Talk:Dextropropoxyphene/Archive 1

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My thoughts

Hey guys, I say this article is blatantly unfair to dextropropoxyphene! Dextropropoxyphene has a very limited abuse potential. Yes, it is an opioid, and it can be addictive... but it is among the least addictive of the opioids (its' addiction potential has been described as "qualitively similar to codeine, although quantitively less") According to studies I have read on the subject (I hope to provide sources in the future) in almost *every* recorded death from dextropropoxyphene overdose, there were significant histories of mental illness, strife with other persons, etc, etc. This lead the researcher to ask whether dextropropoxyphene was addictive to the general population, or only to the vulnerable. In another study, inpatient psychiatric patients were allowed unlimited access to dextropropoxyphene. The level of use was found to be roughly co-related to the level of personality disturbance, but no patients overdosed. Further studies seem to back up this conclusion that to mentally healthty individuals, dextropropoxyphene (being a weak opioid) is simply not significantly addictive. Cases of dextropropoxyphene addiction among those without a background of emotional problems or personality disturbance are extremely rare. -- Eliyohub 11:41, 8 October 2005

First, let me explain that the poisonings by opioid medications are rarely, if ever, a result of slow chronic build-up. even in a chronic user, a poisoning is almost always caused by voluntarily taking a dose significantly higher or significantly more frequently than the prescribed or normal dose. it is this acute toxicity i mean, not "long-term abuse," when i cite "abuse" of the drug -- it impacts many patients.
I see plenty of instances of Darvocet crises, and i have seen it in both the respiratory-depressing and liver-toxicity types. None have died. However, in profiling patients, sufficiently many new addiction cases exist without pre-existing histories to keep the question open that you have so eloquently sought to close.
While most modern research indicates patients stop increasing a pain-management dose once the initial euphoria fades, the concern with darvocet is that the euphoria tends to fade more quickly in its users than in users of any other opioid-agonist medication, causing users to significantly increase their doses in proportions much higher than those of other opioids.
Moreover, a great many patients present with upset stomach, nausea, emesis, cramping and other similar symptoms that cause a range of misdiagnosis from UTI to IBS. a trick i've recently used is a one-two punch: check liver enzymes (blood draw) and inject IM naloxone. if the patient develops a runny nose and watery eyes, your patient is borderline poisoned by a schedule III (us) narcotic.
This potential, though remote, is serious enough that i avoid prescribing anything containing APAP except when thoroughly necessary (either to protect myself, as in a non-heart patient in need of short-term pain management or because Schedule II drugs are simply tough here in the states (see below). -- DrMorelos 20:32, 19 February 2006
Fist, let me say that I greatly appreciate your response. I, unlike you, am no pysician.
I don't know where you are located, but you refer to Darcovet overdose and toxicity. Darcovet (as I am sure you are aware) is a combination of dextropropoxyphene and acetaminophen, so you will get "liver toxicity.
I am located in australia. The most commonly (ab)used form here is Doloxene (100mg pure Dextropropoxyphene napsylate, with no acetaminophen, readily available) so liver damage is virtually unheard of.
Most abusers are usually also abusers of other (stronger) opioids such as heroin so "respiratory-depressing" fatalities are rare. Most only use dextropropoxyphene when unable to obtain their opioid of choice.
Note: the study I mentioned above, of fatalities in san francisco, dealt only with deaths as a result of dextropropoxyphene - not co-related acetaminophen poisoning (which often happens faster).
My recommendation? If someone is going to abuse dextropropoxyphene, give them the pure stuff, as we do here. You'll get far fewer problems - and no shredded livers.
The issue of abuse liability in the "mentally healthy" remains open. I'd love to hear your thoughts. -- 203.36.217.79 07:52, 5 March 2006
Well said. You're right on all counts. And generally the people who abuse the stuff are those who are likely to abuse all sorts of things. I have changed the "acetaminophen toxicity" to "liver toxicity" which is correct (thank you), though upon re-reading the paragraph I still don't like it. A big problem we're having in the US is the different way drugs are tracked: a combination drug is easy to prescribe, easy to administer and not subject to the same scrutiny or requirements of documentation as a pure narcotic is. For example, Tylenol #3 is one of the most-prescribed pain medications whereas I see a pure codeine solution (even for inpatient administration) used perhaps once every 100 times the combinations are used. And to be honest, it's very hard to overdose on a pure narcotic, even with minimal supervision. They're just safe medications. I am strongly in favour of making most narcotic medications OTC (or at LEAST tracking them differently). Please find your way to my Elvis example for a more complete answer to the propoxyphene napsylate-abuse issue. -- DrMorelos

