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首页> 外文期刊>Egyptian Journal of Medical Human Genetics >Mitochondrial alterations in children with chronic liver disease
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Mitochondrial alterations in children with chronic liver disease

机译：慢性肝病患儿的线粒体改变

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Background Over recent years it has become apparent that the hepatocyte mitochondrion functions both as a cause and as a target of liver injury. Resultant dysfunction of mitochondria yields deficient oxidative phosphorylation, increased generation of reactive oxygen species, impairment of other metabolic pathways and activation of both necrotic and apoptotic pathways of cellular death. Methods This study was conducted on 26 children and adolescents with chronic liver disease who presented to or were following up in the Pediatric Hepatology Clinic, Children’s Hospital, Ain-Shams University. They were divided into three groups according to the aetiology of liver disease (GI=patients with Wilson’s disease (WD), GII=patients with chronic hepatitis C, GIII=patients with chronic liver disease other than Wilson’s and chronic hepatitis C). Ultrasound-guided gun liver biopsies were performed, under local anaesthesia for all the 26 patients, using a modified 18-gauge truecut needle. Two liver biopsy cores were taken from each patient. One for light and electron microscopic examinations and the other was immediately immersed in liquid nitrogen to be frozen and used for studying mitochondrial DNA deletions by PCR. Results Liver steatosis was higher in the group of patients with Wilson’s disease and other liver diseases. Electron microscopic examination of the mitochondria revealed significant mitochondrial pleomorphism in patients with Wilson’s disease and patients with chronic hepatitis C infection. Enlarged mitochondria were found to be more prevalent among patients with chronic hepatitis C infection. Three of our patients (11.53%) had mitochondrial DNA deletions. We developed a scoring system for mitochondrial affection in our patients, 7 patients (32%) were considered to have mild mitochondrial affection, 9 patients (41%) had moderate mitochondrial affection, while 6 patients (27%) had severe mitochondrial affection. Four of the studied patients had no mitochondrial affection. Conclusion Mitochondria affection is common in chronic liver disease. This mitochondrial affection might be responsible for some of the chronic liver disease manifestation such as easy fatiguability and steatosis.
机译：背景技术近年来，很明显，肝细胞线粒体既作为肝损伤的原因又作为肝损伤的靶标。导致的线粒体功能异常会导致氧化磷酸化不足，活性氧的生成增加，其他代谢途径的损伤以及细胞死亡的坏死和凋亡途径的激活。方法本研究是针对26名患有慢性肝病的儿童和青少年进行的，这些儿童和青少年就诊于或正在Ain-Shams大学儿童医院的儿科肝病诊所接受随访。根据肝病的病因将其分为三组（GI =威尔逊病（WD）患者，GII =慢性丙型肝炎患者，GIII =除了Wilson和慢性C型肝炎以外的其他慢性肝病患者）。所有26例患者均在局麻下使用改良的18号truecut针进行了超声引导的枪肝活检。从每个患者中取出两个肝活检核心。一种用于光镜和电子显微镜检查，另一种立即浸入液氮中冷冻并用于通过PCR研究线粒体DNA缺失。结果威尔逊氏病和其他肝病患者的肝脂肪变性更高。线粒体的电子显微镜检查显示，威尔逊氏病患者和慢性丙型肝炎患者存在明显的线粒体多态性。发现线粒体扩大在患有慢性丙型肝炎的患者中更为普遍。我们的三名患者（11.53％）具有线粒体DNA缺失。我们为患者的线粒体疾病建立了评分系统，其中7例（32％）被认为是轻度线粒体疾病，9例患者（41％）被认为是中度线粒体疾病，而6例患者（27％）被严重的线粒体疾病。研究的四名患者没有线粒体感染。结论线粒体感染在慢性肝病中很常见。这种线粒体的影响可能是某些慢性肝病表现的原因，例如易疲劳和脂肪变性。

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