Stockler-Ipsiroglu Sylvia, van Karnebeek Clara, Longo Nicola, Korenke G Christoph, Mercimek-Mahmutoglu Saadet, Marquart Iris, Barshop Bruce, Grolik Christiane, Schlune Andrea, Angle Brad, Araújo Helena Caldeira, Coskun Turgay, Diogo Luisa, Geraghty Michael, Haliloglu Goknur, Konstantopoulou Vassiliki, Leuzzi Vincenzo, Levtova Alina, Mackenzie Jennifer, Maranda Bruno, Mhanni Aizeddin A, Mitchell Grant, Morris Andrew, Newlove Theresa, Renaud Deborah, Scaglia Fernando, Valayannopoulos Vassili, van Spronsen Francjan J, Verbruggen Krijn T, Yuskiv Nataliya, Nyhan William, Schulze Andreas
Department of Pediatrics, University of British Columbia, Vancouver, BC, Canada.
Department of Pediatrics, University of British Columbia, Vancouver, BC, Canada; Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, BC, Canada.
Mol Genet Metab. 2014 Jan;111(1):16-25. doi: 10.1016/j.ymgme.2013.10.018. Epub 2013 Nov 7.
We collected data on 48 patients from 38 families with guanidinoacetate methyltransferase (GAMT) deficiency. Global developmental delay/intellectual disability (DD/ID) with speech/language delay and behavioral problems as the most affected domains was present in 44 participants, with additional epilepsy present in 35 and movement disorder in 13. Treatment regimens included various combinations/dosages of creatine-monohydrate, l-ornithine, sodium benzoate and protein/arginine restricted diets. The median age at treatment initiation was 25.5 and 39 months in patients with mild and moderate DD/ID, respectively, and 11 years in patients with severe DD/ID. Increase of cerebral creatine and decrease of plasma/CSF guanidinoacetate levels were achieved by supplementation with creatine-monohydrate combined with high dosages of l-ornithine and/or an arginine-restricted diet (250 mg/kg/d l-arginine). Therapy was associated with improvement or stabilization of symptoms in all of the symptomatic cases. The 4 patients treated younger than 9 months had normal or almost normal developmental outcomes. One with inconsistent compliance had a borderline IQ at age 8.6 years. An observational GAMT database will be essential to identify the best treatment to reduce plasma guanidinoacetate levels and improve long-term outcomes.
我们收集了来自38个患有胍基乙酸甲基转移酶(GAMT)缺乏症家庭的48例患者的数据。44名参与者存在以言语/语言发育迟缓及行为问题为最主要受累领域的全面发育迟缓/智力残疾(DD/ID),其中35名存在额外的癫痫,13名存在运动障碍。治疗方案包括一水肌酸、L-鸟氨酸、苯甲酸钠的各种组合/剂量以及蛋白质/精氨酸限制饮食。轻度和中度DD/ID患者开始治疗的中位年龄分别为25.5个月和39个月,重度DD/ID患者为11岁。通过补充一水肌酸联合高剂量L-鸟氨酸和/或精氨酸限制饮食(250mg/kg/d L-精氨酸),可实现脑内肌酸增加及血浆/脑脊液胍基乙酸水平降低。在所有有症状的病例中,治疗均与症状改善或稳定相关。4名9个月前接受治疗的患者发育结局正常或几乎正常。1名依从性不一致的患者在8.6岁时智商处于临界水平。一个观察性GAMT数据库对于确定降低血浆胍基乙酸水平及改善长期结局的最佳治疗方法至关重要。