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NSAIDs including potency list


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Int J Cancer. 2010 May 20. [Epub ahead of print]

Associations of aspirin, non-steroidal anti-inflammatory drug and paracetamol use with PSA-detected prostate cancer: findings from a large, population-based, case-control study (the ProtecT study).

Murad AS, Down L, Smith GD, Donovan JL, Lane JA, Hamdy FC, Neal DE, Martin RM.

Department of Social Medicine, University of Bristol, Canynge Hall, 39 Whatley Road, Bristol, BS8 2PS, UK.


Evidence from laboratory studies suggests that chronic inflammation plays an important role in prostate cancer aetiology. This has resulted in speculation that non-steroidal anti-inflammatory drugs may protect against prostate cancer development. We analysed data from a cross-sectional case-control study (n(cases)= 1,016; n(controls)= 5,043), nested within a UK-wide population-based study that used PSA-testing for identification of asymptomatic prostate cancers, to investigate the relationship of aspirin, non-steroidal anti-inflammatory drug (NSAID) and paracetamol use with prostate cancer. In conditional-logistic regression models accounting for stratum matching on age (5-year age-bands) and recruitment centre, use of non-aspirin NSAIDs (odds ratio, OR = 1.32, 95% CI: 1.04 to 1.67) or all NSAIDs (OR = 1.25; 1.07 to 1.47) were positively associated with prostate cancer. There were weaker, not conventionally statistically significant, positive associations of aspirin (OR = 1.13; 0.94 to 1.36) and paracetamol (OR = 1.20; 0.90 to 1.60) with prostate cancer. Mutual adjustment for aspirin, non-aspirin NSAIDs or paracetamol made little difference to these results. There was no evidence of confounding by age, family history of prostate cancer, body mass index or self-reported diabetes. Aspirin, NSAID and paracetamol use were associated with reduced serum PSA concentrations amongst controls. Our findings do not support the hypothesis that NSAIDs reduce the risk of PSA-detected prostate cancer. Our conclusions are unlikely to be influenced by PSA detection bias because the inverse associations of aspirin, NSAID and paracetamol use with serum PSA would have attenuated (not generated) the observed positive associations.

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A new study, below, finds NSAID use to be associated with PCa risk. The results seemingly contradict a number of previous studies.

Earlier this year, Mahmud (http://www.ncbi.nlm....pubmed/20091856) was able to report:

"The association between use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of prostate cancer remains controversial despite many observational epidemiological studies."

My own interest in cancer-related inflammation is not specifically to COX-2 generation, but an upstream event - activation of NFkB. Inhibit NFkB & we inhibit COX-2 & much else. In addition, my understanding is that NFkB inhibition becomes more important with time. Any NSAID benefit related to COX inhibition, would tend to be more apparent in the years following diagnosis. i.e. it should show up in advanced PCa statistics.

Although NSAIDs may inhibit NFkB, they do so "with highly variable efficacy" http://www.ncbi.nlm.nih.gov/pubmed/1548 ... t=Abstract.

The cited study concludes with:

"Overall these results indicate that aspirin and ibuprofen are least potent, while resveratrol, curcumin, celecoxib, and tamoxifen are the most potent anti-inflammatory and antiproliferative agents of those we studied."

Back in 2008, Stock stated (http://www.ncbi.nlm....pubmed/18698582):

"Observed anti-cancer effects of non-steroidal anti-inflammatory drugs (NSAIDs) have consisted largely of those that inhibit inflammatory mechanisms thought to promote an aggressive disease phenotype."

& reported:

"a possible negative association between NSAID use and disease aggressiveness"

- a fairly weak conclusion.

In 2006, Liu suggested that the NSAID response varied depending on genes. Search PubMed.com for 16931544 Liu concluded:

"any potential chemoprevention of prostate cancer by NSAIDs may be most appropriate for men with the LTA +80CC genotype"

But, returning to the current study, why would NSAID use seemingly increase the possibility of PCa? Why take a daily NSAID? Implies that a person is trying to deal with an inflammatory condition. Does not necessarily imply total success. Perhaps a C-reactive protein test would have shed light on the degree of residual inflammation.

In a very recent study, McArdle (http://www.ncbi.nlm....pubmed/20395655) writes:

"C-reactive protein {is a} significant independent predictor of prostate cancer-specific survival."

"the presence of a systemic inflammatory response, at diagnosis, independently predicts poor long-term cancer outcome in patients with localised prostate cancer"


PMID: 20506261 Forum: Every little bit helps Title: NSAIDs including potency list

This extract can be found on http://PubMed.com, and is in the public domain.

On PubMed.com there will be a link to the full paper (often $30, sometimes free).

Any highlighting (except the title) is not by the author, but by Jim Marshall.

Jim is not a doctor.

This page was found on the Advanced Prostate Cancer Community for Australian men at http://advancedprost...lia.ipbhost.com.

The link is hard to remember.

An easier way to find it is to go to JimJimJimJim.com and click on Prostate.

That's the word Jim four times, no spaces, followed by .com.

If you need other help - to perhaps find someone to talk to or a local support group:

Click on the Contact Jim button at http://JimJimJimJim.com.

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