Pain management: the 24 hour OxyContin wait
Disclaimer: none of the stores I've worked in have ever been held up. I've never had anyone shove any weapons into my face and demand XYZ controlled substance. Those of you who have experienced this may think differently.
All of the pharmacies I work in, save my home store, have mandatory 24 hour OxyContin waiting periods. I used to be envious of these stores, but the more I learn think about it, and about pain management in general, the more I think maybe it's a stupid rule. Why was I envious of those other stores at first?
Well people that bring in scripts for CIIs — especially OxyContin — seem to bring in 2 or 3 at a time. And they usually come in packs of 2-3 people at a time. Almost like they're all friends or something. ("Hey guys let's hang out and take some Oxies tonight!" "Yeah, OK!") I have no idea why. Maybe it's just my area. Anyway, that means you've got anywhere between 6 and 9 OxyContin scripts to fill. These people often choose to wait. Filling 9 prescriptions for CIIs really gums up the works. Most retail pharmacies keep their CIIs in a safe, and only a pharmacist has access to them for theft reasons. This means that the pharmacist is tied up for about 15-20 minutes doing nothing but working on these prescriptions. That's a royal pain in the ass for everyone else. Those of you familiar with retail pharmacy understand that ours is an interrupt-driven business. You just don't have time to concentrate exclusively on one task for 15 or 20 minutes to the exlusion of all else. The rest of the place falls apart because the pharmacist is the bottleneck through which all prescriptions must pass.
It's easier if there are two pharmacists on, because one can pick up the slack, but at most smaller retail pharmacies, there is no pharmacist overlap.
Anyway, as I said, my attitudes have changed. While I don't think it's often necessary for these people who wait for their Oxy scripts to do so, I do think retail pharmacies should re-think the "mandatory" 24 hour wait period so that (ostensibly) we can order OxyContin for the next day.
Random aside: Ordering OxyContin for the next day is complete and utter BS anyway, as you pharmacists will know. It takes at least two days for the requisite 222 form to make it to the supplier. In fact, there's just one pharmacist per pharmacy allowed to sign off on a CII order, and s/he doesn't work 7 days a week, usually. So next-day ordering is out most of the time. The idea is that this policy will trick people into thinking that your retail store doesn't actually have any OxyContin on the premises for safety reasons.
Back on topic: people who are on maintenance doses of OxyContin don't usually need to wait. In stores where there's a 24-hour wait policy, these people happily drop off their prescriptions and pick them up the next day.
Last night we had a person who had been in a serious accident involving a tractor trailer get released from the hospital. She had 3 prescriptions, one of which was for OxyContin. I had to turn her away — which made me mad because we had it in stock, and I sent her up the street to my home store where we don't have any waiting rules — for what amounted to no reason. I guess this "rule" is in place for "safety" reasons. Though any criminal is going to know — not guess — that this rule is complete BS, which isn't going to prevent him from holding you up in the first place.
If you're at one of these 24-hour wait stores, are you really going to try to convince some dude sticking a .44 magnum in your face that you really don't have any OxyContin in the safe? Somehow I doubt it. It's just not worth the risk.
So we've created a rule that merely offers the illusion of protection. It keeps the honest opioid users honest, won't deter those bent on breaking the law, and prevents those who may legitimately need a prescription for OxyContin today (first-time fillers) from getting their medication.
What a wonderful, pointless system we've created. I think it would be more effective if we simply advertised the fact that we keep less than 100 tablets of OxyContin in the store at all times. That, at least, sounds somewhat believable.
While this post was more introspective and rant-ish, I have lots more to say about the clinical aspects of pain management in the near future, especially about the castigation of opioid users by pharmacy staff, and the backwards attitudes of (usually older) pharmacists when it comes to pain management.
[tags]Medicine, pharmacy, OxyContin[/tags]
Goodbye, generic Plavix (for real)
So it looks like at the end of next week, we're going to run out of generic Plavix. I've not followed the business drama of Big Pharma in a little while because I find it dull, so I have no commentary on the outcome of the lawsuit, which I presume has been settled in S-A and BMS's favor. Apotex had a good run while it lasted. I mentioned in September that we were warned that this might happen.
In any event, it looks like it's for real. As far as I know, this is the only time in recent history where a generic has been withdrawn. I think I recall similar things happening for Lanoxin (digoxin) and Synthroid (levothyroxine), but generics for those drugs were withdrawn because of problems with bioequivalence rather than as a result of litigation.
It's going to suck explaining the reasons why clopidogrel is temporarily going the way of the Dodo. People don't take too kindly to the idea of their copayments doubling (or more). I'm thinking I should write a little handout for people explaining what happened so we don't have to have the same conversation 500 times. After telling something a dozen or so times, you've heard all the wisecracks and complaints that such a topic engenders, and it just gets redundant and tiresome.
I also think the idea of jerking patients/consumers around like this is ethically wrong, patents and the justice system be damned. But then morality is entirely dependent on one's point of view, now isn't it?