Is pure dextropropoxyphene actually schedule III in the US?! I am rather surprised! Here in australia it's schedule IV, available on regular prescription and subject to similar documentation and supervision requirements as benzodiazipines (which are pretty run-of-the-mill). My understanding is that serious abuse is pretty rare, and I suspect the reason is simple: why abuse dextropropoxyphene when you can get methadone? If your'e an opioid addict, getting on the methadone program is pretty simple. The US DEA claims on its' website (http://www.dea.gov/pubs/abuse/4-narc.htm) that "This narcotic is associated with a number of toxic side effects and is among the top 10 drugs reported by medical examiners in drug abuse deaths." I am shocked! Please explain? Are these deaths mostly "respiratory depression", or are they "liver toxicity"? How can such a weak opioid kill so many people (unless it's the acetaminophen that's killing them)? And why do people go for it if they can get methadone? Or is it hard to get on a methadone program in the US?

Let me begin by saying that yes, the acetaminophen is what's killing people. Methadone programs are easy to join, but mostly (in my opinion) worthless. Heroin clinics here brag about getting 80% of patients off heroin. They leave out the part that says "We replaced their street drug with our laboratory drug and now they have to waste 30-60min of every day coming here to get their daily dose." In my clinical opinion, this is not how you cure a dependency or an addiction. I have been lobbying desperately for permission to perform an (1x monthly) Ibogaine + (1x bi-weekly) MDMA + (weekly) cognitive therapy (double-blind) study on a small group of worst-case addicts. I will never receive the permission and the study will never be performed, but I would bet my life and everything in it that this is the way to turn dependency or addiction into symptomless loss of the need for opioids. -- DrMorelos
Methadone also beats both naloxone and naltrexone in terms of receptor affinity, so if the user decides to pursue euphoria with it there's an enormous potential for guaranteed death by respiratory depression. I have never, and will never, prescribe(d) methadone as a pain management drug. It is (in my opinion, again) dangerous and inappropriate when reversible and equally potent opioids are options. -- DrMorelos
Have you heard of buprenorphine? This one is pretty amazing in many ways. The partial mu-agonist and mu-antagonist activity enables receptors to "take a break" and work on reshaping themselves to better match the user's endorphins. I have heard of 9-day, asymptomatic, complete withdrawals from long-term use through transition to buprenorphine. Apparently, though, one must wait until whatever other opioid was cleared nearly entirely from their system (they need to become symptomatic - night sweats, diarrhoea, etc.) before starting ultra-low-dose buprenorphine. -- DrMorelos

Oh... and just out of curiousity, is it practically possible to overdose on the napsylate form (as opposed to the hydrochloride form)? I thought there was a "ceiling" on absorbtion, and that was why we here in australia rarely see doloxene deaths. (doloxene is pure dextropropoxyphene napsylate). It would take some sort of combination (such as with alcohol or a benzodiazipine) to kill, wouldn't it? Oh... and today, I happened to stumble on a report on the matter at http://www.unodc.org/unodc/en/bulletin/bulletin_1960-01-01_1_page003.html Their conclusions are fascinating, and the reprorted phenomena observed seem frankly somewhat bizarre. If and when u have a chance to explain this puzzle to me, I would be grateful.

A very quick response - some patients get a different and much more high-energy euphoria from dextropropoxyphene than any other opioids they can get prescribed to them. Sorry; if you have a back ache I'm not giving you sufentanil on your first visit. Bye-bye, Mr. License and reputation. In the US, BZDs are in the "Pretend Schedule" and dextropropoxyphene without liver poison is Schedule III. In addition, the blockage can cause an Elvis-style death (he liked the codeine sulfate; I guess his CYP2E1 worked) by (perhaps two-months of) amazingly intense constipation and then septic shock. In fact, propoxyphenes are incredibly 'drying' and extretion-blocking; maybe more so than any other opioid I have met. With propoxyphene-n, respiratory depression doesn't generally become an issue, but bradycardia can. Also, the N can kill you but it is harder to do with no APAP. Thus, propoxyphene-n abusers can die from different abuse results than dextropropoxyphene+apap patients. Does that help? --[DrMorelos]]

Why has this chemical lost its license in the UK? The fact of potential for abuse should not trump the legitimate use by those whose metabolism works best with these properties. 96.228.137.222 (talk) 09:50, 4 August 2008 (UTC)

Why use it at all?

