title: Hypertriglyceridemia and lowered apolipoprotein C-II/C-III ratio in uremia: effect of a fibric acid, clinofibrate.
abstract: We examined the effects of a fibric acid, clinofibrate, on lipoprotein metabolism in 12 hyperlipidemic patients with uremia treated on continuous ambulatory peritoneal dialysis during a 24 week treatment. Daily dose of clinofibrate was 200 mg for the initial four weeks, 400 mg for the second four weeks, and 600 mg for the subsequent 16 weeks. Serum and very-low density lipoprotein (VLDL) triglyceride were decreased by 36% and 48%, respectively. Neither total cholesterol nor apolipoprotein B changed significantly, whereas cholesterol was decreased in VLDL and increased in low (LDL) and high density lipoprotein (HDL) fractions. Post-heparin plasma lipoprotein lipase (LPL) before treatment was not lower than the normal value, and we found no change in LPL activity following clinofibrate. Hepatic triglyceride lipase also did not change. Apolipoprotein (apo) C-II/C-III ratio was low as compared to the normal value before treatment, and the ratio was increased by 38% after the treatment. Decrease in VLDL triglyceride was associated with increase in apo C-II/C-III ratio in all the cases. Abnormal enrichment with triglyceride of LDL and HDL fractions was improved by clinofibrate. Although one patient had a transient and asymptomatic elevation of serum creatine phosphokinase, no patient had muscle pain. There was no accumulation of the drug in the 24 week trial. These results suggest that clinofibrate is an effective and safe approach to the management of dyslipidemia in CAPD patients.
authors.affiliation: Second Department of Internal Medicine, Osaka City University Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nishizawa
authors.forename: T
authors.initials: T
authors.lastname: Shoji
authors.forename: H
authors.initials: H
authors.lastname: Nishitani
authors.forename: M
authors.initials: M
authors.lastname: Yamakawa
authors.forename: T
authors.initials: T
authors.lastname: Konishi
authors.forename: K
authors.initials: K
authors.lastname: Kawasaki
authors.forename: H
authors.initials: H
authors.lastname: Morii
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D053304:Apolipoprotein C-II; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C / Q000032:analysis*; D002784:Cholesterol / Q000097:blood; D005260:Female; D006493:Heparin / Q000494:pharmacology; D006801:Humans; D015228:Hypertriglyceridemia / Q000188:drug therapy* / Q000209:etiology*; D008049:Lipase / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood / Q000737:chemistry; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008875:Middle Aged; D010642:Phenoxyacetates / Q000493:pharmacokinetics / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood; D014511:Uremia / Q000097:blood*
chemical_list: D053304:Apolipoprotein C-II; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C; D008075:Lipoproteins, HDL; D010642:Phenoxyacetates; D014280:Triglycerides; C006231:clinofibrate; D006493:Heparin; D002784:Cholesterol; D008049:Lipase