Bergman R, Kasif Y, Aviram M, Maor I, Ullman Y, Gdal-On M, Friedman-Birnbaum R
Department of Dermatology, Rambam Medical Center, Haifa, Israel.
Acta Derm Venereol. 1996 Mar;76(2):107-10. doi: 10.2340/0001555576107110.
The lipid compositions of 8 normolipidemic xanthelasma palpebrarum (XP) lesions were analyzed using thin-layer chromatography, with the adjacent uninvolved skin used as control. The lesions were found to be composed predominantly of cholesterol, mostly cholesteryl ester, whereas in the control specimens phospholipids predominated. The degradation rates of 125I-low-density lipoprotein (LDL), oxidized LDL, and acetyl LDL, and the rates of intracellular cholesterol synthesis from 1,2-(14)C-acetate, in blood monocyte-derived macrophages (MDM) from 3 normolipidemic patients, were similar to those of MDM from 3 normal control subjects. The mean levels of lipid peroxides and conjugated dienes under basal conditions, as well as following the addition of a free radical-generating compound (2,2-azobis-2-amidinopropane hydrochloride) to the plasma of 14 normolipidemic XP patients were significantly higher than those of 14 age- and sex-matched normal controls. We conclude that the predominant lipid accumulated in normolipidemic XP lesions is cholesteryl ester, but there is no evidence for intrinsic cellular cholesterol metabolism derangement in blood MDM from patients which could account for this. Since macrophage cholesterol accumulation can also result from enhanced uptake of increased levels of oxidized LDL, the increased plasma lipid peroxidation (derived from oxidized LDL) might lead to accumulation of cholesterol in macrophages and formation of foam cells via this mechanism.
使用薄层色谱法分析了8例血脂正常的睑黄瘤(XP)病变的脂质组成,并以相邻未受累皮肤作为对照。发现病变主要由胆固醇组成,大部分为胆固醇酯,而对照标本中磷脂占主导地位。3例血脂正常患者血液单核细胞衍生巨噬细胞(MDM)中125I-低密度脂蛋白(LDL)、氧化LDL和乙酰LDL的降解率,以及1,2-(14)C-乙酸盐合成细胞内胆固醇的速率,与3例正常对照受试者的MDM相似。在基础条件下,以及向14例血脂正常的XP患者血浆中添加自由基生成化合物(2,2-偶氮双-2-脒基丙烷盐酸盐)后,脂质过氧化物和共轭二烯的平均水平显著高于14例年龄和性别匹配的正常对照。我们得出结论,血脂正常的XP病变中积累的主要脂质是胆固醇酯,但没有证据表明患者血液MDM中存在内在的细胞胆固醇代谢紊乱可解释这一现象。由于巨噬细胞胆固醇积累也可能源于氧化LDL水平升高导致的摄取增加,血浆脂质过氧化增加(源自氧化LDL)可能通过这种机制导致巨噬细胞中胆固醇积累和泡沫细胞形成。