Startseite Medizin Exploring pathogenic pathways in carpal tunnel syndrome: sterile inflammation and oxidative stress
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Exploring pathogenic pathways in carpal tunnel syndrome: sterile inflammation and oxidative stress

  • Mohd. Sajid Arshad , Bhawna Mattoo ORCID logo und Iqbal Alam EMAIL logo
Veröffentlicht/Copyright: 29. Mai 2024

Abstract

Objectives

The main objective of the current study was to find the association between oxidative stress, inflammatory markers, and electrophysiological profile with symptom severity in patients of carpal tunnel syndrome (CTS).

Methods

Thirty-two carpal tunnel syndrome patients and 32 controls were included in the study. Boston CTS questionnaire along with plasma oxidative stress markers including superoxide dismutase, malondialdehyde, and nitric oxide and inflammatory markers including IL-6 and TNF-α were compared with the electrophysiological parameters derived from nerve conduction studies. Statistical significance of the levels between groups was calculated using unpaired-t test after checking for normality with D’Agostino & Pearson omnibus normality test.

Results

We found that the median nerve conduction velocity was prolonged, amplitude was decreased, while the levels of oxidative stress markers like malondialdehyde (MDA), superoxidase dismutase (SOD), and nitric oxide (NO) were increased in CTS patients compared to controls. Inflammatory markers like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were also increased in CTS patients. We found that plasma SOD and TNF-α correlated well with the median motor amplitude. There was no other significant correlation between oxidative stress markers and inflammatory markers with nerve conduction studies or disease severity. Patients with mild disease also showed lesser levels of SOD, NO, IL-6, and TNF-α markers than patients with severe disease.

Conclusions

CTS is probably a disease of sterile inflammation and disbalance of oxidative stress, with higher inflammatory and oxidative stress markers pointing to a more severe disease.


Corresponding author: Prof. Iqbal Alam, Professor and Head, Department of Physiology, 421037 Hamdard Institute of Medical Sciences and Research, Jamia Hamdard , New Delhi, India, E-mail:

  1. Research ethics: Study was conducted in accordance with the Declaration of Helsinki. Ethical approval was obtained from Institutional review board.

  2. Informed consent: Informed consent was obtained from all individuals included in this study.

  3. Author contributions: BM Conceived and designed the analysis; performed the analysis , manuscript preparation MSA collected the data; contributed data or analysis tools; wrote the paper IA: supervised the study, data analysis , manuscript preparation. The authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  4. Competing interests: Authors state no conflict of interest.

  5. Research funding: None declared.

  6. Data availability: The raw data can be obtained on request from the corresponding author.

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Received: 2024-01-11
Accepted: 2024-05-11
Published Online: 2024-05-29

© 2024 Walter de Gruyter GmbH, Berlin/Boston

Heruntergeladen am 6.2.2026 von https://www.degruyterbrill.com/document/doi/10.1515/jbcpp-2024-0004/pdf
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