Zielonka Matthias, Makhseed Nawal, Blau Nenad, Bettendorf Markus, Hoffmann Georg Friedrich, Opladen Thomas
Division of Neuropediatrics and Metabolic Medicine, Department of General Pediatrics, University Hospital Heidelberg, Im Neuenheimer Feld 430, 69120, Heidelberg, Germany.
Pediatric Department, Jahra Hospital, Qadisiya, Kuwait.
JIMD Rep. 2015;24:109-13. doi: 10.1007/8904_2015_450. Epub 2015 May 26.
Sepiapterin reductase (SR) deficiency is a rare autosomal recessively inherited error of tetrahydrobiopterin (BH4) biosynthesis, resulting in disturbed dopaminergic and serotonergic neurotransmission. The clinical phenotype is characterized by dopa-responsive movement disorders including muscular hypotonia, dystonia, and parkinsonism. Due to the rarity of the disease, the phenotype of SR deficiency is far from being completely understood. Here, we report a 7-year-old boy, who was referred for diagnostic evaluation of combined psychomotor retardation, spastic tetraplegia, extrapyramidal symptoms, and short stature. Due to discrepancy between motor status and mental condition, analyses of biogenic amines and pterins in CSF were performed, leading to the diagnosis of SR deficiency. The diagnosis was confirmed by a novel homozygous mutation c.530G>C; p.(Arg177Pro) in exon 2 of the SPR gene. Because of persistent short stature, systematic endocrinological investigations were initiated. Insufficient growth-hormone release in a severe hypoglycemic episode after overnight fasting confirmed growth-hormone deficiency as a cause of short stature. In addition, central hypothyroidism was present. A general hypothalamic affection could be excluded. Since dopamine is known to regulate growth-hormone excretion, IGF-1, IGF-BP3, and peripheral thyroid hormone levels were monitored under L-dopa/carbidopa supplementation. Both growth-hormone-dependent factors and thyroid function normalized under treatment. This is the first report describing growth-hormone deficiency and central hypothyroidism in SR deficiency. It extends the phenotypic spectrum of the disease and identifies dopamine depletion as cause for the endocrinological disturbances.
蝶呤还原酶(SR)缺乏症是一种罕见的常染色体隐性遗传的四氢生物蝶呤(BH4)生物合成缺陷病,导致多巴胺能和5-羟色胺能神经传递紊乱。临床表型的特征为对多巴反应性运动障碍,包括肌张力减退、肌张力障碍和帕金森综合征。由于该疾病罕见,SR缺乏症的表型远未被完全了解。在此,我们报告一名7岁男孩,因精神运动发育迟缓、痉挛性四肢瘫、锥体外系症状和身材矮小而前来接受诊断评估。由于运动状态与精神状况不符,对脑脊液中的生物胺和蝶呤进行了分析,从而诊断为SR缺乏症。通过SPR基因第2外显子的一个新的纯合突变c.530G>C;p.(Arg177Pro)确诊。由于身材持续矮小,启动了系统的内分泌学检查。过夜禁食后严重低血糖发作时生长激素释放不足证实生长激素缺乏是身材矮小的原因。此外,还存在中枢性甲状腺功能减退。可以排除一般性下丘脑病变。由于已知多巴胺调节生长激素分泌,在补充左旋多巴/卡比多巴的情况下监测了IGF-1、IGF-BP3和外周甲状腺激素水平。治疗后生长激素依赖因子和甲状腺功能均恢复正常。这是第一份描述SR缺乏症中生长激素缺乏和中枢性甲状腺功能减退的报告。它扩展了该疾病的表型谱,并确定多巴胺耗竭是内分泌紊乱的原因。