Postprandial hemorrheology and apolipoprotein B metabolism in patients with familial hypertriglyceridemia.

Impaired postprandial lipoprotein metabolism has been found to be related to the extent of coronary artery disease. Moreover, since dyslipoproteinemias are associated with impaired hemorrheology, we investigated the effect of postprandial hypertriglyceridemia on hemorrheological parameters before and after triglyceride-lowering therapy. Triglyceride-rich lipoproteins (TRLs) separated by ultracentrifugation (d < 1.006 g/dL) and chylomicrons and chylomicron remnants (quantified by apolipoprotein [apo] B-48 determination) were determined after a fat load in 10 patients with familial hypertriglyceridemia before and after therapy with gemfibrozil (900 mg daily). Lipid and hemorrheological parameters (plasma and whole-blood viscosity [PV and BV], red cell aggregation [RCA], hematocrit, and fibrinogen) were determined at baseline and every hour up to 6 hours postprandially. Fasting total triglycerides and TRL triglycerides significantly decreased with gemfibrozil therapy (P < .01). Total triglycerides postprandially increased from 9.53 +/- 1.72 to 14.47 +/- 2.07 mmol/L (TRL triglycerides by 61%) before therapy (P < .05) and from 4.61 +/- 1.28 to 7.17 +/- 0.99 mmol/L (TRL triglycerides by 57%) after therapy (P < .05). The postprandial TRL apo B increase was reduced with gemfibrozil (from 11.6 +/- 2.8 to 20.7 +/- 5.0 mg/dL with therapy v 19.0 +/- 7.6 to 33.0 +/- 12.5 mg/dL before therapy, P < .05, respectively) with a proportionally greater increase in apo B-48 (119% and 169%, respectively) compared with apo B-100 (64% and 64%, respectively). Fasting RCA was improved with lipid-lowering therapy (P < .05), but PV, BV, RCA, and fibrinogen did not show any statistically significant postprandial changes either before or after lipid-lowering therapy. In summary, we did not find any statistically significant changes in hemorrheological parameters, despite a strong postprandial increase of triglycerides. In particular, these findings were independent of fasting triglyceride levels. We conclude that triglyceride-lowering therapy by gemfibrozil had no substantial beneficial effects with respect to hemorrheology in patients with familial hypertriglyceridemia.

Primary chylomicronemia in patients with severe familial hypertriglyceridemia responds to long-term treatment with (n-3) fatty acids.

Because it disturbs microcirculation, chylomicronemia can cause severe clinical complications such as acute pancreatitis. Dietary measures are very important in the prevention and treatment of this condition. Dietary supplementation with (n-3) fatty acids has been shown to be of benefit in short-term treatment of chylomicronemia. To evaluate the long-term efficacy of (n-3) fatty acids we added 2.16 or 4.32 g/d (for 3 mo) and 3.24 g/d (for a further 8 mo after 1 mo of no treatment) (n-3) fatty acids to the diet of eight patients with primary chylomicronemia. Serum triglycerides decreased significantly from 15.0 +/- 2.5 to 9.9 +/- 2.8 mmol/L (P < 0.01) after 11 mo of treatment, and VLDL triglycerides decreased from 12.3 +/- 2.8 to 9.0 +/- 2.4 mmol/L (P < 0.01), resulting in a significant decrease of plasma viscosity from 1.56 +/- 0.17 mPa-s to 1.47 +/- 0.12 mPa.s (P < 0.01). Total cholesterol, HDL and LDL cholesterol as well as lipoprotein (a) and fibrinogen concentrations were not affected by fish oil treatment. The presence of chylomicrons and chylomicron remnants (apolipoprotein B 48 concentration in the lipoprotein fraction with a density lower than 1.006 kg/L) was significantly reduced from 4.82 +/- 1.08 to 1.06 +/- 0.38 mg/L (P < 0.01). Body weight increased significantly from 71.0 +/- 4.6 kg to 75.2 +/- 5.3 kg after 11 mo of treatment with (n-3) fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)