Mayes Kelly, Tan Maw, Morgan Colin
Department of Clinical Chemistry, Alder Hey Childrens' Hospital, Alder Road, Liverpool, UK.
JPEN J Parenter Enteral Nutr. 2014 Jan;38(1):92-8. doi: 10.1177/0148607112467036. Epub 2012 Nov 20.
Hyperalimentation describes the increase in glucose, amino acids (AAs), and lipid intake designed to overcome postnatal growth failure in preterm infants. Preterm infants are dependent on phenylalanine metabolism to maintain tyrosine levels because of tyrosine concentration limits in parenteral nutrition (PN). We hypothesized that hyperalimentation would increase individual AA levels when compared with the control group but avoid high phenylalanine/tyrosine levels.
To compare the plasma AA profiles on days 8-10 of life in preterm infants receiving a hyperalimentation vs a control regimen.
Infants <29 weeks' gestation were randomized to receive hyperalimentation (30% more PN macronutrients) or a control regimen. Data were collected to measure macronutrient (including protein) intake and PN intolerance, including hyperglycemia, insulin use, urea, and AA profile. Plasma profiles of 23 individual AA levels were measured on days 8-10 using ion exchange chromatography.
One hundred forty-two infants were randomized with 118 AA profiles obtained on days 8-10. There were no differences in birth weight or gestation between groups. There was an increase (P < .05) in 8 of 23 median individual plasma AA levels when comparing hyperalimentation (n = 57) with controls (n = 61). Only tyrosine levels (median; interquartile range) were lower with hyperalimentation: 27 (15-52) µmol/L vs 43 (24-69) µmol/L (P < .01). Hyperalimentation resulted in more insulin-treated hyperglycemia. No difference between the groups was apparent in tyrosine levels when substratified for insulin-treated hyperglycemia. All insulin vs no insulin comparisons showed lower tyrosine levels with insulin treatment (P < .01).
Hyperalimentation can result in paradoxically low plasma tyrosine levels associated with an increase in insulin-treated hyperglycemia.
高营养疗法是指增加葡萄糖、氨基酸（AA）和脂质的摄入量，旨在克服早产儿出生后的生长发育迟缓。由于肠外营养（PN）中酪氨酸浓度有限，早产儿依赖苯丙氨酸代谢来维持酪氨酸水平。我们假设，与对照组相比，高营养疗法会增加个体氨基酸水平，但避免苯丙氨酸/酪氨酸水平过高。
比较接受高营养疗法与对照方案的早产儿出生后第8至10天的血浆氨基酸谱。
将孕周小于29周的婴儿随机分为接受高营养疗法（PN宏量营养素多30%）或对照方案的两组。收集数据以测量宏量营养素（包括蛋白质）摄入量和PN不耐受情况，包括高血糖、胰岛素使用情况、尿素和氨基酸谱。在出生后第8至10天，使用离子交换色谱法测量23种个体氨基酸水平的血浆谱。
142名婴儿被随机分组，在出生后第8至10天获得了118份氨基酸谱。两组之间的出生体重或孕周无差异。将高营养疗法组（n = 57）与对照组（n = 61）进行比较时，23种个体血浆氨基酸水平的中位数中有8种有所升高（P < .05）。高营养疗法组的酪氨酸水平（中位数；四分位间距）较低：27（15 - 52）µmol/L对43（24 - 69）µmol/L（P < .01）。高营养疗法导致更多接受胰岛素治疗的高血糖病例。在根据接受胰岛素治疗的高血糖情况进行分层时，两组之间的酪氨酸水平无明显差异。所有胰岛素治疗组与未接受胰岛素治疗组的比较均显示，接受胰岛素治疗组的酪氨酸水平较低（P < .01）。
高营养疗法可能会导致血浆酪氨酸水平反常降低，并伴有接受胰岛素治疗的高血糖病例增加。
