肌酸激酶(CK)与神经病变有关,但是机制是不确定的。我们假设,与一般人群中年龄和性别匹配的对照相比,患有持续性CK升高(高CK血症)的受试者的周围神经功能受损。参与者是从挪威基于人口的Tromsø研究中招募的。神经病变损伤评分(NIS),神经传导研究(NCS)和肌电图(EMG)在患有持续性高CK血症的受试者中(n=113;51名男性,62名女性)和对照组(n=128;61名男性,67名妇女)进行了表演。高CK血症组的NIS评分高于对照组(p=0.050)。胫神经的NCS显示复合运动动作电位振幅降低(p<0.001),运动传导速度降低(p<0.001),F波潜伏期增加(p=0.044)。此外,中位数的感觉幅度降低,尺骨,然后发现了腓肠神经.EMG在所有检查的肌肉中显示出平均运动单位电位幅度显着增加。CK与糖化血红蛋白、非空腹血糖呈正相关。虽然不控制协变量。在高CK血症组中表现出的长度依赖性多发性神经病是无法解释的,但推测CK渗漏和参与糖代谢。
Creatine kinase (CK) has been associated with neuropathy, but the mechanisms are uncertain. We hypothesized that peripheral nerve function is impaired in subjects with persistent CK elevation (
hyperCKemia) compared to age- and sex matched controls in a general population. The participants were recruited from the population based Tromsø
study in Norway. Neuropathy impairment score (NIS), nerve conduction studies (NCS) and electromyography (EMG) in subjects with persistent
hyperCKemia (n = 113; 51 men, 62 women) and controls (n = 128; 61 men, 67 women) were performed. The
hyperCKemia group had higher NIS score than the controls (p = 0.050). NCS of the tibial nerve showed decreased compound motor action potential amplitude (p < 0.001), decreased motor conduction velocity (p < 0.001) and increased F-wave latency (p = 0.044). Also, reduced sensory amplitudes of the median, ulnar, and sural nerves were found. EMG showed significantly increased average motor unit potential amplitude in all examined muscles. CK correlated positively with glycated hemoglobin and non-fasting glucose in the hyperCKemia group, although not when controlled for covariates. The length dependent polyneuropathy demonstrated in the
hyperCKemia group is unexplained, but CK leakage and involvement of glucose metabolism are speculated on.