Re: Farmas USA
Después de volverme loco buscando me parece que el artículo es este:
Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio
Haruo Ohnishi1), Yasushi Saito2)
1) Mochida Pharmaceutical Co. Ltd. 2) Chiba University Graduate School of Medicine.
https://www.jstage.jst.go.jp/article/jat/advpub/0/advpub_18002/_article
La revista es japonesa. No pude seguir todo el adcom, pero sí recuerdo que algunas de las objeciones al Jeli era precisamente era que el artículo no estaba publicada en USA y que la población en el estudio era solo japonesa, y en su mayor parte, creo recordar, mujeres, por lo que no se consideraba una muestra representativa. Había más objeciones, pero no escuché mas sobre este tema
Os dejo el abstract:
The clinical efficacy of fish oil and high-purity eicosapentaenoic acid ethyl ester (hp-EPA-E) for treating cardiovascular disease (CVD) has been reported. Fish oil contains saturated and monounsaturated fatty acids that have pharmacological effects opposite to those of ω3 fatty acids (ω3). Moreover, ω3, such as EPA and docosahexaenoic acid (DHA), do not necessarily have the same metabolic and biological actions. This has obscured the clinical efficacy of ω3. Recently, the Japan EPA Lipid Intervention Study (JELIS) of hp-EPA-E established the clinical efficacy of EPA for CVD, and higher levels of blood EPA, not DHA, were found to be associated with a lower incidence of major coronary events. A significant reduction in the risk of coronary events was observed when the ratio of EPA to arachidonic acid (AA) (EPA/AA) was >0.75. Furthermore,theratioofprostaglandin (PG) I3andPGI2 to thromboxane A2 (TXA2) ([PGI2+PGI3]/TXA2) was determined to have a linear relationship with the EPA/AA ratio as follows: (PGI2+PGI3)/TXA2=λ+π* (EPA/AA). Like PGI2, PGI3 not only inhibits platelet aggregation and vasoconstriction, but also is assumed to reduce cardiac ischemic injury and arteriosclerosis and promote angiogenesis. Thus, the effects of EPA in reducing the risk of CVD could be mediated by biological action of PGI3 in addition to hypotriglyceridemic action of EPA. Compared with DHA, EPA administration increases the EPA/AA ratio and the (PGI2+PGI3)/TXA2 balance to a state that inhibits the onset and/or progression of CVD.
AMRN
