Introduction to Deficiencies of Apolipoproteins CII and EIII With Some Associated Clinical Findings
Introduction to Deficiencies of Apolipoproteins CII and EIII With Some Associated Clinical Findings
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介绍载脂蛋白 CII 和 EIII 的缺陷以及一些相关的临床发现
DOI：
10.1007/978-1-4612-6071-4_127
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
V. McGuire
中科院分区：
文献类型：
--
作者：
J. Little;D. Cox;W. Breckenridge;V. McGuire
III型高脂蛋白血症(HLP)是Fredrickson等人的特点。(1967年)具有密度小于1.006的β迁移性脂蛋白。他们提到了Gofman等人(1954)之前的描述，即成人起病的结节状黄色瘤患者，过早的缺血性血管疾病，SF 0-12降低，12-400脂蛋白增加，可能患有III型。他们怀疑这可能是继发于异常脂蛋白的存在，以及来自家族性研究的“几个突变的等位基因”可能决定III型HLP。几个小组的一些发现进一步描述了这种疾病的特征：β-甚低密度脂蛋白中胆固醇/甘油三酯比率增加；肝素锰沉淀异常的极低密度脂蛋白；极低密度脂蛋白中富含精氨酸的载脂蛋白(Apo E)浓度增加，并描述为由于乳糜蛋白和极低密度脂蛋白分解代谢残留物的积累而导致的β-β脂蛋白血症。
Type III hyperlipoproteinemia (HLP) was characterized by Fredrickson et al. (1967) as having β migrating lipoproteins with a density less than 1.006. They referred to a prior description by Gofman et al.(1954) of patients with adult onset tuberous xanthomata, premature ischemic vascular disease, decreased Sf 0-12 and increased 12–400 lipoproteins, as probably having Type III. They suspected that it was “likely to be secondary to the presence of an abnormal lipoprotein” and from family studies that “several mutant alleles” might determine Type III HLP. A number of discoveries by several groups have further characterized the disorder: an increase in the cholesterol/glyceride ratio in β-VLDL; the precipitation of abnormal VLDL by heparin manganese; the increased concentration of arginine rich apolipoprotein (apo E) in VLDL and its description as a dysbetalipoproteinemia due to an accumulation of remnants from chy- lomicron and VLDL catabolism.