden think that Potion X, Herb Y, or whatever is some really good shit. How do they know? Because “some dude” said so? People listen to trusted friends a lot more than to doctors, so the damage can be real and immediate. If I have a patient on warfarin to prevent a deadly blood clot, and their nephew tells them that Potion Zed is good for blood clots, and Potion Zed just happens to have some vitamin K in it, my patient may die. I’m not making this up—ask any doctor in practice for their latest horror stories.
Intervening in human health is serious business, and people will listen to advice from anyone, knowledgeable or not. Sometimes my patient’s greatest enemy is a well-meaning friend.