keeping low platelates by aspirin may help in hcc. as this article suggests:
full article: http://www.pnas.org/content/early/2012/07/18/1210296109.full.pdf
Platelets harness the immune response to drive liver cancer
Mala K. Maini and Anna Schurich
Division of Infection and Immunity, University College London, London WC1 E6JF, United Kingdom
I have found these paragraphs interesting have a look:
So where do platelets come into this scenario? Previous groundbreaking work from Iannacone et al. (8) revealed an un-
precedented role for activated platelets in mediating CTL-induced liver damage in mouse models of acute viral hepatitis. In the study of Sitia et al. (2), from the same laboratory, the authors go on to show that platelet activation is a critical driver of the fatal sequelae of chronic HBV infection.To do this, Sitia et al. (2) take advantage of a mouse model that has previously been shown to allow persistent, high-level ex-pression of the HBsAg transgene in all hepatocytes, and to result in the de-velopment of high rates of HCC in a CD8 T cell-dependent manner (9). In this elegant study, in 540 mice carefully monitored for their lifetime, Sitia et al.(2) demonstrate that the administration of drugs able to block platelet activation [aspirin and clopidogrel (Asp/Clo)] potently reduces the development of HCC, thereby markedly enhancing sur-
vival. The development of cirrhosis cannot be assessed in this model, but, importantly, the authors also observe significant ame-lioration in the progression of liver fibrosis.Reductions in these outcomes are accom-panied by a decrease in the number of HBV-specific CD8 and nonspecific in-flammatory cells accumulating in the livers of the transgenic mice expressing high levels of the HBV surface protein (i.e.,HBsAg) (Fig. 1) (2). Although platelets could have procarcinogenic effects in-dependent of T cells, Sitia et al. (2) show that antiplatelet drugs are unable to block carcinogenesis in a model of liver cancer that is not dependent on an in flammatory infiltrate (2). They therefore conclude that the capacity of Asp/Clo to block the in-trahepatic accumulation and/or expan-sion of CTL is responsible for the striking reductions in HCC.
Could antiplatelet drugs constitute a sim-ple, well-tolerated, and cheap additional approach to the prevention of HCC? The use of drugs that antagonize platelet ag-gregation seems counterintuitive in patients with liver disease, who are already considered to be at increased risk of bleeding. However, recent work suggests that liver disease may conversely increase thrombotic tendencies, perhaps justifying trials of antiplatelet drugs in these patients (14). Blocking platelet activation also carries the risk of interfering with their emerging protective roles against various infections, as exempli
fied by the ability of aspirin to block platelet-mediated killing of malaria parasites (15). Weighed against this, antiplatelet drugs are widely used to prevent cardiovascular disease, and, in such studies, have additionally been found to reduce the rates of overall cancer deaths (16). Prospective studies to specif-ically address the effects of Asp/Clo on the development of HCC in patients with chronic HBV infection will require ex-tended follow-up, but viral load, and the
progression offibrosis, will be easier outcomes to measure. Initial studies could use the woodchuck hepatitis virus
model (closely related to HBV) to assess the impact of antiplatelet drugs on vire-mia, liver inflammation, and HCC.
does this article suggests:
1. the platelates in lower normal range is good?
2. is Aspirin useful in fibrosis and HCC?
i think if platelates can be kept in lower normal range by aspirin that may be good idea. people at high risk may consider after disscussion with their doctor, but following question needs answers, may be researchers who may follow us may answer:
its effectiveness against HCC in long run, interference with nucs, interferron and vit d.
it suggests nothing they are just guesses by vitro/animal, you need thousands and thousands of patients followed for a decade at least for hcc to prove that thought exactly like they did for simvastatin, vit k2 and fish oil
noting that hcc prevention is so high by nucs, simvastatin, vit k2 and fish oil that there is no need to add toxic drugs, aspirin even if low dose is too toxic for liver and gut, plus we dont know the benefit long term of making platlets low so in the end this needs full proof and might end up making more damage than good
ok,aspirin may not be good option. for moment forget aspirin to reduce platelate count.
study is about platelates role in developement of hcc. study is suggesting low platelate count is beneficial in reducing future risk for hcc. ok. so question is does keeping platelates count (at least theoratically) in lower-normal range(still normal) is useful for future liver health. or present lower platelate count with normal liver is indication of less future complications. just an academic type question for disscussion to conclude something, based on this research paper or on other studies.
fish oil already does about the same thing as aspirin with no sides effects and with already proof of low hcc on humans, prevention of fatty liver and cardio vascular diseases...plus the low platlets count is an effect of activated immune response in the liver which makes liver damage and inflammation which in turn makes hcc......i dont think lowering platlets can work in the opposite direction
the ways of reducing hcc are already there simvastain, fish oil and probably the substances in fibroguard too like curcumin, reservtrol and so on, they all lower inflammation and not platlets and hcc development is connected with inflammation...aspirn lowers inflammation too but it has sdes effects so it is not a good option
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