Mintz M
University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School at Camden 08103, USA.
J Child Neurol. 1995 Nov;10 Suppl 2:S40-4.
There is an increasing body of evidence that subgroups of patients infected with human immunodeficiency virus type 1 possess carnitine deficiency. Secondary carnitine deficiencies in these individuals may result from nutritional deficiencies, gastrointestinal disturbances, renal losses, or shifts in metabolic pathways. However, tissue depletion precipitated by drug toxicities, particularly zidovudine, is a major etiology and concern. Carnitine deficiency may impact on energy and lipid metabolism, causing mitochondrial and immune dysfunction. There are convincing laboratory data showing the in vitro ameliorative effects of L-carnitine supplementation of zidovudine-induced myopathies and lymphocyte function. Studies measuring the impact of L-carnitine supplementation on clinical characteristics are ongoing.
越来越多的证据表明，感染1型人类免疫缺陷病毒的患者亚群存在肉碱缺乏。这些个体的继发性肉碱缺乏可能源于营养缺乏、胃肠道紊乱、肾脏损失或代谢途径的改变。然而，药物毒性，特别是齐多夫定引起的组织消耗是一个主要病因和关注点。肉碱缺乏可能影响能量和脂质代谢，导致线粒体和免疫功能障碍。有令人信服的实验室数据表明，补充L-肉碱对齐多夫定诱导的肌病和淋巴细胞功能有体外改善作用。测量补充L-肉碱对临床特征影响的研究正在进行中。
