A case control study of the relationship between persistent serum creatine kinase elevation and polyneuropathy

Abstract 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 w...

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Bibliographic Details
Published in:Scientific Reports
Main Authors: Svein I. Bekkelund, Karin Abeler, Hallvard Lilleng, Sissel Løseth
Format: Article in Journal/Newspaper
Language:English
Published: Nature Portfolio 2024
Subjects:
Creatine kinase
HyperCKemia
Nerve conduction study
Electromyography
Polyneuropathy
Medicine
R
Science
Q
Tromsø
Online Access:https://doi.org/10.1038/s41598-024-64555-x
https://doaj.org/article/9917a7e6317a432fb6ef6fc4293bbeef
Description
Summary:Abstract 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.

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