Why did we use it atall when Codeine is cheaper to produce I believe, and has a much higher theraputic index.


To be frank, it takes a freakishly different metabolic pathway. Moreover, many patients respond better to propoxyphenes than codones at lower TI and exhibit the "defective" codeine -> morphine pathway leaving us with only the propoxyphenes to treat them.
People who don't have the defective CYP2D6 can exhibit much different reactions with propoxyphenes because they tend to do more at brain sites than codeine (prior to its metabolism into morphine); often times here in the states we'll begin with an irregular migraine patient and skip the "migraine drugs" in favor of old-school Darvocet. The reasoning is if they're not having migraines all the time, preventative drugs are pointless; dextropropoxyphene or propoxyphene-n seem to do -very- well at doses around 60mg for migraine patients with very little of the dryness, urinary and fecal retention, or euphoric side effects. This is clinical experience talking, so give it whatever authority you'd like. Recognize, please, though that about half my irregular migraine patients are using darvocet and I can write them scripts once every 3 months for 20 pills; the pills last. -- DrMorelos
There are some people who cannot tolerate Codeine or Paracetamol/Acetaminophen. Straight Propoxyphene Napsylate (Darvon-N 100 which is NOT to be confused with Darvocet-N 100!) is what works for them. Codeine intolerance runs in my father's side of my ancestry, and I have it too. I spent most of a week in hospital puking my guts out, even though my father told them I couldn't take Codeine, they gave me pills with it anyway! Five minutes after taking ONE pill of something without Codeine, I was fine.) Fortunately I don't have a problem with Paracetamol/Acetaminophen (AKA Tylenol), but it gives my father terrible headaches. He is a disabled veteran with chronic pain and Propoxyphene Napsylate is the only thing that works. —Preceding unsigned comment added by Bizzybody (talkcontribs) 00:49, 6 December 2008 (UTC)

Enzymes

I altered the article to reflect this - the enzyme in question is CYP2D6 which is vital to convert codeine to morphine - Eliyohub (amatuer psychopharmacologist)

