Zirn B, Steinberger D, Troidl C, Brockmann K, von der Hagen M, Feiner C, Henke L, Müller U
Institut für Humangenetik, University of Giessen, Schlangenzahl 14, D-35392 Giessen, Germany.
J Neurol Neurosurg Psychiatry. 2008 Feb;79(2):183-6. doi: 10.1136/jnnp.2007.128413. Epub 2007 Sep 26.
We performed a systematic study on the frequency of point mutations and deletions of the gene GCH1 in dopa-responsive dystonia (DRD). A total of 136 dystonia patients were studied. Fifty of these had a sustained response to oral L-Dopa therapy (group 1: definite diagnosis of DRD), whereas the response to L-Dopa was incomplete or not tested in 86 patients (group 2: possible diagnosis of DRD). We found a GCH1 point mutation in 27 patients of group 1 (54%) and in four patients of group 2 (5%). Of these, nine single and one double mutation have not been described before. GCH1 deletions were detected in four patients of group 1 (8%) and in one patient of group 2 (1%). Among GCH1 point-mutation-negative patients with a definite diagnosis of DRD (group 1), the frequency of GCH1 deletions was 17% (4/23). We conclude that GCH1 deletion analysis should be incorporated into the routine molecular diagnosis of all patients with DRD with a sustained response to L-Dopa.
我们对多巴反应性肌张力障碍(DRD)患者中GCH1基因点突变和缺失的频率进行了系统研究。共研究了136例肌张力障碍患者。其中50例对口服左旋多巴治疗有持续反应(第1组:明确诊断为DRD),而86例患者对左旋多巴的反应不完全或未进行检测(第2组:可能诊断为DRD)。我们在第1组的27例患者(54%)和第2组的4例患者(5%)中发现了GCH1点突变。其中,9个单突变和1个双突变以前未曾报道过。在第1组的4例患者(8%)和第2组的1例患者(1%)中检测到GCH1缺失。在明确诊断为DRD且GCH1点突变阴性的患者(第1组)中,GCH1缺失的频率为17%(4/23)。我们得出结论,GCH1缺失分析应纳入所有对左旋多巴有持续反应的DRD患者的常规分子诊断中。