This is a flawed analysis on many levels.
(1) There is a continuum of risk for pancreatitis that expresses itself above 500mg/dl and increases dramatically over 1000 mg/dl in most cases
(2) There is a continuum of cardiovascular risk for TG>150 and increases proportionately (though not linearly) thereafter and exists both above and below 500mg/dl.
A dichotomous > and < 500mg/dl approach to risk: benefit analysis that relegates a pancreatitis risk to above 500 and a CV risk to below 500 is therefore illogical.
Further, the pancreatitis "risk" that we are treating in TG>500 is an idiosyncratic one albeit correlated with the chronicity of the TG>500 exposure. So we would have to continue the Lovaza "ad infinitum" to prevent pancreatitis and stopping it arbitrarily after 12 weeks would not serve any purpose.
Lastly, the adverse risk of the DHA in Lovaza has hitherto been ascribed to the LDL rise that DHA containing drugs elicit. It has been portrayed as being negated by co-administering statin. In fact, there may very well be a direct deleterious effect of DHA independent of the LDL effect, just as there is an independent beneficial effect of EPA independent of its LDL effects. This being the case, a prolonged duration of consuming DHA containing products would neither be desirable for the patient or ethical for the prescriber. If we wish to treat pancreatitis risk and maintain CV risk lowering simultaneously the logical choice for TG>500 is Vascepa, albeit with a 10% lower TG lowering c/w Lovaza that could be mitigated by just increasing the EPA dosage. As an aside, once the TG risk gets above the 750mg/dl range there is always a need for polypharmacy (just as with severe hypercholesterolemia where statin or statin plus ezetimibe will not cut it if your starting LDL is >250mg/dl)
HK.