Thank you so much for doing that. The pathway of metabolism is so incredibly important and, as the other gentleman said, the metabolic differences make it so people with defective CYP2D6 enzymes (10% of the US population, roughly) are precluded from using codeine for anything but making themselves throw up. The first time my life-partner's (don't believe in marriage, sorry, and irrelevant) enzyme became evident I realized two things: (1) it's tough to hold a girl's hair back while she's having a bout of projectile vomiting and (2) codeine never makes it to the morphine stage in these bad CYP2D6 folks. Thank you all for cleaning this up so much and adding links, references and simply excellent pharmacology and toxicology components. This article began as my baby, and it's grown into something worth reading here on wikipedia. -- DrMorelos
Moreover, and THIS IS EXTREMELY IMPORTANT TO ME, we should include just a couple other things on the CYP2E1 enzyme which is how most propoxyphene abusers wind up on (and not making it near the top of) the liver transplant list, then dying. It would make this article much more robust. APAP is an interesting drug with a horrible TI which in small doses can help but which in large doses causes either half day-long bouts of vomiting (biliary pH becomes distorted and liver gets extremely upset) or worse yet, death by liver failure (which, disgustingly, comes between 4-7 days after the patient thinks he or she has recovered - they start turning yellow and by the time they are admitted it's just too late; we start a morphine + diazepam drip and if necessary add fentanyl patches and the patient dies comfortably but way too young. It hurts a clinician or physician to see this theme recurring because of APAP. Some kind of solid tie-in would be meaningful to our less knowledgeable readers. Anyone willing? -- DrMorelos
I would also love it if someone would be willing to help me construct a paragraph about using cimetidine (Tagamet in US) in larger-than-recommended doses to completely inhibit CYP2E1 and prevent APAP issues. I have experimented with this myself and played Russian Roulette: [ Removed per WP:BEANS] (Paracetamol) three hours after taking [Removed WP:BEANS]; the next day I took 12 more of the same APAP with no extra cimetidine; that's [Removed WP:Beans] of acetaminophen within 16 hours (guaranteed liver poisoning). Think of it as a small meal consisting of nothing but Paracetamol. -- DrMorelos
Though it was dangerous and stupid, I would rather poison myself than any other and please do not repeat this as it is simply (how should I put it) the most irresponsible and dangerous single thing I have ever done. Again, please do not repeat this self-experiment; YOU COULD DIE A HORRIBLE, PAINFUL DEATH. Perhaps I have a strangely potent and tolerant CYP2e1 or perhaps the cimetidine worked as an inhibitor to prevent the APAP from being converted into its toxic metabolites (studies in other mammals have repeatedly demonstrated that cimetidine help prior to dosing but not after the APAP has been ingested). Just three days after the second day's dose, and since I exhibited NO symptoms of any problems, I asked a colleague who did not know what I had done to order me some blood work ("to check my cholesterol;" it looks less suspicious that way). Generally patients who poison themselves with Paracetamol initially get sick and then think they're recovering for four to five days; at day six or seven, the one-way trip begins. -- DrMorelos
My AST returned 16 (clinically healthy is between 10 and 40, inclusive). My ALT returned 12 (many labs say 15-45 is acceptable while many other labs will say anything below 36 is healthy). Perhaps, as I suggested, my liver is "special." My other liver were also on the low side of healthy. YOU MUST UNDERSTAND: DO NOT REPEAT THIS EXPERIMENT ON YOURSELF, ANOTHER PERSON OR A PATIENT. YOU MAY BE IN GRAVE DANGER. I thought it would be interesting for intelligent and educated professional clinicians and amateur pharmacologists to know about this SINGLE-CASE, STATISTICALLY MEANINGLESS AND WILDLY IRRESPONSIBLE self-experiment. -- DrMorelos
Dr Morelos, I greatly respect you, and you seem to be extremely knowledgable, but all I can say after reading this russian roulette self-experiment is YOU WERE AN IDIOT! Do you realize that you could have killed yourself?! You don't need to worry about me trying anything so stupid and dangerous, I can assure you.
The problem, I suspect, in using this method in an emergency setting is that by the time one catches acetaminophen poisoning, it's usually too late. That said, I could see it being very useful in dealing with people who confess in the early stages.

22:09, 27 April 2006 (UTC) use NSAIs, Paracetamol or semi-synthetic morphine analogues.

In my clinical and pharmacological opinion, this is a bad option. NSAIDs (other than 81-162mg aspirin) are contraindicated in heart patients; Paracetamol (Tylenol / APAP) is contraindicated in patients with decreased liver function; semi-synthetic morphine analogues (I think you mean Thebaine-derived semi-synthetic opioids such as hydrocodone or oxycodone, which have fierce abuse potential) are generally too much for a typical patient where codeine or dextropropoxyphene would be indicated. Now, if your patient is liver-compromised, you must avoid the APAP (Paracetamol) component of the opioid and write a script for Schedule III (US) vicoprofen hydrocodone+ibuprofen; for non-heart patients only) or you have to skip straight to Schedule II (US again) and prescribe an elixir or pill of pure, strong opioid. This is a huge liability for any medical practitioner and the difference in paperwork (we have to write a 'check' which has to be called into the DEA and cleared as opposed to a simple script) between Schedule II and Schedule III medications is intensely time-consuming. -- DrMorelos

The source of the vast majority of APAP overdoses

Most APAP od's come from what are usually called "cry-for-help" suicide attempts; made, most frequently, by teenage girls. Girls who, for whatever reason, decide to down the bottle of Tylenol one day. They are almost never aware of the hepatotoxicity of acetaminophen and more than few end up on the Liver Donation Needed list.

If you have kids, esp girls, make them aware than there are much better ways to get attention than an APAP overdose.

It only requires 10-15 500mg tablets to kill you. And, as cited above, by the time treatment can be administered (there is an antidote acetylcysteine, trade name Mucomyst, normally used in treating cysticfibrosis [sp?] I believe), it's usually too late to save the liver, thus condemning the patient to an agonizing death (as noted above).

