Yoshino M, Aoki K, Akeda H, Hashimoto K, Ikeda T, Inoue F, Ito M, Kawamura M, Kohno Y, Koga Y, Kuroda Y, Maesaka H, Murakamisoda H, Sugiyama N, Suzuki Y, Yano S, Yoshioka A
Department of Pediatrics and Child Health, Kurume University School of Medicine, Japan.
Pediatr Int. 1999 Apr;41(2):132-7. doi: 10.1046/j.1442-200x.1999.4121044.x.
Therapeutic modalities in acute metabolic decompensation in maple syrup urine disease (MSUD) are variable, and outcomes of each therapeutic measure have been known only individually. Factors that affect neurological outcome are not clear.
A questionnaire was sent throughout Japan to each pediatrician treating any of the 42 MSUD patients.
Necessary information was available for 13 patients through the questionnaire, and through a publication for one patient. In nine of the 14 patients episodes of metabolic decompensation developed in the neonatal period. In the other five, the onset of disease was delayed until infancy or later. In the nine patients with neonatal onset, a pretreatment level of plasma leucine greater than 40 mg/100 mL or a duration of altered level of alertness longer than 10 days was associated with a poor neurological outcome. The therapeutic measures employed included intravenous infusion of glucose and electrolyte solution or hypertonic glucose and electrolyte solution, exchange transfusion, peritoneal dialysis, a large dose of thiamine and intravenous hyperalimentation. All patients had survived the episodes and were alive at the time of the survey. Five of the nine patients with neonatal onset have developed neurological sequelae to varying degrees. Episodes of metabolic decompensation in infancy or thereafter did not affect, or only minimally affected, the neurological outcome.
Therapeutic goals to improve neurological outcome are to shorten the duration of the altered level of consciousness, and to minimize the peak plasma leucine level as much as possible.
枫糖尿症(MSUD)急性代谢失代偿的治疗方式多种多样,且每种治疗措施的结果仅为个案报道。影响神经学预后的因素尚不清楚。
向日本各地治疗42例MSUD患者中任何一例的每位儿科医生发送了一份调查问卷。
通过调查问卷获得了13例患者的必要信息,并通过一篇文献获得了1例患者的信息。14例患者中,9例在新生儿期出现代谢失代偿发作。另外5例患者的发病延迟至婴儿期或更晚。在9例新生儿期发病的患者中,血浆亮氨酸预处理水平大于40mg/100mL或意识改变水平持续时间超过10天与不良神经学预后相关。所采用的治疗措施包括静脉输注葡萄糖和电解质溶液或高渗葡萄糖和电解质溶液、换血、腹膜透析、大剂量硫胺素和静脉高营养。所有患者均度过发作期,在调查时仍存活。9例新生儿期发病的患者中有5例出现了不同程度的神经后遗症。婴儿期或之后的代谢失代偿发作未影响或仅轻微影响神经学预后。
改善神经学预后的治疗目标是缩短意识改变水平的持续时间,并尽可能降低血浆亮氨酸峰值水平。