Gilbert Jeffrey, Ibdah Jamal A
Division of Gastroenterology, Department of Internal Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
Med Hypotheses. 2005;64(3):586-9. doi: 10.1016/j.mehy.2004.07.032.
Intestinal pseudo-obstruction can be caused by mitochondrial disorders. Understanding the association between genetic alterations in mitochondrial function and development of intestinal pseudo-obstruction may provide insight into the pathogenesis of this disorder. Although the association between mitochondrial DNA defects and pseudo-obstruction is documented, little is known about the relationship between mitochondrial beta-oxidation disorders, which are caused by defects in nuclear genes, and development of intestinal pseudo-obstruction. Mitochondrial beta-oxidation defects have emerged recently as an important group of recessively inherited inborn errors of metabolism with multiple phenotypes. Here we report the case history of a 25-year-old patient with mitochondrial trifunctional protein (MTP) deficiency, the eldest known living patient with this disorder. MTP is an enzyme complex that consists of 4alpha and 4beta subunits and catalyzes the last three steps in the beta-oxidation cycle. The patient's MTP deficiency is secondary to a compound heterozygosity for two mutations in the MTP beta-subunit. Over the past 5 years, the patient had worsening symptoms consistent with intestinal pseudo-obstruction associated with progressive skeletal myopathy and polyneuropathy. We hypothesize that impairment of mitochondrial beta-oxidation causes intestinal pseudo-obstruction secondary to accumulation of intracellular long chain fatty acids, activation of extramitochondrial fatty acid oxidation pathways, and generation of excessive reactive oxygen species leading to visceral myopathy.
肠道假性梗阻可由线粒体疾病引起。了解线粒体功能的基因改变与肠道假性梗阻的发展之间的关联,可能有助于深入了解这种疾病的发病机制。尽管线粒体DNA缺陷与假性梗阻之间的关联已有文献记载,但对于由核基因缺陷引起的线粒体β-氧化障碍与肠道假性梗阻发展之间的关系却知之甚少。线粒体β-氧化缺陷最近已成为一组重要的隐性遗传先天性代谢缺陷,具有多种表型。在此,我们报告一例25岁线粒体三功能蛋白(MTP)缺乏症患者的病例史,该患者是已知患有这种疾病的年龄最大的在世患者。MTP是一种由4个α亚基和4个β亚基组成的酶复合物,催化β-氧化循环的最后三个步骤。该患者的MTP缺乏是由于MTPβ亚基中两个突变的复合杂合性所致。在过去5年中,该患者的症状不断恶化,与肠道假性梗阻相关,并伴有进行性骨骼肌病和多发性神经病。我们推测,线粒体β-氧化受损导致肠道假性梗阻,继发于细胞内长链脂肪酸的积累、线粒体外脂肪酸氧化途径的激活以及导致内脏肌病的过量活性氧的产生。