[tags]Medicine, pharmacy, big pharma, plavix, clopidogrel, ethics[/tags]
How do you tell a patient that their doctor is incompetent?
We get scripts from a particular doctor in my neck of the woods about 2-3 times a day. He's a really nice guy, and he's about 80 years old. His scripts are always for the same antibiotic. Ampicillin: 500mg b.i.d. for seven days. Now that I'm working more, I've noticed this trend, and the disturbing tendency for these patients to come back a week later with prescriptions for different antibiotics, usually prescribed by someone at the ER. Probably as high as 50%.
Curious, I started conducting an informal Q&A to find out what this doctor was prescribing for. There are some head-scratchers among them:
- pneumonia
- UTI
- GI infection of unknown etiology
- sinus infection
- ear infection
- H. pylori
- Acne
Sure, you might use ampicillin for an ear infection. Maybe even a sinus infection. But pneumonia? Probably not. It's also an unlikely choice for UTI — yeah it's got some activity against Proteus, but is it really the best choice? Acne? Hmm…
I might be inclined to give him the benefit of the doubt; we certainly get some head-scratchers sometimes, and they usually work out okay. If we call an office, we usually get a reasonable explanation. But this is the only antibiotic this guy writes for. Ever. Quinolone? What's that? Cephalosporin? Who needs it! Macrolide? Hah!
I don't mean to be a smartass, or to disrespect this guy, but I've never seen a script that shows any amount of cognitive effort behind it. It's always ibuprofen 600mg t.i.d. or ampicillin. Usually ampicillin.
I'm trying to come up with a nice way of telling people this probably won't work very well for your condition and more importantly, you need to find a real doctor. When does it become my business to get involved? I worry about things like our MDRO problem. I don't like to see patients have to go to the ER when it's totally avoidable. Does being nice make up for not having a clue about modern treatment paradigms for bacterial infections? Should I not tell them that they're probably wasting their time and money?
[tags]Medicine, pharmacy, antibiotics[/tags]
More on reversing Type 1 diabetes
This past summer, I went on an article-printing spree, and one of the things I printed was this NYTimes article about the work of Dr. Denise Faustman, a diabetes researcher out of MGH in Boston. I read it early last week, and had been idly wondering what became of her research, thinking I should dig and see if anything newer had happened. Fast-forward to last night, I was cruising digg, and I came across more results involving the same protocol that she used back in 2003.
In March of this year, three other labs confirmed that Dr. Faustman's protocol could reverse Type 1 diabetes in non-obese diabetic (NOD) mice. Those results were inconclusive on the role of spleen cells in the recovery of insulin-producing pancreatic islets. The new data from the NIH provide a fourth confirming study, and more significantly, the role of spleen cells in islet regeneration.
In the 2001 and 2003 studies, Faustman and colleagues treated end-stage nonobese diabetic (NOD) mice with Freund's complete adjuvant, a substance that suppresses the activity of the immune cells that destroy islets in type 1 diabetes. They also introduced donor spleen cells to retrain the immune system not to attack islets and found that the protocol not only halted the immune destruction caused by diabetes but also allowed the insulin-producing pancreatic islet cells to regenerate. Evidence indicated that the spleen cells were the source of at least some of the regenerated islet cell and hastened the restoration of blood sugar levels.
The direct contribution of spleen cells to islet recovery, first described in the 2003 study, is confirmed in the current work. NIH researchers used cell lineage tracking in the form of Y-chromosomal fluorescence in situ hybridization (FISH), in combination with insulin staining, to follow the fate of male spleen cells transplanted into female recipients. The female mice that received male donor cells consistently showed Y-chromosome-positive insulin-producing islet cells, indicating that the introduced spleen cells contribute to islet recovery. The current study also showed that the degree of spleen cell contribution is influenced by mouse age at the start of treatment. Spleen cells appear to contribute to islet recovery more in mice who are older and with more advanced diabetes compared with younger mice with less advanced diabetes, in which regeneration of remaining islets may be the dominant mechanism.
With four studies confirming the success of the diabetic reversal, I am wondering when Phase I human trials will begin. From an economic standpoint, FCA and BCG are both good choices, since they are both orphaned drugs. FCA is incredibly old — Dr. Freund, the guy who created it, died in 1960.
While I'm glad to see the success of these studies, it's still a long way from mice to people. I have my doubts about the side effect profile of this treatment as well. FCA is a biologic made (usually) from killed M. tuberculosis, and is forbidden for use in humans. It has a high incidence of painful reaction and potential tissue damage. So that leaves BCG, a similar, but less potent biologic made from M. bovis, found in TB vaccines. The NYT article states that BCG was used in Dr. Faustman's 2003 work, but the original research paper (PDF) indicates that it was actually FCA.
This leaves me wondering two things: 1) will BCG have a similar effect and 2) if BCG is not successful, will FCA be approved for use in humans?