As a chronic pain patient who takes two CII drugs daily (Dilaudid and Oxycontin), I can tell you that things have loosened up tremendously in the last ten years regarding the prescription of Schedule II & III drugs, especially the former. I suffer from interstitial cystitis--a debilitating, incredibly painful condition--and have since I was 19 (I'm now 37). When I first began to suffer from it (1989-90), trying to get CIII, let alone CII out of DR's, esp since I didn't have health insurance then and had to resort to ERs, was like pulling teeth; I was once flat-out accused of being a "drug seeker", a statement which nearly led to the doctor needing a new grill I was so pissed; fortunately the attitude towards pain has shifted dramatically for the better. Especially with the (relatively) new specialty of pain management (usually neurologists looking for a new niche). These MDs and ODs take upon the paperwork requirements and monitoring of patient compliance with Narcotic Contracts and dosing instructions (my pain mgmnt doc actually had me take a piss test, I was extremely annoyed at the blatant implication of mistrust, but I like and respect this doctor and I understand this helps cover his ass with the Feebs).

Also, DrMorelos, the paperwork requirements vary by state. In California, for example, a special, triplicate prescription form is required for CIIs. In my state of Nevada, there is no such requirement. And while, of course, the DEA keeps a close eye on these drugs, as long as the provider follows the rules, keeps proper paperwork, sees the patient every month, he or she is unlikely to come under undue scrutiny.

What irks is me is how doctor-patient confidentiality goes right out the window when it comes to these drugs. State and Federal regulators don't even need a warrant to access your pharmacy records (i.e. those kept by the state). Where as to get their hands on your chart they have to get a judge's assent. It's an absurd end-run around the Fourth and Fourteenth Amendments; yet another product of the anti-drug hysteria generated by the failed "War on Drugs". PainMan (talk) 09:00, 24 April 2008 (UTC)

There's a bunch of stuff on this page that really shouldn't be here. This page is to discuss improvements to the article, not the subject of the article. Having said that... Yes, paracetamol is involved in very many overdose deaths, but this isn't an article about paracetamol. Dextropropoxyphene (in the form of coproxamol) was, for many years, the main drug used in suicides in the UK, and was involved in many accidental overdoses. Dextropropoxyphene is much quicker to kill than paracetamol - dextropropoxyphene kills within an hour, paracetamol has a window of a few hours for you to get an antidote. All this is verifiable sourced and referenced in the article. Dan Beale-Cocks 09:28, 24 April 2008 (UTC)

DANGER

Allow me a comment about Darvocet, it is extremely DANGEROUS. I was alarmed to see the suicide statistics for people who were prescribed this drug. Surely it cannot be considered as a medication. In 1997 I had shoulder surgery and was prescribed Darvocet. Shortly after taking the prescribed dosage I would attempt to sleep. Regardless of whether it was in the middle of the day or at night I began having halucinagenic dreams shortly after falling asleep. These dreams were Horrible and involved horrific monsters attacking me in a subconscious state it was always the same outcome, I would begin screaming and screaming. If it was at night my wife was terrified, and tried to wake me. If it was in the daytime and I was home alone I could not wake from this horrific state easily. PLEASE DO NOT EVER TAKE THIS DRUG, YOU COULD SERIOUSLY HURT YOURSELF. Jmmanuto 03:24, 3 February 2007 (UTC)

This drug is prescribed in limited capitcy because of it's drug rating. I think your had a reaction that most people don't have. ShadowWriter 17:09, 18 February 2007 (UTC)


ShadowWriter is correct. Jmmanuto's reaction is what's called "idiopathic;" i.e. unique to him or herself and one that hasn't shown up in the required clinical trials.
As a chronic pain patient whose taken Darvocet I can say two things: 1.) There's 99.99999% chance you will NOT have a reaction such as the one cited above and 2.) it just doesn't work better than non-narcotic OTC preparations such as aspirin, ibuprofen, naproxyn (sp?), etc. While it does have a mild and brief euphoric effect after the first couple of doses (similar to feeling of a beer on an empty stomach), it's neither very addictive (or, to be more medically specific, it's potential for addiction is quite low) and almost totally ineffective as a pain killer. Admittedly the last clause is my personal experience.
PainMan (talk) 08:38, 24 April 2008 (UTC)

Darvodan?

I seem to remember a pill called "Darvodan" but Google shows no reliable hits except one document on Yahoo! Answers where it is described as it was described to me, as "Darvon and aspirin." "Darvadan" gives 88 hits, but nothing reliable (mostly lyrics from this one song). Has anyone else heard of Darvodan?0702034 18:57, 6 February 2007 (UTC)

Trouble breathing?

