{"title":"与 SURF1 基因突变相关的利氏病的独特影像标记:一项儿科病例研究","authors":"Rama Krishna Narra, Reshma Vemuri","doi":"10.12659/AJCR.944514","DOIUrl":null,"url":null,"abstract":"<p><p>BACKGROUND Leigh disease (LD) is a rare progressive mitochondrial neurodegenerative disorder characterized by subacute necrotizing encephalopathy and symmetrical spongiform lesions in the brain. Cytochrome C oxidase deficiencies due to SURF1 Cytochrome C Oxidase Assembly Factor (SURF1) gene mutations are seen only in 15% of LD cases. Consideration of these genetic mutations in young patients is crucial for early diagnosis, intervention, and further genetic counseling. Although only a few cases of the SURF1 mutation have been reported, there are anecdotal case reports describing imaging features. CASE REPORT We report a case of a 2-year-old boy with developmental delay, hypotonia, involuntary movements, shortness of breath, and reduced activity since age 6 months. On blood examination there was mildly elevated lactate levels and increased lactate to pyruvate ratio and cerebrospinal fluid lactate levels. Magnetic resonance imaging findings showed symmetrical lesions in the dentate nucleus, subthalamic nucleus, midbrain (substantia nigra, periaqueductal gray matter), posterolateral pons, and olivary nucleus of the medulla extending into the cervical spinal cord, with mild elevation of the lactate peak on magnetic resonance spectroscopy. CONCLUSIONS These findings prompted further genetic analysis, which indicated a mitochondrial type IV deficiency with the SURF1 gene defect, an intranuclear type 1 mutation (MC4DN1) (OMIM 220110). Treatment is usually supportive with vitamins supplementation and physiotherapy, and genetic counseling of the parents is mandatory.</p>","PeriodicalId":39064,"journal":{"name":"American Journal of Case Reports","volume":null,"pages":null},"PeriodicalIF":1.0000,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11318735/pdf/","citationCount":"0","resultStr":"{\"title\":\"Distinct Imaging Markers of Leigh's Disease Linked to SURF1 Mutation: A Pediatric Case Study.\",\"authors\":\"Rama Krishna Narra, Reshma Vemuri\",\"doi\":\"10.12659/AJCR.944514\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>BACKGROUND Leigh disease (LD) is a rare progressive mitochondrial neurodegenerative disorder characterized by subacute necrotizing encephalopathy and symmetrical spongiform lesions in the brain. Cytochrome C oxidase deficiencies due to SURF1 Cytochrome C Oxidase Assembly Factor (SURF1) gene mutations are seen only in 15% of LD cases. Consideration of these genetic mutations in young patients is crucial for early diagnosis, intervention, and further genetic counseling. Although only a few cases of the SURF1 mutation have been reported, there are anecdotal case reports describing imaging features. CASE REPORT We report a case of a 2-year-old boy with developmental delay, hypotonia, involuntary movements, shortness of breath, and reduced activity since age 6 months. On blood examination there was mildly elevated lactate levels and increased lactate to pyruvate ratio and cerebrospinal fluid lactate levels. Magnetic resonance imaging findings showed symmetrical lesions in the dentate nucleus, subthalamic nucleus, midbrain (substantia nigra, periaqueductal gray matter), posterolateral pons, and olivary nucleus of the medulla extending into the cervical spinal cord, with mild elevation of the lactate peak on magnetic resonance spectroscopy. CONCLUSIONS These findings prompted further genetic analysis, which indicated a mitochondrial type IV deficiency with the SURF1 gene defect, an intranuclear type 1 mutation (MC4DN1) (OMIM 220110). Treatment is usually supportive with vitamins supplementation and physiotherapy, and genetic counseling of the parents is mandatory.</p>\",\"PeriodicalId\":39064,\"journal\":{\"name\":\"American Journal of Case Reports\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2024-07-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11318735/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American Journal of Case Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.12659/AJCR.944514\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Case Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12659/AJCR.944514","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
摘要
背景利氏病(LD)是一种罕见的进行性线粒体神经退行性疾病,以亚急性坏死性脑病和大脑对称性海绵状病变为特征。由于 SURF1 细胞色素 C 氧化酶组装因子(SURF1)基因突变导致的细胞色素 C 氧化酶缺乏症仅见于 15%的 LD 病例。考虑年轻患者的这些基因突变对于早期诊断、干预和进一步的遗传咨询至关重要。虽然只有少数 SURF1 基因突变的病例被报道,但也有描述影像学特征的轶事病例报道。病例报告 我们报告了一例 2 岁男童的病例,他自 6 个月大开始出现发育迟缓、肌张力低下、不自主运动、呼吸急促和活动减少等症状。血液检查显示乳酸水平轻度升高,乳酸与丙酮酸比值和脑脊液乳酸水平升高。磁共振成像结果显示,齿状核、丘脑下核、中脑(黑质、纹状体周围灰质)、大脑后外侧和延髓橄榄核对称性病变,并延伸至颈脊髓,磁共振波谱检查显示乳酸峰值轻度升高。结论 这些发现促使人们进一步进行基因分析,结果表明该患者患有线粒体 IV 型缺乏症,SURF1 基因缺陷,核内 1 型突变(MC4DN1)(OMIM 220110)。治疗方法通常是补充维生素和物理治疗,同时必须对父母进行遗传咨询。
Distinct Imaging Markers of Leigh's Disease Linked to SURF1 Mutation: A Pediatric Case Study.
BACKGROUND Leigh disease (LD) is a rare progressive mitochondrial neurodegenerative disorder characterized by subacute necrotizing encephalopathy and symmetrical spongiform lesions in the brain. Cytochrome C oxidase deficiencies due to SURF1 Cytochrome C Oxidase Assembly Factor (SURF1) gene mutations are seen only in 15% of LD cases. Consideration of these genetic mutations in young patients is crucial for early diagnosis, intervention, and further genetic counseling. Although only a few cases of the SURF1 mutation have been reported, there are anecdotal case reports describing imaging features. CASE REPORT We report a case of a 2-year-old boy with developmental delay, hypotonia, involuntary movements, shortness of breath, and reduced activity since age 6 months. On blood examination there was mildly elevated lactate levels and increased lactate to pyruvate ratio and cerebrospinal fluid lactate levels. Magnetic resonance imaging findings showed symmetrical lesions in the dentate nucleus, subthalamic nucleus, midbrain (substantia nigra, periaqueductal gray matter), posterolateral pons, and olivary nucleus of the medulla extending into the cervical spinal cord, with mild elevation of the lactate peak on magnetic resonance spectroscopy. CONCLUSIONS These findings prompted further genetic analysis, which indicated a mitochondrial type IV deficiency with the SURF1 gene defect, an intranuclear type 1 mutation (MC4DN1) (OMIM 220110). Treatment is usually supportive with vitamins supplementation and physiotherapy, and genetic counseling of the parents is mandatory.
期刊介绍:
American Journal of Case Reports is an international, peer-reviewed scientific journal that publishes single and series case reports in all medical fields. American Journal of Case Reports is issued on a continuous basis as a primary electronic journal. Print copies of a single article or a set of articles can be ordered on demand.