Talk:Non-steroidal anti-inflammatory drug

From Wikipedia, the free encyclopedia

Non-steroidal anti-inflammatory drug is part of WikiProject Pharmacology, a project to improve all Pharmacology-related articles. If you would like to help improve this and other pharmacology articles, please join the project. All interested editors are welcome.
B This article has been rated as B-Class on the quality scale.
Top This article has been rated as top-importance for this Project's importance scale.
WikiProject Medicine This article is within the scope of WikiProject Medicine. Please visit the project page for details or ask questions at the doctor's mess.
B This page has been rated as B-Class on the quality assessment scale
High This article has been rated as high-importance on the importance assessment scale

Contents

[edit] The ideal wikipedia article

The ideal wikipedia article about a drug should include the inventor, the patent number URL/link, and the year in which it was invented, for every drug. --SystemBuilder 19:49, 23 February 2007 (UTC)

This is a drug class, not a drug. Also, while I sort of agree with you, I work in this area and rarely see that kind of information. I'm not sure how easy it is to come by. josta59 28 February 2008

[edit] Should this be here?

Omega-3 Fatty Acids Drakcap 06:14, 9 October 2006 (UTC)

In Addition Celbrex is a NSAID, but I am not sure which type it is.

Celebrex is a COX-2-inhibiting NSAID. Fatty acids are not NSAIDs; does that answer your question?josta59 28 February 2008

[edit] Adverse risks of COX-2 inhibitors

The risk of COX-2 inhibitors causing MI's and other prothrombotic disorders is anecdotal. It might have to do with thromboxane etc. The bottom line is, that statistical evidence is lacking. A huge study would be required that is sufficienty powered for this finding. JFW 12:12, 4 Apr 2004 (UTC)

looking more and more likely, though. gzuckier 2 july 2004

also, i put in a piece on history of nsaids i had lying around (not copyright anywhere else) but it's unwikipediafied as yet. I'll get back to it sometime, but anyone who wants to can obviously chip in. gzuckier 2 july 2004

"In 2001, NSAIDs accounted for 70,000,000 prescriptions and 30 billion over-the-counter sales annually in the United States. (Green, 2001)." This seems incorrect; it implies that the average person in the US purchases NSAIDs every 4 days. Perhaps it is really 30 billion doses? 21 Oct 2004

While I did not originally put that statement in, I checked that this was the exact wording from the article by Green (2001) when I did the formatting revision a while back. Now that I've looked at the article again, that statement is actually only present in the abstract, and not referenced; so it's perhaps a poor source. But you are right - I wonder if it might perhaps refer to USD$30 billion? Techelf 11:56, 22 Oct 2004 (UTC)

Hmm. This guy says 30 billion over-the-counter tablets sold annually in the United States, which offhand sounds closer to reasonable, but there still is no link to the primary source.

This guy says 30 billion over the counter tablets, but it looks like just a copy of the previous item.

This guy sounds like he's saying $2billion over the counter: "In addition, sales of over-the-counter (OTC) oral analgesics were also very high; about 3 billion dollars were spent, and about 60% of those analgesics included nonsteroidals and aspirin". Most of the articles I looked at also seem to say on the order of $1billion for OTC nsaids, so I think we can rule out $30billion.

this guy says 730 million doses per day in Germany (pop 82 million) with 5% being over the counter, which comes out to..... about .5 doses OTC per person per day, or about 50 billion pills per year for the US. Not too far from 30 billion, considering all the handwaving.

This guy says 26 billion OTC tablets a year, but the original link is gone.

On the preponderance of the evidence, I'd guess it's 30 billion doses/tablets per year, not 30 billion OTC sales, where a sale is a bottle of pills. Agree? Of course, this now opens the can of worms that most of these OTCs seem to count 2 tablets as 1 dose, and the above seem to use tablet and dose interchangably. Then there's the question of whether the 70,000,000 prescriptions cited in the paper are doses or actual prescripotions.... Oy. Gzuckier 16:52, 22 Oct 2004 (UTC)

[edit] What does "irreversibly inhibit" mean?