Is Darvocet known to cause trouble breathing? I just took a pill and I am having mild difficulty breathing - mostly like I am not getting enough oxygen and I feel the need to hyperventilate, leading to light-headedness. However, I have taken Darvocet before and I have never had this difficulty in the past, so I wonder if there is another reason for this. I did not overdose.

I wonder if I will faint... I was warned that fainting could be a possible side affect by the doctor who first prescribed Darvocet to me, but I have never before fainted, although I do get dizzy, and I often sleep for an hour after the Darvocet takes effect.

Sorry for using the talk page for a personal matter, but perhaps this message will inspire someone to do some research that will improve the article.

Thank you,
Armedblowfish (talk|mail) 05:02, 9 February 2007 (UTC), 05:04, 9 February 2007 (UTC)

U.S. doses

The article had said that the U.S. prescribed dosage ranges up to 60/325, but in fact my prescription was for 100/650 tablets -- and in fact, one of the pictures in the article shows exactly that tablet. --Andersonblog 14:55, 1 July 2007 (UTC)

Yeah, mine's 100/650 too. linas 02:34, 11 July 2007 (UTC)

propox nap with apap

What the heck is "propox nap with apap"? Is "apap" supposed to be an abbreviation for aceominaphen? This article should clarify, as this seems to be the common compound that is prescribed. linas 02:34, 11 July 2007 (UTC)

Yes, "apap" is code for Acetaminophen; See http://www.drugs.com/ppa/acetaminophen-n-acetyl-p-aminophenol-apap.html I would like to know why Propoxyphene redirects to this article, myself; and what's Propoxyphene-n -- Guest 1111:39pm, 4 2008-Sept-4 —Preceding unsigned comment added by 71.131.25.65 (talk) 06:40, 5 September 2008 (UTC)

Typo: paracetamol instead of Dextropropoxyphene?

"It is often combined with paracetamol (Acetaminophen) in the preparation co-proxamol, however, there is no evidence that this combination is any more effective than paracetamol alone"

Common sense would dictate that the second occurrence of paracetamol is incorrect. It doesn't make sense that an opioid would be entirely ineffective compared to an OTC pain reliever, as anyone who has taken either can verify. I believe this was a typo, and should, instead, say Dextropropoxyphene. AlanM1 (talk) 13:19, 7 February 2008 (UTC)

No. The sentence is correct. Coproxamol contains a sub-therapeutic dose of paracetamol. There's no evidence that a dose of coproxamol is any more effective than a therapeutic dose of paracetamol alone. This is a referenced quote. I think it comes from the Committee for the safety of medication - an old UK organisation. Don't forget that coproxamol contains a small amount of a _weakly_ acting opiod analgesic, and a less than a therapeutic dose of paracetamol. Dan Beale-Cocks 13:45, 7 February 2008 (UTC)
Here's a link to a quote for that very nearly that sentence: Google show pdf as html result

The MHRA took the decision to remove co-proxamol from the UK market in January 2005 because of safety concerns and lack of evidence for efficacy. Early in 2007 it stated that “Co-proxamol is implicated in 300 to 400 deaths from overdose a year. There is growing concern prompted by UK research which shows that co-proxamol is implicated in almost one fifth of drug related suicides and is secondary only to tricyclic antidepressants as an agent of fatal overdose”. There is no good evidence that co-proxamol is any more effective than full strength paracetamol taken regularly for either acute or chronic pain. There is also no identifiable patient group in whom the risk: benefit ratio of co-proxamol is positive.

One of the problems of pain killers is the strong placebo effect. There's a study somewhere showing that 40% of people suffering from long term pain reported relief when given a placebo. Dan Beale-Cocks 13:48, 7 February 2008 (UTC)

OK. From my experience with people on this drug, I don't believe it, but thanks for the cite. AlanM1 (talk) 20:24, 7 February 2008 (UTC)

UK CoProxamol ban / suicide risks

Coproxamol contains 32.5 mg of dextropropoxyphene and 325 mg of paracetamol. Two tablets does not provide a therapeutic dose of paracetamol, and provides a dose of a weak, but toxic, analgesic. About 250 - 400 per year were dying from coproxamol overdose in the UK. Most of these people died in their homes, or on the way to hospital. To be clear: This isn't the paracetamol killing people, it's the opioid. The dangers were first raised in 1977. Coproxamol has had several clear warnings since then. Coproxamol was the second most used med in suicide attempts (after anti-depressants), but is considerably more toxic than other meds when taken in overdose. There's no evidence that coproxamol is any more effective than a therapeutic dose of paracetemol alone.

