Clinical features of Guillain-Barré syndrome patients with elevated serum creatine kinase levels

• Published in: BMC neurology 2020-05, Vol.20 (1), p.214-214, Article 214
• Main Authors: Hosokawa, Takafumi, Nakajima, Hideto, Sawai, Taiki, Nakamura, Yoshitsugu, Sano, Eri, Tsukahara, Akihiro, Unoda, Kiichi, Ishida, Shimon, Sakane, Sadaki, Kimura, Fumiharu, Arawaka, Shigeki
• Format: Article
• Language: English
• Subjects: AIDP; AMAN; Cranial nerves; Creatine; Creatine kinase; Demyelination; Diabetes; Diabetic neuropathy; Disability; Ganglioside GM1; Guillain-Barre syndrome; Guillain-Barré syndrome; Inflammation; Laboratories; Neurodegeneration; Neuropathy; Patients; Polyneuropathy; Reversible conduction failure; Sensory neurons
• ISSN: 1471-2377; 1471-2377
• DOI: 10.1186/s12883-020-01796-z

It is not well defined whether Guillain-Barré syndrome (GBS) patients with elevated serum creatine kinase (CK) levels have characteristic clinical features and are related to the subgroups of GBS. We retrospectively studied 51 consecutive patients with GBS, who visited our hospital, and compared clinical, laboratory and electrophysiological findings between patients with and without elevated CK levels. Of 51 patients, 14 patients (27%) showed an elevation of serum CK levels. When compared with patients with the normal CK levels, the ratios of male, antecedent infections, and anti-GM1 antibody positivity were significantly higher in patients with elevated CK levels. The ratios of hypoesthesia, cranial nerve involvement, and urinary retention were significantly less in patients with elevated CK levels. There were no significant differences in disability at peak between two groups. In the electrophysiological examination, sensory nerve abnormalities were not observed. Although some patients with elevated CK levels showed prolongation of distal motor latencies (DMLs) and increase of durations in the initial examination, development of the prolongation of DMLs and increase of durations was not observed in the follow-up examinations. The findings were consistent with acute motor axonal neuropathy (AMAN) with reversible conduction failure (RCF) but not acute inflammatory demyelinating polyneuropathy (AIDP). The results suggest that the GBS patients with elevated CK levels represent not a group of AIDP but a group of AMAN with axonal degeneration or RCF even though the initial electrophysiological examination shows AIDP pattern.