Bolla K I, Milstien S, Briefel G, Wieler L, Kaufman S
Department of Neurology, Francis Scott Key Medical Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224.
Neurology. 1991 Nov;41(11):1806-9. doi: 10.1212/wnl.41.11.1806.
Although increased levels of aluminum (Al) are present in patients with dialysis encephalopathy (DE), it is unclear if the association is causal. The enzyme dihydropteridine reductase (DHPR) plays a critical role in neurotransmitter formation and its activity. Elevated levels of Al are reported to decrease DHPR activity, which would alter neurotransmitter metabolism, thus producing DE. We examined the association between erythrocyte DHPR activity and Al levels, attention/psychomotor skills, and depression in a group of 21 patients with end-stage renal disease. DHPR activity was not related to Al level, mental status, psychomotor ability, or depression score. After administration of deferoxamine (an Al chelating agent), Al level increased significantly but DHPR activity remained the same. Our results suggest that the mechanism for the development for DE does not involve alterations of neurotransmitter metabolism caused by Al-mediated reductions in DHPR activity.
尽管透析性脑病(DE)患者体内铝(Al)水平升高,但尚不清楚这种关联是否具有因果关系。二氢蝶啶还原酶(DHPR)在神经递质形成及其活性中起关键作用。据报道,铝水平升高会降低DHPR活性,这会改变神经递质代谢,从而导致透析性脑病。我们研究了21例终末期肾病患者的红细胞DHPR活性与铝水平、注意力/精神运动技能和抑郁之间的关联。DHPR活性与铝水平、精神状态、精神运动能力或抑郁评分无关。给予去铁胺(一种铝螯合剂)后,铝水平显著升高,但DHPR活性保持不变。我们的结果表明,透析性脑病的发生机制不涉及铝介导的DHPR活性降低引起的神经递质代谢改变。