[tags]Medicine, diabetes, type 1 diabetes, fca, bcg, biochemistry, physiology[/tags]
"About me" — let's clarify a couple of things…
I just finished reading "Cardiorenal Effects of Celecoxib As Compared With the Nonsteroidal Anti-Inflammatory Drugs Diclofenac and Ibuprofen" and I decided that I need a break from reading clinical papers. Earlier today, I was poking through my Technorati link love, and Kevin refers to me several times as a pharmacist, something I hadn't really noticed before. I've never referred to myself as a pharmacist on this blog, though I've also never gone out of my way to tell my readers that I'm not. It just never seemed terribly relevant. I'm not a pharmacist, though my background is pharmacy, and I work in a pharmacy. I went about halfway through pharmacy school, not really knowing if that's what I wanted to do with my life. I enjoyed retail, the only pharmacy experience I had. I was good at it. Really good at it. You might think "It's retail… does it really matter how "good" you are?" — but if you've ever had to change pharmacies because of negative experiences with the staff and then found one that was truly great, you know exactly what I mean. It's not trivial.
Money was one of the main appeals of pharmacy when I first started, but that'll only compel you to just barely get by. Ultimately there was something about it (retail pharmacy) that I didn't like. A couple of things, actually. It was too limiting. I didn't like the fact that from a business point of view, the pharmacist was answerable to someone who may not have any background in medicine or pharmacy whatsoever. That seems wrong. I also don't like the emphasis on numbers over all else. Numbers are a great way to measure some aspects of the business, but hardly all.
I still work retail, but I make it more interesting for myself. I ask more questions than perhaps I should. I like to ask questions. I always have. In the way of making my job more interesting… I do consulting for Medicare patients with an eye towards lowering drug costs and improving therapeutic outcomes. That's probably my favorite part of my job — working with a patient's doctor(s) and lowering their drug costs in a meaningful, measurable way. It's also forced me to learn a lot more about certain things than I would have learned on my own. You don't have a conversation with an MD about diabetes, for example, unless you know WTF you're talking about, particularly when there are other significant comorbidities involved. (And I must admit that I am not blind to the fact that many docs look down on pharmacists, which bothers me, and is another motivation for my being up on my therapeutic knowledge before I write a letter or make a phone call.)
I spend my lunch breaks (if I have time to sit down) with my nose buried in Facts and Comparisons, a CGP textbook, or a general therapeutics textbook. Most of my free time outside of work is spent buried in clinical literature. Medicine has suddenly become my hobby and my passion. It's not just something I study while I'm at school, or do for a job. And it happened overnight. Literally.
You're wondering where this is going, I know. Here it is:
Something a little off-topic…
I was poking around the blogosphere today, and I found something that might be of use to those information gluttons (like myself) that like to save useful things: printing to PDF of journal articles and CEs that are of interest for easy searching later.
Unfortunately the instructions only apply to Mac OS X, but you can do the same thing on Windows with a couple of extra programs.
[tags]Technology, search[/tags]
Januvia is going to eat Byetta's lunch
Januvia hit our shelves this past week, and I marveled at how inexpensive it was for a brand new drug. (~$300, if dim memory serves.) I think Merck's going to have a runaway hit on their hands, and Amylin and Lilly are going to be the ones that lose out. I almost feel like I'm stating the obvious here — heck, maybe I am, I haven't kept with any business news and speculation in several months.
Exenatide (Byetta) is a glucagon-like peptide analog that responds to glucose by stimulating insulin release and inhibiting glucagon release. It also slows gastric emptying, inhibits synthesis of glucagon, and stimulates beta cell neogenesis by preventing beta cell death. It only responds in the presence of glucose, which means there's low risk for hypoglycemia.
Unfortunately, GLP-1 is broken down by DPP-IV, which limits native GLP-1 half-life to about 90 seconds. GLP-1 is also efficiently cleared by the kidneys. The other downside to Byetta is the fact that it's injected.
Sitagliptin (Januvia) prevents the breakdown of the body's own GLP-1 (and other incretin hormones) by inhibiting DPP-IV. As an oral tablet, patient compliance is likely to be higher, or at the very least, it's more convenient than poking oneself.
Despite having entirely different mechanisms of action, the net effect is the same: higher levels of GLP-1 in the body, with low risk of hypoglycemia. Both Byetta and Januvia are likely to help patients lose weight as well. There's been some talk about possibly getting Byetta approved as a weight-loss drug — I don't know how far along this idea is, however.
It's only a matter of time before we start getting insurance rejections for prior authorizations telling us that the doctor needs to try Januvia before they'll approve Byetta. This is good news for those seniors on Medicare Part D plans as well — Januvia can save them a pile of money because it's just so much cheaper than Byetta.
So to recap:
- Easier to store (no refrigeration)
- Oral tablet vs injection
- Once a day dosing instead of twice a day poking
- Cheaper
I think all the pieces are in place for Merck is going to eat Eli Lilly and Amylin's lunch here. It seems one investment house is also predicting something similar. (PDF)
[tags]Medicine, pharmacy, diabetes, byetta, januvia, sitagliptin, exenatide[/tags]