Breckenridge W C, Little J A, Steiner G, Chow A, Poapst M
N Engl J Med. 1978 Jun 8;298(23):1265-73. doi: 10.1056/NEJM197806082982301.
A 59-year-old man with severe hypertriglyceridemia and no post-heparin lipolytic activity was studied because of a marked fall in plasma triglyceride concentrations after a blood transfusion. An apolipoprotein activator (apolipoprotein C-II) for lipoprotein lipase could not be detected by polyacrylamide-gel electrophoresis of apoproteins, immunodiffusion of the plasma against anti-apolipoprotein CII or activation assays for lipoprotein lipase. Furthermore, the patient's triglyceride-rich lipoproteins would not serve as substrate for lipoprotein lipase. The patient had latent post-heparin lipolytic activity, which appeared after the addition of apolipoprotein CII to the post-heparin plasma. After a transfusion of 1 unit of plasma from a normal subject the patient's plasma triglycerides fell, within one day, from 1000 to 250 mg per deciliter and remained below preinfusion concentrations for six days. We conclude that this patient's hyperlipoproteinemia resulted from a deficiency of apolipoprotein C-II.
一名59岁男性，患有严重的高甘油三酯血症且无肝素后脂解活性，因输血后血浆甘油三酯浓度显著下降而接受研究。通过载脂蛋白的聚丙烯酰胺凝胶电泳、血浆与抗载脂蛋白CII的免疫扩散或脂蛋白脂肪酶的激活试验，均未检测到脂蛋白脂肪酶的载脂蛋白激活剂（载脂蛋白C-II）。此外，患者富含甘油三酯的脂蛋白不能作为脂蛋白脂肪酶的底物。该患者具有潜在的肝素后脂解活性，在肝素后血浆中加入载脂蛋白CII后出现。输注1单位正常受试者的血浆后，患者的血浆甘油三酯在一天内从每分升1000毫克降至250毫克，并在六天内维持在输注前浓度以下。我们得出结论，该患者的高脂蛋白血症是由载脂蛋白C-II缺乏引起的。