Here's some quality refs:-

[[[linkification: http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1365-2125.2004.02252.x%7Chttp://www.blackwell-synergy.com/doi/pdf/10.1111/j.1365-2125.2004.02252.x]] A multicentre study of coproxamol poisoning suicides based on coroners’ records in England]

[[[linkification: http://cebmh.warne.ox.ac.uk/csr/rescoprox.html%7Chttp://cebmh.warne.ox.ac.uk/csr/rescoprox.html]] Co-proxamol and suicide]

[[[linkification: http://www.nyrdtc.nhs.uk/docs/dud/DU_31_co-proxamol.pdf%7Chttp://www.nyrdtc.nhs.uk/docs/dud/DU_31_co-proxamol.pdf]] DRUG UPDATE]

[[[linkification: http://www.mhra.gov.uk/home/idcplg?IdcService=SS_GET_PAGE&useSecondary=true&ssDocName=CON2025739&ssTargetNodeId=387%7Chttp://www.mhra.gov.uk/home/idcplg?IdcService=SS_GET_PAGE&useSecondary=true&ssDocName=CON2025739&ssTargetNodeId=387]] MHRA] UK government agency

I am unable to edit the article. I would be unable to maintain NPOV. Dan Beale 19:55, 11 April 2007 (UTC)

"There's no evidence that coproxamol is any more effective than a therapeutic dose of paracetemol (sic) alone." User Dan Beale states.
My own Empirical experience would suggest otherwise. My experience is probably no less a NPOV than your beliefs. I have been prescribed Co-Proxamol (in the UK) for moderate to severe pain caused by a spinal injury since the late 1990's. I have used it safely and only experienced constipation after the need to take the maximum daily dosage during particularly severe periods of pain. I have had periods of between 12-18 months where the pain has not needed to be managed by co-proxamol or indeed anything else other than living carefully (eg. no horse riding, bungee jumping, rollercoaster riding etc.)
Co-Proxamol continues to be available within the NHS on a limited "named patient" basis (my understanding of the term 'new patients are not prescribed it' but I am not certain of this). For a period of about a year, when the "ban" came into effect, pharmacy supplies in my area disappeared entirely. Fortunately, for me at least, this co-incided with a period where medicinal pain relief was unnecessary. But recently I have needed pain relief when the injury was aggravated by other factors. My GP initially offered Co-Codamol, which from previous experience has no discernable effect on my pain. I declined the offer, not wishing to waste my money (£6.85 prescription fee) on what (for me) is an ineffectual pain reliever. In a remark I made to the GP merely intended as a humourous aside I said "No thanks, I'll go an buy a tube of Smarties instead. They're cheaper than a prescription of Co-Codamol and have no effect on the pain either but they taste nicer. Pity Co-Proxamol is 'banned', thats the only one that ever worked". To which my GP replied that their pharmacy had started to be resupplied. This was much to my surprise as I thought the drug had been banned. After studying my previous history, my GP prescribed me Co-Proxamol again.
I am only one man and that is from a wikipedia point of view original research. However, in the suspected suicide of Dr David Kelly Co-Proxamol was partly implicated along with the cutting of his left wrist. More detailed UK Media interest in the event touched upon Co-Proxamol and some web based news services gave a more detailed background of the drug. This peaked my interest at the time because I was familiar with the name of the drug. Ever the inquisitive type, I looked into the background of the drug via the net. I do not recall the sources I read at the time but I discovered the following from the most basic of google searches ...