From the article: "Aspirin, the only NSAID able to irreversibly inhibit COX-1,"

As a layman, I don't understand "irreversibly". In someone taking aspirin just once, COX-1 is inhibited until death? I suspect not. :-) Isidore 20:33, 22 Apr 2005 (UTC)

you are an observant "layman", Izz. i believe it does do it irreversibly, but this refers to "PLATELET" COX, and what limits the duration of its effect is that platelets only live about a week. Sfahey 02:21, 23 Apr 2005 (UTC)
Indeed, aspirin irreversibly inhibits COX-1. Platelets are unable to synthesise new COX-1 and thus so platelet COX-1 is inhibited for the duration of the platelet's "life" as Sfahey noted. COX-1 in other cells is also irreversibly inhibited, but new COX-1 can be (and is) synthesised in those cells. Techelf 03:32, 23 Apr 2005 (UTC)

Thanks, both. I considered updating the article to clarify this for future readers and, broadening my search, looked at http://www.medicinenet.com/aspirin_and_antiplatelet_medications/article.htm. This also mentions thromboxane A-2 and says aspirin's inhibition of COX-1 lasts much longer than other NSAIDs (not irreversibly). At this point I decided I wasn't qualified to update the article! Isidore 16:55, 23 Apr 2005 (UTC)

Can I suggest to the "layman" that COX-1 inhibition actually refers to inhibition of the cyclooxgenase 1 enzyme rather than the cox1 gene, and so inhibition is irreversible in that it acts until 'death' of the enzyme rather than death of the patient. enzynes have variable lifespan and are continually replaced. Specifically asprin acts by covalent modification of the cyclooxygenase (addition of an acetyl group to Serine 530 residue of the enzyme therby blocking the active site).

Yes, we were referring to the enzyme COX-1, not the gene. -Techelf 04:10, 14 May 2006 (UTC)

I think the anonymous poster is right, though; "irreversibly" refers to the life of the enzyme, not the platelet. If inhibited by aspirin, it will be inactive for its lifetime, unlike with other, reversible NSAIDs that bounce on and off, competing with substrate (arachidonic acid) for COX-1's active site. The above posters are correct, though, in that platelets cannot produce new COX-1. They contain a lot of it, but they do only live nine to ten days. josta59 28 February 2008

[edit] NSAIDs and healing

NSAIDs reduce inflammation, but is that actually good for the healing process? Some papers indicate otherwise:

  • A. Beck et al, 2003, "Influence of diclofenac (group of nonsteroidal anti-inflammatory drugs) on fracture healing", Archives of Orthopaedic and Trauma Surgery, 123(7):327-332

(conclusion: NSAIDs delay healing, reduce bone density after trauma in rats)

  • D. Marsolais et al, 2003, "Nonsteroidal Anti-Inflammatory Drug Reduces Neutrophil and Macrophage Accumulation but Does Not Improve Tendon Regeneration", Laboratory Investigation, 83:991-999.

Both of these two papers deal with acute trauma rather than chronic inflammation.

On the other hand, arthritis-related papers seem to be only studying symptomatic relief and reduction of gastrintestinal complications when using NSAIDs. So, have there been any studies relating to chronic inflammation and rehabilitation of sports injuries (where most of the problems are related to overuse) that are studying the healing process rather than the symptomatic relief? --Olethros 15:08, 28 March 2006 (UTC)

NSAIDs are not used to heal things, only to provide symptomatic relief of inflammatory conditions. And you're quite right, they may well be counterproductive in the healing process. -Techelf 11:04, 29 March 2006 (UTC)

[edit] Vet uses and misuse

Diclofenac causes death due to renal failre in vultures Use of diclofenac in farm animals in India has lead to a 95% decline in the vulture population, who eat the dead carcasses. Meloxicam seems to safe for vultues. Snowman 09:07, 22 June 2006 (UTC)

[edit] Non-selective NSAIDs

Non-selective NSAIDs are safe, despite recent claims that even ibuprofen could worsen cardiovascular risk[1]. So no panic. But naproxen is not protective, knocking a hole in the common defense against the VIGOR study results. JFW | T@lk 16:51, 9 July 2006 (UTC)

The following drugs, acetylsalicylic acid, salicylic acid and dicrofenac have been found to increase permeability of the intestine allowing food antigens, some potentially allergenic into the system, the effect is augmented by exercise and cause anaphylaxis, a condition that can compicate preexisting cardiovascular risk. The most dangerous of the risk is exercise induced anaphylaxis, with a number of studies showing that aspirin and similar drugs can elevate risk, including low dose aspirin therapy.

