Bahi-Buisson Nadia, Eisermann Monica, Nivot Sylvie, Bellanné-Chantelot Christine, Dulac Olivier, Bach Nathalie, Plouin Perrine, Chiron Catherine, de Lonlay Pascale
Department of Paediatric Neurology and Metabolic Disease, Hôpital Necker Enfants Malades, Paris, France.
J Child Neurol. 2007 Sep;22(9):1147-50. doi: 10.1177/0883073807306272.
Activating mutations in the Kir6.2 subunit of the adenosine triphosphate-sensitive potassium (KATP) channel is a cause of neonatal diabetes associated with various neurological disorders that include developmental delay, epilepsy, and neonatal diabetes (known together as DEND syndrome). This article reports a girl who developed infantile spasms and early onset diabetes mellitus at the age of 3 months and revealed DEND syndrome with a heterozygous activating mutation in Kir6.2. Infantile spasms with hypsarrhythmia on the electroencephalogram were severe and refractory to steroids. Steroids combined with oral sulfonylurea, a drug that closes the ATP-sensitive potassium channel by an independent mechanism, allowed partial and transitory control of the epilepsy. However, the child still exhibited severe encephalopathy and died of aspiration pneumonia. The role of oral sulfonylurea as an anticonvulsant in DEND syndrome associated with Kir6.2 mutation is discussed.
三磷酸腺苷敏感性钾(KATP)通道的Kir6.2亚基中的激活突变是导致新生儿糖尿病的原因之一,该疾病与多种神经障碍相关,包括发育迟缓、癫痫和新生儿糖尿病(统称为DEND综合征)。本文报告了一名3个月大时出现婴儿痉挛和早发性糖尿病的女孩,经检测发现其患有DEND综合征,且Kir6.2存在杂合激活突变。脑电图显示伴有高峰节律紊乱的婴儿痉挛严重,对类固醇治疗无效。类固醇与口服磺脲类药物联合使用,后者通过独立机制关闭ATP敏感性钾通道,可使癫痫得到部分且短暂的控制。然而,该患儿仍表现出严重的脑病,并死于吸入性肺炎。本文还讨论了口服磺脲类药物在与Kir6.2突变相关的DEND综合征中作为抗惊厥药的作用。