Clinic for Special Children, Strasburg, PA 17579, USA.
Mol Genet Metab. 2011 Sep-Oct;104(1-2):93-106. doi: 10.1016/j.ymgme.2011.07.003. Epub 2011 Jul 12.
Striatal degeneration from glutaryl-CoA dehydrogenase deficiency (glutaric aciduria type 1, GA1) is associated with cerebral formation and entrapment of glutaryl-CoA and its derivatives that depend on cerebral lysine influx. In 2006 we designed a lysine-free study formula enriched with arginine to selectively block lysine transport across cerebral endothelia and thereby limit glutaryl-CoA production by brain. Between 2006 and present, we treated twelve consecutive children with study formula (LYSx group) while holding all other treatment practices constant. Clinical and biochemical outcomes were compared to 25 GA1 patients (PROx group) treated between 1995 and 2005 with natural protein restriction (dietary lysine/arginine ratio of 1.7±0.3 mg:mg). We used published kinetic parameters of the y+and LAT1 blood-brain barrier transporters to model the influx of amino acids into the brain. Arginine fortification to achieve a mean dietary lysine/arginine ratio of 0.7±0.2 mg:mg was neuroprotective. All 12 LYSx patients are physically and neurologically healthy after 28 aggregate patient-years of follow up (current ages 28±21 months) and there were no adverse events related to formula use. This represents a 36% reduction of neurological risk (95% confidence interval 14-52%, p=0.018) that we can directly attribute to altered amino acid intake. During the first year of life, 20% lower lysine intake and two-fold higher arginine intake by LYSx patients were associated with 50% lower plasma lysine, 3-fold lower plasma lysine/arginine concentration ratio, 42% lower mean calculated cerebral lysine influx, 54% higher calculated cerebral arginine influx, 15-26% higher calculated cerebral influx of several anaplerotic precursors (isoleucine, threonine, methionine, and leucine), 50% less 3-hydroxyglutarate excretion, and a 3-fold lower hospitalization rate (0.8 versus 2.3 hospitalizations per patient per year). The relationship between arginine fortification and plasma lysine indicates that transport competition exists at both cerebrovascular and gastrointestinal barriers, suggesting their co-administration is key to efficacy. Monitoring the ratio between lysine and arginine in diet and plasma may prove a useful strategy for treating children with GA1.
谷氨酸酰辅酶 A 脱氢酶缺乏症(戊二酸血症 1 型,GA1)导致纹状体退化,与脑内谷氨酸酰辅酶 A 及其衍生物的形成和截留有关,而这些物质依赖于脑内赖氨酸的流入。2006 年,我们设计了一种富含精氨酸的无赖氨酸研究配方,选择性地阻断脑内皮细胞中的赖氨酸转运,从而限制大脑中谷氨酸酰辅酶 A 的产生。在 2006 年至现在期间,我们用研究配方(LYSx 组)治疗了 12 名连续的患儿,同时保持其他治疗方法不变。将临床和生化结果与 25 名 GA1 患儿(PROx 组)进行比较,PROx 组患儿于 1995 年至 2005 年期间接受天然蛋白限制治疗(饮食中赖氨酸/精氨酸比值为 1.7±0.3mg:mg)。我们使用血脑屏障 y+和 LAT1 转运体的已发表动力学参数来模拟氨基酸进入大脑的情况。精氨酸强化可使平均饮食中赖氨酸/精氨酸比值达到 0.7±0.2mg:mg,具有神经保护作用。在 28 名患儿的 28 个聚合患者年随访(当前年龄 28±21 个月)后,所有 12 名 LYSx 患儿在身体和神经方面都健康,且没有与配方使用相关的不良事件。这代表神经系统风险降低了 36%(95%置信区间为 14%-52%,p=0.018),我们可以直接将其归因于氨基酸摄入的改变。在生命的第一年,LYSx 患儿的赖氨酸摄入量降低 20%,精氨酸摄入量增加两倍,与血浆赖氨酸降低 50%、血浆赖氨酸/精氨酸浓度比降低 3 倍、脑内赖氨酸平均计算流入量降低 42%、脑内精氨酸计算流入量增加 54%、几种生酮氨基酸前体(异亮氨酸、苏氨酸、蛋氨酸和亮氨酸)的计算流入量增加 15-26%、3-羟基戊二酸排泄量减少 50%以及住院率降低 3 倍(0.8 次/患儿/年,2.3 次/患儿/年)有关。精氨酸强化与血浆赖氨酸之间的关系表明,在脑血管和胃肠道屏障中都存在转运竞争,这表明两者同时给药是其疗效的关键。监测饮食和血浆中赖氨酸和精氨酸的比值可能是治疗 GA1 患儿的一种有用策略。