Abstract
The effects of gemfibrozil on plasma lipoprotein distribution and composition and on platelet function were investigated in 11 patients with stable hypertriglyceridemia, six belonging to Fredrickson type IIb and five to type IV. Gemfibrozil (600 mg twice a day) significantly reduced total and very low density lipoprotein (VLDL)-associated triglyceridemia (respectively -32.4% and -40.4%, after 6 weeks of treatment). No significant variations were noted in the lipid components of low-density lipoproteins; by contrast, a marked increase (18%) was detected in high-density lipoprotein (HDL)-associated cholesterol. Comparison of the two patient groups (type IIb and type IV) showed that those with type IIb had both a more significant reduction of triglyceridemia and a more marked increase of HDL-cholesterol. Apolipoprotein B levels were reduced in both groups (-12%) with no change in apolipoprotein AI. The cholesterol content in the HDL subfractions, separated by rate zonal ultracentrifugation, was raised in HDL3 (18%) and in HDL2 (14%). Both particles also showed significant increases of the cholesterol/protein and the cholesterol/phospholipid ratios. A non-statistically significant decrease in collagen-induced aggregation and in the release of thromboxane B2 was noted after treatment. These findings suggest that, similar to what was recently reported in normal individuals and in laboratory animals, the probable mode of action of gemfibrozil is in reducing the secretion of atherogenic lipoproteins, particularly VLDL, while stimulating the production of small HDL particles.
| Original language | English |
|---|---|
| Pages (from-to) | 279-286 |
| Number of pages | 8 |
| Journal | The Journal of Laboratory and Clinical Medicine |
| Volume | 110 |
| Issue number | 3 |
| Publication status | Published - 1987 |
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ASJC Scopus subject areas
- Medicine(all)
- Pathology and Forensic Medicine
Cite this
Effects of gemfibrozil on plasma lipoprotein-apolipoprotein distribution and platelet reactivity in patients with hypertriglyceridemia. / Sirtori, C. R.; Franceschini, G.; Gianfranceschi, G.; Sirtori, M.; Montanari, G.; Tremoli, E.; Maderna, P.; Colli, S.; Zoppi, F.
In: The Journal of Laboratory and Clinical Medicine, Vol. 110, No. 3, 1987, p. 279-286.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of gemfibrozil on plasma lipoprotein-apolipoprotein distribution and platelet reactivity in patients with hypertriglyceridemia
AU - Sirtori, C. R.
AU - Franceschini, G.
AU - Gianfranceschi, G.
AU - Sirtori, M.
AU - Montanari, G.
AU - Tremoli, E.
AU - Maderna, P.
AU - Colli, S.
AU - Zoppi, F.
PY - 1987
Y1 - 1987
N2 - The effects of gemfibrozil on plasma lipoprotein distribution and composition and on platelet function were investigated in 11 patients with stable hypertriglyceridemia, six belonging to Fredrickson type IIb and five to type IV. Gemfibrozil (600 mg twice a day) significantly reduced total and very low density lipoprotein (VLDL)-associated triglyceridemia (respectively -32.4% and -40.4%, after 6 weeks of treatment). No significant variations were noted in the lipid components of low-density lipoproteins; by contrast, a marked increase (18%) was detected in high-density lipoprotein (HDL)-associated cholesterol. Comparison of the two patient groups (type IIb and type IV) showed that those with type IIb had both a more significant reduction of triglyceridemia and a more marked increase of HDL-cholesterol. Apolipoprotein B levels were reduced in both groups (-12%) with no change in apolipoprotein AI. The cholesterol content in the HDL subfractions, separated by rate zonal ultracentrifugation, was raised in HDL3 (18%) and in HDL2 (14%). Both particles also showed significant increases of the cholesterol/protein and the cholesterol/phospholipid ratios. A non-statistically significant decrease in collagen-induced aggregation and in the release of thromboxane B2 was noted after treatment. These findings suggest that, similar to what was recently reported in normal individuals and in laboratory animals, the probable mode of action of gemfibrozil is in reducing the secretion of atherogenic lipoproteins, particularly VLDL, while stimulating the production of small HDL particles.
AB - The effects of gemfibrozil on plasma lipoprotein distribution and composition and on platelet function were investigated in 11 patients with stable hypertriglyceridemia, six belonging to Fredrickson type IIb and five to type IV. Gemfibrozil (600 mg twice a day) significantly reduced total and very low density lipoprotein (VLDL)-associated triglyceridemia (respectively -32.4% and -40.4%, after 6 weeks of treatment). No significant variations were noted in the lipid components of low-density lipoproteins; by contrast, a marked increase (18%) was detected in high-density lipoprotein (HDL)-associated cholesterol. Comparison of the two patient groups (type IIb and type IV) showed that those with type IIb had both a more significant reduction of triglyceridemia and a more marked increase of HDL-cholesterol. Apolipoprotein B levels were reduced in both groups (-12%) with no change in apolipoprotein AI. The cholesterol content in the HDL subfractions, separated by rate zonal ultracentrifugation, was raised in HDL3 (18%) and in HDL2 (14%). Both particles also showed significant increases of the cholesterol/protein and the cholesterol/phospholipid ratios. A non-statistically significant decrease in collagen-induced aggregation and in the release of thromboxane B2 was noted after treatment. These findings suggest that, similar to what was recently reported in normal individuals and in laboratory animals, the probable mode of action of gemfibrozil is in reducing the secretion of atherogenic lipoproteins, particularly VLDL, while stimulating the production of small HDL particles.
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M3 - Article
C2 - 3475394
AN - SCOPUS:0023630285
VL - 110
SP - 279
EP - 286
JO - Journal of Laboratory and Clinical Medicine
JF - Journal of Laboratory and Clinical Medicine
SN - 0022-2143
IS - 3
ER -