[[http://www.theyworkforyou.com/whall/?id=2007-01-17b.340.0]] [[http://www.patient.co.uk/thread.asp?thread=563&noscript=noscript]] [[http://petitions.pm.gov.uk/Co-Proxamol/]]

These contain empirical Co-Proxamol users evidence that contradicts the statement "There's no evidence...".
Further to add to the details of my own experience, I do not preclude the possiblity that Co-Proxamol continues to have a placebo effect on me. But when I first took it, I had no knowledge of the drug's effects and experienced a sensation similar to drunkenness. This effect is no longer experienced by me, perhaps due to Drug tolerance.
I have no doubt, that as user Dan Beal, I suffer from confirmation bias, so I will not be editing the article and anyway I do not consider myself qualified to do so. I would welcome the input from others who could maintain rigorous neutrality. If only because I would like to know if there is "no evidence" why does the drug work for me when Co-Codamol and regular Paracetamol don't? GordonTG 08:52, 15 November 2007 (UTC)
Oh and I should add, NSAIDs were contraindicated in my case due to other factors. And that just because my own experience was positive it does not mean the drug is suitable for you 'CARE SHOULD BE TAKEN AT ALL TIMES WHEN USING THIS DRUG. ALWAYS FOLLOW THE INSTRUCTIONS. NEVER EXCEED THE STATED DOSE'. I've added this just incase people reading this decide to self diagnose and think this is the drug for them.
I hope that's clear :) I was a bit concerned having read this and other drug related talk pages, that people may use Wikipedia for health advice. Wikipedia is here information, not health advice. If you want health advice, see a Doctor. signed GordonTG 09:31, 15 November 2007 (UTC)

Re: Suicide Risks. Types of suicide are related to the availability of lethal agents. If hand guns are widely available in a given population, hand guns will be used in a high proportion of suicides. If a very high bridge is available for people to jump off, that very high bridge will be used in a high proportion of suicides. As with all potentially dangerous things, they are not a problem when used with the appropriate caution. If individuals choose to abuse dangerous things we are powerless to stop them. For if we tried, we might just as well wrap cotton wool around everything and remove all sharp objects from the planet.

Deaths by suicide and self-inflicted injury in the UK for 2002 - 4,066 persons [[http://www.who.int/whosis/database/mort/table1_process.cfm]](Direct link not possible, manually select country and year)

Grim reading. If we had removed one lethal agent like Co-Proxamol would that have saved lives? Quite possibly or maybe they would have chosen something else. As with all the other lethal agents involved in suicide a balance of benefit versus risk must be struck. Does the potential for abuse outweigh the benefit? In my own case it does, for a life without effective pain management is extremely unpleasant. GordonTG 10:36, 15 November 2007 (UTC)

Replying to GordonTG - 1) "No evidence" isn't my POV, it's peer-reviewed published opinion that's accepted by most UK agencies. 2)Why does co-proxamol work for you when other stuff doesn't? Because pain has complex causes and placebo effect plays an important part of pain relief - 40% of users with chronic pain report relief from that pain when given sugar pills (I'll find a ref later). 3) Removing means of suicide is an important factor of suicide prevention. Suicide by overdose tends to be impulsive, co-proxamol kills quickly, removing co-proxamol removes a quick-acting means of death. Switching to other meds means a swithc to less fatal meds. 4) Dr kelly - slashing wrists is a paiful and difficult way to kill yourself, co-proxamol is remarkably easy, as can be seen by the number of accidental co-proxamol deaths. But, again, I have a clear POV, and will try not to edit the article. I appreciate your comments. Dan Beale-Cocks 20:44, 30 December 2007 (UTC)

About efficacy Paracetamol plus dextropropoxyphene in postoperative pain

Structural Image Change

I'm changing the structural image, as it looks slightly misleading as the carbonyl oxygen looks like its cyclized, although this isn't possible, it's still slightly misleading visually. Also, the new image is using the ACS settings in ChemDraw. If anyone has a problem, let me know. Ccroberts @ 01:52, 16 February 2008 (UTC)

Unjustified description

I removed the following description of the drug:

citing its highly addictive nature

The drug is Schedule IV under the Controlled Substances Act of 1970. CIV's, as they are known in the jargon on the medical trade, are not considered to have a high potential for abuse/addiction.

It has about the same potential for the last as does Diazepam or Xanax or the opioid pentazocine.

Many of the most common narcotic/opioid drugs are Schedule II, including morphine, Fentanyl, Dilaudid, etc.

I'm a chronic pain patient and I've been treated with most of the narcotics in the pharmacopeia and Darvocet isn't in the same ballpark. To quote Quentin Tarantino "it's not even the same [deleted] sport."

(My CV: I took a vocational program and worked as (hospital) pharmacy tech.)

PainMan (talk) 07:41, 13 March 2008 (UTC)