I have observed discrepancies in the measurement of serum pancreatic lipase(LIP, Triacylglycerol acylhydrolase, EC 3.1.1.3) activities by non-enzymatic and enzymatic methods using diglyceride(1,2-dilinoleoyl-2-palmitoyl-glycerol, DLPG) as a substrate. The greatest discrepancies were seen in the post-heparin sera of patients with acute coronary syndrome(ACS). It is well-known that serum levels of lipoprotein lipase(LPL, EC 3.1.1.34) and hepatic triglyceride lipase(HTL, EC 3.1.1.3) show a significant increase after the administration of heparin in hemodialysis patients, and even larger quantities of heparin are administered before cardioangiography for ACS. Moreover, inhibitors of LPL and HTL induce almost complete reduction of increased LIP activity in post-heparin serum as measured by enzymatic assays. Pseudohyperlipasemia and positive interference from post-heparin serum LIP activity in enzymatic assays are considered to largely reflect LPL and HTL activities. Therefore, enzymatic reagent kits need improvement.