Inflammatory question...
December 4, 2007 9:39 AM   Subscribe

If musculoskeletal pain responds well to acetaminophen (paracetamol), but does not respond at all to anti-inflammatory meds, does this tell us anything about the origin or cause of the pain? Other than, "it's obviously not inflammatory pain".

As an example, my friend had sore tendons in their arms, legs, wrists and ankles for weeks.

Having had good success with anti-inflammatories such as Aspirin, Aleve, Advil, etc. for back aches and things, this was what he took for several days (dunno which ones exactly). No let up in the pain at all.

He had never bothered with acetaminophen before for anything except headaches, but eventually tried some, and bingo! - instant relief for the day.

I can't understand why that kind of pain would respond better to that kind of painkiller... and if it had been me, I might never have bothered trying the acetaminophen.

So what kinds of pain respond to what kinds of painkiller? The internets just kind of says, "try different ones to find out what works", but hopefully science knows more than that these days... yes? no?
posted by blue_wardrobe to Health & Fitness (10 answers total) 5 users marked this as a favorite
 
I'm no expert, but I'd say that if your friend was a regular user of aspirin / ibuprofen / naproxen (they're all basically related drugs), then he probably has some kind of resistance to it (I know I do, as I spent a lot of my younger days with a bad back and a bad doctor that just scripted me heavy doses of IB and sent me away). I hardly ever take acetaminophen, but when I do, pain goes away like magic, while anti-inflammatories often leave me hanging.

To answer your question more to the point: anti-inflammatories usually treat muscle pains, while acetaminophen is usually reserved for things like headaches. But, I've seen both used for both. I do know that anti-inflammatories tend to take down swelling, though.
posted by General Malaise at 10:56 AM on December 4, 2007


Most bottles of ibuprofen say to take 1 tablet (which is actually a pretty small dose), and then take a 2nd tablet if the pain doesn't respond. Many bottles of acetaminophen say to take 2 tablets. Honestly, my guess is that he just didn't take enough ibuprofen.
posted by selfmedicating at 11:02 AM on December 4, 2007


paracetamol can inhibit COX3.
posted by NucleophilicAttack at 11:36 AM on December 4, 2007


Best answer: This is a complex subject. First of all, although acetaminophen (called paracetamol in Europe) and the nonsteroidal anti-inflammatory drugs (NSAIDs) are known to act on very similar enzyme systems, we now know that the particular enzyme subtypes the NSAIDs react most strongly with are distributed all over the body (and are particularly concentrated in areas of inflammation) whereas the enzyme substrates for acetaminophen are found pretty much exclusively in the central nervous system.
In other words, NSAIDs are best for inflammatory pain (that's why they can be very effective in cream/gel form for superficial inflammatory pains) whereas acetaminophen reduces pain processing in the brain. It does so in a dose-dependent manner, so the more you take, the stronger the effect will be - however at doses above 4 grams per day, your liver can be damaged (that's why you can kill yourself with acetaminophen poisoning). Fatal liver failure is common at doses above 10 grams per 24 hours, and this has given acetaminophen a bad name.
It is however coming back into "fashion" as it is now available with a built-in liver protection agent, and the NSAIDs have pretty dangerous side effects as well in existing kidney impairment, severe asthma, and blood coagulation deficits. In recent years it has been realised that you can get excellent analgesia with a combination of the two.
Bear in mind that for moderately severe pain, you need to saturate your system with the painkiller(s), and that will take 5 dosing intervals, i.e. around 30 hours. It should also be remembered, that there are huge interpersonal differences between peoples' responses to acetaminophen and the (large numbers of) different NSAIDs - these interindividual differences are probably as big as, or bigger than, differences between common aches and pains. Lastly, certain (atypical) pains will respond poorly or not at all to these so-called "simple" (i.e. non-opioid) analgesics, e.g. nerve pain such as sciatica.

