PLASMA TRIGLYCERIDE AND LDL HETEROGENEITY IN FAMILIAL COMBINED HYPERLIPIDEMIA

被引:94
作者
HOKANSON, JE
AUSTIN, MA
ZAMBON, A
BRUNZELL, JD
机构
[1] UNIV WASHINGTON, SCH MED,DEPT MED,DIV METAB ENDOCRINOL & NUTR, RG-26, SEATTLE, WA 98195 USA
[2] UNIV WASHINGTON, SCH PUBL HLTH & COMMUNITY MED, DEPT EPIDEMIOL, SEATTLE, WA 98195 USA
来源
ARTERIOSCLEROSIS AND THROMBOSIS | 1993年 / 13卷 / 03期
关键词
TRIGLYCERIDES; LDL; FAMILIAL COMBINED HYPERLIPIDEMIA;
D O I
10.1161/01.ATV.13.3.427
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Familial combined hyperlipidemia (FCHL) is a genetic disorder characterized by increases in plasma cholesterol and/or triglyceride, elevated apolipoprotein B, and heterogeneous low density lipoprotein (LDL). To examine the relation between plasma triglyceride concentrations and LDL heterogeneity, 13 hypertriglyceridemic FCHL patients with a predominance of small LDL (LDL subclass phenotype B) were treated with gemfibrozil. The distribution of LDL was determined using nondenaturing gradient gel electrophoresis and nonequilibrium density gradient ultracentrifugation. Mean plasma triglyceride levels decreased 55% (p<0.01) after 3 months of treatment. Mean LDL peak particle size remained small (247 +/- 4 versus 249 +/- 5 angstrom), and the correlation between change in plasma triglyceride concentrations and a change in LDL peak particle size was not significant. Individual changes in LDL flotation rate (R(f)) were, however, inversely correlated with changes in triglyceride concentration (R=0.60, p<0.05). Although mean LDL Rf increased during treatment (p<0.005) due to an increase in buoyant LDL, dense LDL remained elevated compared with that of a control population. Thus in FCHL patients, small, dense LDL persists despite decreases in plasma triglyceride concentrations.
引用
收藏
页码:427 / 434
页数:8
相关论文
共 29 条
[1]
APOPROTEIN MEASUREMENTS AND THEIR CLINICAL-APPLICATION [J].
ALBERS, JJ ;
BRUNZELL, JD ;
KNOPP, RH .
CLINICS IN LABORATORY MEDICINE, 1989, 9 (01) :137-152
[2]
ARMITAGE P, 1971, STATISTICAL METHODS
[3]
AUSTIN M A, 1988, Journal of the American Medical Association, V260, P1917, DOI 10.1001/jama.260.13.1917
[4]
AUSTIN MA, 1988, AM J HUM GENET, V43, P838
[5]
INHERITANCE OF LOW-DENSITY-LIPOPROTEIN SUBCLASS PATTERNS IN FAMILIAL COMBINED HYPERLIPIDEMIA [J].
AUSTIN, MA ;
BRUNZELL, JD ;
FITCH, WL ;
KRAUSS, RM .
ARTERIOSCLEROSIS, 1990, 10 (04) :520-530
[6]
ATHEROGENIC LIPOPROTEIN PHENOTYPE - A PROPOSED GENETIC-MARKER FOR CORONARY HEART-DISEASE RISK [J].
AUSTIN, MA ;
KING, MC ;
VRANIZAN, KM ;
KRAUSS, RM .
CIRCULATION, 1990, 82 (02) :495-506
[7]
BIMODALITY OF PLASMA APOLIPOPROTEIN-B LEVELS IN FAMILIAL COMBINED HYPERLIPIDEMIA [J].
AUSTIN, MA ;
HOROWITZ, H ;
WIJSMAN, E ;
KRAUSS, RM ;
BRUNZELL, J .
ATHEROSCLEROSIS, 1992, 92 (01) :67-77
[8]
LARGE BUOYANT LDL-LIKE PARTICLES IN HEPATIC LIPASE DEFICIENCY [J].
AUWERX, JH ;
MARZETTA, CA ;
HOKANSON, JE ;
BRUNZELL, JD .
ARTERIOSCLEROSIS, 1989, 9 (03) :319-325
[9]
REGRESSION OF CORONARY-ARTERY DISEASE AS A RESULT OF INTENSIVE LIPID-LOWERING THERAPY IN MEN WITH HIGH-LEVELS OF APOLIPOPROTEIN-B [J].
BROWN, G ;
ALBERS, JJ ;
FISHER, LD ;
SCHAEFER, SM ;
LIN, JT ;
KAPLAN, C ;
ZHAO, XQ ;
BISSON, BD ;
FITZPATRICK, VF ;
DODGE, HT .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (19) :1289-1298
[10]
BRUNZELL JD, 1983, J LIPID RES, V24, P147