Wamelink Mirjam M C, Ramos Ruben J J F, van den Elzen Annette P M, Ruijter George J G, Bonte Ramon, Diogo Luisa, Garcia Paula, Neves Nelson, Nota Benjamin, Haschemi Arvand, Tavares de Almeida Isabel, Salomons Gajja S
Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, De Boelelaan 1117, 1081HV, Amsterdam, The Netherlands,
J Inherit Metab Dis. 2015 Sep;38(5):889-94. doi: 10.1007/s10545-014-9809-1. Epub 2015 Feb 3.
We present the first two reported unrelated patients with an isolated sedoheptulokinase (SHPK) deficiency. The first patient presented with neonatal cholestasis, hypoglycemia, and anemia, while the second patient presented with congenital arthrogryposis multiplex, multiple contractures, and dysmorphisms. Both patients had elevated excretion of erythritol and sedoheptulose, and each had a homozygous nonsense mutation in SHPK. SHPK is an enzyme that phosphorylates sedoheptulose to sedoheptulose-7-phosphate, which is an important intermediate of the pentose phosphate pathway. It is questionable whether SHPK deficiency is a causal factor for the clinical phenotypes of our patients. This study illustrates the necessity of extensive functional and clinical workup for interpreting a novel variant, including nonsense variants.
我们报告了首例两个互不相关的孤立性景天庚酮糖激酶(SHPK)缺乏症患者。首例患者表现为新生儿胆汁淤积、低血糖和贫血,而第二例患者表现为先天性多发性关节挛缩、多处挛缩和畸形。两名患者的赤藓糖醇和景天庚酮糖排泄均升高,且均在SHPK基因中存在纯合无义突变。SHPK是一种将景天庚酮糖磷酸化为景天庚酮糖-7-磷酸的酶,而景天庚酮糖-7-磷酸是磷酸戊糖途径的重要中间产物。SHPK缺乏是否是我们患者临床表型的致病因素尚存在疑问。本研究说明了对包括无义变异在内的新变异进行广泛功能和临床检查的必要性。