I should probably say that I am a medically qualified pain therapist. I am also copying this response to another similar enquiry on AskMeFi.
posted by kairab at 11:46 AM on December 4, 2007 [10 favorites]


Well, I'd say kairab deserves a flag for best answer...
posted by Slarty Bartfast at 1:34 PM on December 4, 2007


If I may add several details for future reference (this may begin to show why I said this is a complex subject...) - there has been a lot of publicity and controversy relating to the different enzyme subtypes affected by NSAIDs: Cyclo-oxygenase (COX)-1 is widely distributed throughout the body, and is inhibited by all classic NSAIDs; COX-2 is increased especially in inflammatory conditions, and is preferentially or selectively inhibited by COX-2 NSAIDs (e.g. Celebrex/celecoxib). These agents were developed by "big pharma" in the hope that they would do just as good a job for pain but without the risk of gastric ulceration that classic NSAIDs carry. It was however belatedly realised that the flipside of this particular coin is that you lose the cardioprotective platelet-inhibiting side effects of the older NSAIDs (the reason why low-dose Aspirin is good for you), and consequently patients with coronary heart disease started dying while on COX-2 inhibitors. Big legal mess ensued...and most COX-2 inhibitors have been withdrawn, with massive financial crises for big pharma! This is one of the reasons why acetaminophen/paracetamol is making a comeback (another is its recent availability as an intravenous preparation for hospital inpatients). It is a specific COX-3 inhibitor, but that is primarily of academic interest. For what it's worth, some small studies suggest that a combination of full-dose classic (COX-1) NSAID and acetaminophen is approximately 30% more potent than NSAID alone.
Ibuprofen and naproxen have perhaps the best (question of definition here) reputation among the classic NSAIDs - the former being the least harmful (but not particularly good against inflammation) and the latter being both potent and the most cardioprotective besides Aspirin (which is really tough on the stomach in full dosage).
Another factor to consider for some is that Aspirin and other NSAIDs are among the most allergenic common medications (roughly on a par with penicillin), and a severe allergic reaction can kill you! Although allergy to acetaminophen is not unknown, it is very rare. I hope this helps (or at least doesn't confuse you totally).
posted by kairab at 2:17 PM on December 4, 2007


Response by poster: Simplistic review: does this mean that since his pain responded well to acetaminophen, and since acetaminophen "reduces pain processing in the brain" (per kairab), but didn't respond well to NSAIDs, that the origin of the pain is *within* the nervous system rather than external to it.

Does this question make sense, and if so can we say such a thing?
posted by blue_wardrobe at 2:26 PM on December 4, 2007


To come back to the original question: From the description offered (many different painful joints) it sounds like an inflammatory polyarthritis/synovitis to me - this is often a manifestation of the body's overactive immune response to a viral infection (I've had this myself, and it can be a bloody painful nightmare) and should - in theory - be helped by any NSAID. If NSAIDs didn't help on this occasion, this could be (a) because the dose or duration of therapy was too small, or (b) because the indivdual just doesn't respond particularly well to the particular NSAIDs taken (others may happen to work better).
Not least because of its central CNS action, paracetamol is perhaps less specific/dependent on individual responsiveness. Most people who find acetaminophen unhelpful don't take enough of it for a sufficiently long period of time (i.e. more than 30 hours), or have difficulty absorbing it into their system, e.g. when nausea & retching or diarrhoea are prominent.
posted by kairab at 2:56 PM on December 4, 2007


caveat: I have something wrong with a knee. Doc said it was arthritis, but he was just a GP and I think that is incomplete. Anyway, the Ibuprofen doesn't do much. But then I had a cold, and took some Nyquil. Very weird, my knee stopped hurting for several days. Pharmacist thought it was the Paracetamol in the Nyquil (at least, as formulated in South Africa, and sold by a different name, but still Vicks, and still with alcohol).
posted by Goofyy at 3:58 AM on December 5, 2007


In recent years it has been realised that you can get excellent analgesia with a combination of the two. [acetaminophen & NSAIDS]

I have chronic hip pain, and a while ago my mother (who suffers from arthritis) gave me the same tip. Her rheumatologist told her to take one Tylenol and one Aleve -- taken together, this gives me much better pain relief than two tablets of either. I didn't even have Tylenol in my medicine cabinet before, but it sure does work well when combined with NSAIDS.
posted by vorfeed at 3:02 PM on December 5, 2007


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