Patzold T, Sindern E, Ossege-Pohle L, Malin J P
Neurologische Klinik der Ruhr-Universität, BG-Kliniken Bergmannsheil, Bochum, Germany.
J Neurol. 1998 Dec;245(12):803-8. doi: 10.1007/s004150050290.
We determined serum and cerebrospinal fluid (CSF) levels of the soluble 60-kDa tumour necrosis factor (TNF) receptor (sTNF-R p60) in 50 patients with relapsing-remitting multiple sclerosis (MS) and in 18 patients with Guillain-Barré syndrome (GBS). Neither in serum nor in CSF samples was there a statistically significant difference between mean receptor concentrations of patients with MS (serum: 1064, SD 262 pg/ml; CSF: 555, SD 130 pg/ml), with other noninflammatory neurological diseases (serum: 1008, SD 248 pg/ml; CSF: 530, SD 112 pg/ml) and with healthy control subjects (serum: 918, SD 180 pg/ml). In order to determine disease activity, magnetic resonance imaging (MRI) of the brain was performed in all MS patients. The mean sTNF-R p60 levels of patients who showed gadolinium DTPA enhancement on MRI were not different from those without enhancement (1034, SD 274 pg/ml vs 1099, SD 248 pg/ml in serum samples and 546, SD 109 pg/ml vs 565, SD 152 pg/ml in CSF samples). In GBS, the sTNF-R p60 levels of serum and CSF samples were significantly higher than in MS and all control groups except for the group with viral meningitis (VM) (GBS: 1544, SD 834 pg/ml in serum, 882, SD 147 pg/ml in CSF; VM: 1518, SD 375 pg/ml in serum, 1131, SD 611 pg/ml in CSF; P < 0.001 for serum samples and P < 0.005 for CSF samples). Serial serum sTNF-R p60 measurements in 13 patients with GBS showed an increase in receptor levels parallel with the recovery from the disease (1276, SD 374 pg/ml at the time of disease onset, 1554, SD 482 pg/ml 14-24 days later and 1787, SD 525 pg/ml after 28-32 days). From our results and the conflicting data of previous studies, we could not agree with the suggestion that the assessment of sTNF-R p60 in MS patients is a useful marker for disease activity. In GBS, subsequently increasing sTNF-R p60 levels are associated with recovery from the disease. It remains to be shown whether they might represent a relevant pathogenetic factor during this stage of GBS.
我们测定了50例复发缓解型多发性硬化症(MS)患者和18例吉兰 - 巴雷综合征(GBS)患者血清及脑脊液(CSF)中可溶性60 kDa肿瘤坏死因子(TNF)受体(sTNF - R p60)的水平。MS患者(血清:1064,标准差262 pg/ml;脑脊液:555,标准差130 pg/ml)、患有其他非炎性神经系统疾病的患者(血清:1008,标准差248 pg/ml;脑脊液:530,标准差112 pg/ml)以及健康对照者(血清:918,标准差180 pg/ml)的平均受体浓度在血清和脑脊液样本中均无统计学显著差异。为了确定疾病活动度,对所有MS患者进行了脑部磁共振成像(MRI)检查。MRI显示钆喷酸葡胺增强的患者的平均sTNF - R p60水平与未增强患者的水平无差异(血清样本中分别为1034,标准差274 pg/ml和1099,标准差248 pg/ml;脑脊液样本中分别为546,标准差109 pg/ml和565,标准差152 pg/ml)。在GBS中,血清和脑脊液样本中的sTNF - R p60水平显著高于MS患者及除病毒性脑膜炎(VM)组之外的所有对照组(GBS:血清1544,标准差834 pg/ml,脑脊液882,标准差147 pg/ml;VM:血清1518,标准差375 pg/ml,脑脊液1131,标准差611 pg/ml;血清样本P < 0.001,脑脊液样本P < 0.005)。对13例GBS患者进行的系列血清sTNF - R p60测量显示,受体水平随着疾病的恢复而升高(疾病发作时为1276,标准差374 pg/ml,14 - 24天后为1554,标准差482 pg/ml,28 - 32天后为1787,标准差525 pg/ml)。根据我们研究的结果以及既往研究相互矛盾的数据,我们不同意对MS患者评估sTNF - R p60是疾病活动度有用标志物的观点。在GBS中,随后升高的sTNF - R p60水平与疾病的恢复相关。在GBS的这个阶段,它们是否可能代表一个相关的致病因素仍有待证实。