"RESULTS: Four cases were diagnosed with wheat allergy, 3 cases had wheat-dependent, salicylic acid-induced anaphylaxis. SPT and CAP-RAST were positive for wheat and gluten in 5 of 7 cases and 4 of 7 cases, respectively. Dicrofenac enhanced the allergic reactions after wheat ingestion in 1 of 2 cases"PubMed

" Immunoreactive gliadins appeared in the sera of patients during the provocation test with both wheat-exercise and wheat-aspirin challenges in parallel with allergic symptom."PubMed

"Oral challenge tests were positive with prawns and prawn extract only if preceded by NSAIDs. Oral challenges with NSAIDs alone, prawns alone, barnacles with or without NSAIDs and alcohol led to no reaction. A synergistic effect of NSAIDs in inducing anaphylaxis after prawn intake was confirmed." PubMed

Some studies have gone so far as to suggest replacing NSAIDs in patients with a history of sensitivity with omega-3 fatty acid therapy, and the removal of sources of proinflammatory agents, such as arachidonic acid, from the diet. Pdeitiker (talk) 02:19, 11 June 2008 (UTC)


The cardiovascular issue with non-selective NSAIDs is that they raise blood pressure. They don't induce short-term risk of heart attack like COX-2 inhibitors, but over time, increased blood pressure is a serious risk factor. josta59 28 February 2008 —Preceding comment was added at 22:05, 28 February 2008 (UTC)

[edit] Photosensitivity

The last sentence in this section is: "While ibuprofen is somewhat of an exception, having weak absorption, it has been reported to be a weak photosensitising agent." Does this means that a) usualy low-absorption profens have high photosensitising activity, b) ibuprofen has low photosensitising activity compared to other profens (which corresponds to its relatively low absorption), c) ibuprofen has a weak photosensitising effect, however still much, compared to most non-profens, d) something else. Which is it? Thanks... --Edo11en 17:06, 11 January 2007 (UTC)

[edit] Should this be here?

I'm pretty new here, but I always thought that Wikipedia shouldn't dole out health advice, or that this article should have a template warning against using this as medical advice. I'm sure it would be a pain to go through all the pharmacology articles and alter them, as well as make them uglier, but this page just irked me with its direct advice to the reader: "If you are taking a COX-2 inhibitor, you should not use a traditional NSAID (prescription or over-the-counter)." 68.197.26.36 01:11, 29 March 2007 (UTC)

[edit] Adverse effects?

These rather shocking statistics have no cited source:

"These effects are dose-dependent, and in many cases severe enough to pose the risk of ulcer perforation, upper gastrointestinal bleeding, and death, limiting the use of NSAID therapy. An estimated 10-20% of NSAID patients experience dyspepsia, and NSAID-associated upper gastrointestinal adverse events are estimated to result in 103,000 hospitalizations and 16,500 deaths per year in the United States, and represent 43% of drug-related emergency visits."

What proportion of the general population experience dyspepsia? An 'estimated' 10-20% sounds like it was 'estimated' by someone on a whim rather than as a result of any scientific investigation...

16,500 deaths a year in the US as a result of the use of NSAIDS? An amazing statistic if true - but where's the source??

Dean Morrison 14:13, 30 September 2007 (UTC)


[edit] Adverse effects?

These rather shocking statistics have no cited source:

"These effects are dose-dependent, and in many cases severe enough to pose the risk of ulcer perforation, upper gastrointestinal bleeding, and death, limiting the use of NSAID therapy. An estimated 10-20% of NSAID patients experience dyspepsia, and NSAID-associated upper gastrointestinal adverse events are estimated to result in 103,000 hospitalizations and 16,500 deaths per year in the United States, and represent 43% of drug-related emergency visits."

What proportion of the general population experience dyspepsia? An 'estimated' 10-20% sounds like it was 'estimated' by someone on a whim rather than as a result of any scientific investigation...

16,500 deaths a year in the US as a result of the use of NSAIDS? An amazing statistic if true - but where's the source??

Dean Morrison 14:13, 30 September 2007 (UTC)

[edit] NSAIDS cause heart attacks?

I'm curious about the claim that NSAIDS cause heart attacks. The literature I've read suggests that they reduce them. see

this pub med link


or this one

I've looked at the underlying article and it specifically excluded aspirin. Also, it only supported correlation. It did not prove causation. I've adjusted the article accordingly. Can anyone support a causal link?--Ryan Wise (talk) 05:27, 22 March 2008 (UTC)

See [way] above. As you see the advertisement on celebrex, the same is true for most NSAIDs, NSAIDs can cause the microperforations in the mucosa of the small intestine. Strenuous exercise, or even a heavy meal, can cause the induction of food peptides (namely gliadin and crustacean proteins). This can cause exercise-induced anaphylaxis, which is sometimes cause fatal cardiac arrest (among other things). Some of the 'sensitivity' seen to NSAIDs is actually do to allergic reaction to food proteins such as atopy, urticaria, etc. PubMed Pdeitiker (talk) 02:37, 11 June 2008 (UTC) [hope this is 'casual' enough for you]