Robbins J H, Brumback R A, Mendiones M, Barrett S F, Carl J R, Cho S, Denckla M B, Ganges M B, Gerber L H, Guthrie R A
Dermatology Branche, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Brain. 1991 Jun;114 ( Pt 3):1335-61. doi: 10.1093/brain/114.3.1335.
Xeroderma pigmentosum (XP) is an autosomal recessive, neurocutaneous disorder characterized by sunlight-induced skin cancers and defective DNA repair. Many XP children develop a primary neuronal degeneration. We describe 2 unusual XP patients who had a delayed onset of XP neurological disease. Somatic cell genetic studies indicated that they have the same defective DNA repair gene and are both in XP complementation group A. These 2 patients, together with a group A patient previously reported from London, establish as a distinct clinical entity the late onset type of the juvenile onset form of XP neurological disease. The functional capacity of these patients' cultured fibroblast strains to survive after treatment with ultraviolet radiation indicates that their DNA repair defect is less severe than that of typical group A patients who have a more severe neurodegeneration with an earlier symptomatic onset. The premature death of nerve cells in XP patients (which is presumably due to their inherited defects in DNA repair mechanisms) suggests that normal repair of damaged DNA in neurons is required to maintain integrity of the human nervous system.
着色性干皮病(XP)是一种常染色体隐性神经皮肤疾病,其特征为阳光诱发的皮肤癌和DNA修复缺陷。许多XP患儿会出现原发性神经元变性。我们描述了2例不寻常的XP患者,他们的XP神经疾病发病较晚。体细胞遗传学研究表明,他们具有相同的缺陷DNA修复基因,均属于XP互补组A。这2例患者,连同之前伦敦报道的1例A组患者,确立了XP神经疾病青少年发病型的迟发型为一种独特的临床实体。这些患者培养的成纤维细胞株经紫外线照射后存活的功能能力表明,他们的DNA修复缺陷不如典型A组患者严重,典型A组患者有更严重的神经变性且症状出现更早。XP患者神经细胞的过早死亡(推测是由于其DNA修复机制的遗传缺陷)表明,神经元中受损DNA的正常修复对于维持人类神经系统的完整性是必需的。