The objective of this study was to investigate any relationship between peripheral neuropathy and anti-TNF-α therapy used in ankylosing spondylitis (AS). Thirty-nine patients monitored in our clinic with a diagnosis of AS and without neuropathic symptoms were enrolled in the study. Patients were divided into two groups. The first consisted of 21 patients using biological agents for more than one year. The control group was made up of 18 patients of similar age and demographic characteristics receiving non-biological therapy. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores were calculated, and sedimentation rate and C-reactive protein (CRP) levels measured. Motor and sensory nerve conduction analysis for the median, tibial, and sural nerves was performed. The nerve conduction results of the biological therapy group were then compared with those of the non-biological therapy group. Thirty-nine patients with a mean age of 37.05 ± 8.1 were enrolled. Patients were divided into two groups, depending on drugs used. The first group (using anti-TNF-α) consisted of 21 patients with a mean age of 42.2 ± 8.8, and the second (the non-biological group) of 18 patients with a mean age of 35.8 ± 7.5. There was no statistically significant difference between the groups in terms of age, sex, drug use, or duration of disease (p = 0.052, p = 0.55, p = 0.33, and p = 0.72, respectively). Sedimentation rate, CRP, and BASDAI scores were statistically significantly higher in the second group (p = 0.04, p = 0.03, and p = 0.009, respectively). No statistically significant difference was determined in any parameters at nerve conduction analysis between the two groups (p > 0.05). There was a positive correlation between sedimentation rate and median sensory conduction velocity (p = 0.02, r = 0.48) and tibial conduction velocity (p = 0.07, r = 0.43). A negative correlation was determined between duration of disease and median distal motor latency (p = 0.22, r = -0.37) and between length of drug use and median sensory conduction velocity (p = 0.02, r = -0.38). There was no significant correlation between other clinical and demographic data and nerve conduction parameters. No effect on nerve conduction of biological agents in AS patients without neurological symptoms was determined. Clinicians should be alert for signs and symptoms, suggesting neuropathy in patients given anti-TNF-α.
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Cureus
December 2024
Department of Orthopedics, Spine Unit, Hospital Sungai Buloh, Sungai Buloh, MYS.
Spinal cord injuries, including rare cases without radiological abnormalities, pose diagnostic challenges, particularly in cases of delayed neurological deficit development. This case report describes a 55-year-old man with a stable L1 burst fracture who developed delayed neurological deficits two weeks after sustaining a fall despite no evidence of intrinsic or extrinsic spinal cord abnormalities on magnetic resonance imaging (MRI). The patient initially presented with back pain, normal muscle strength across all myotomes, and imaging that showed no canal stenosis or retropulsion fragments.
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Children's Medical Center, Pediatric Center of Excellence, Tehran, Iran.
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January 2025
Longitudinal Studies Section, Translational Gerontology Branch, National Institute On Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
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January 2025
College of Chemical Engineering, Shenyang University of Chemical Technology, Shenyang, Liaoning, 110142, PR China; Institute of Functional Molecules, Shenyang University of Chemical Technology, Shenyang, Liaoning, 110142, PR China. Electronic address:
Acetylcholinesterase (AChE) is a pivotal enzyme in nerve conduction, controlling its activity with its inhibitor (AChEI) is crucial for the treatment of Alzheimer's disease (AD). However, current AChEIs are associated with considerable adverse effects. Previous work has identified 2α,3β,19α,23-tetrahydroxy-12-ene-28-oic acid (RLMS) as a promising natural AChEI.
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Physical Medicine and Rehabilitation, The MetroHealth System, 2500 Metrohealth Dr, Cleveland, OH 44109, USA, Cleveland, Ohio, 44109-1998, UNITED STATES.
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