| High-dose thalidomide increases the risk of peripheral neuropathy in the treatment of ankylosing spondylitis | |
| Alternative Title | High-dose thalidomide increases the risk of peripheral neuropathy in the treatment of ankylosing spondylitis |
| Xue Hongxia; Fu Wenyi; Cui Huadong; Yang Lili; Zhang Ning; Zhao Lijuan | |
| 2015 | |
| Source Publication | Neural Regeneration Research
 |
| ISSN | 1673-5374 |
| Volume | 10Issue:5Pages:814-818 |
| Abstract | Thalidomide is an effective drug for the treatment of ankylosing spondylitis but might induce peripheral neuropathy. This major adverse reaction has attracted much concern. The current study aimed to observe the incidence of thalidomide-induced peripheral neuropathy among ankylosing spondylitis patients for 1 year after treatment. In this study, 207 ankylosing spondylitis cases received thalidomide treatment, while 116 ankylosing spondylitis cases received other treatments. Results showed that the incidence of thalidomide-induced peripheral neuropathy in the thalidomide group was higher than that in the non-thalidomide group. There was no significant difference in the incidence of neuropathy between the < 6 months medication and ≥ 6 months medication groups. There were no differences in the mean age, gender, or daily dose between the two groups. The incidence of peripheral neuropathy among patients receiving 25, 50, 75, or 100 mg thalidomide per day was 4.6%, 8.5%, 17.1%, 21.7%, respectively. The incidence was significantly different between the groups receiving 25 mg and 100 mg thalidomide. In conclusion, thalidomide can induce peripheral neuropathy within 1 year after treatment of ankylosing spondylitis; however, age and gender have no obvious impact on the incidence of peripheral neuropathy. The incidence of peripheral neuropathy is associated with increasing daily doses of thalidomide. |
| Other Abstract | Thalidomide is an effective drug for the treatment of ankylosing spondylitis but might induce peripheral neuropathy. This major adverse reaction has attracted much concern. The current study aimed to observe the incidence of thalidomide-induced peripheral neuropathy among ankylosing spondylitis patients for 1 year after treatment. In this study, 207 ankylosing spondylitis cases received thalidomide treatment, while 116 ankylosing spondylitis cases received other treatments. Results showed that the incidence of thalidomide-induced peripheral neuropathy in the thalidomide group was higher than that in the non-thalidomide group. There was no significant difference in the incidence of neuropathy between the < 6 months medication and ≥ 6 months medication groups. There were no differences in the mean age, gender, or daily dose between the two groups. The incidence of peripheral neuropathy among patients receiving 25, 50, 75, or 100 mg thalidomide per day was 4.6%, 8.5%, 17.1%, 21.7%, respectively. The incidence was significantly different between the groups receiving 25 mg and 100 mg thalidomide. In conclusion, thalidomide can induce peripheral neuropathy within 1 year after treatment of ankylosing spondylitis; however, age and gender have no obvious impact on the incidence of peripheral neuropathy. The incidence of peripheral neuropathy is associated with increasing daily doses of thalidomide. |
| Keyword | active zone stability Drosophila neuromuscular junction dephosphorylation Liprin-α Syd-1 PP2A GSK-3? living scaffolds neural tissue engineering cell transplant biomaterials regeneration neurotrauma neurodegeneration axon pathfinding cell migration injury plasticity neurodegenerative disease brain therapy neuron microglia neural progenitor tissue engineering neuroregeneration repair central nervous system biomaterial regenerative medicine nanotechnology spinal cord injury axonal regeneration exosome extracellular vesicle microRNA microvesicle nerve gap neurite outgrowth peripheral nerve injury Schwann cell stem cell hemodynamic phases cerebral subarachnoid hemorrhage metabolic crises nerve regeneration hypoxic-ischemic brain damage ginsenoside Rg1 neural stem cells cell transplantation cell differentiation cognition nerve reconstruction neural regeneration nerve regeneration brain injury neuroimaging functional magnetic resonance imaging regional homogeneity apoplexy subacute ischemia participants healthy volunteers brain activity NSFC grants neural regeneration nerve regeneration brain injury neuroprotection cerebral ischemia/reperfusion injury lateral intracerebroventricular injection Apelin-13 nerve apoptosis Bcl-2 caspase-3 NSFC grants neural regeneration nerve regeneration fractalkine CX3 chemokine receptor 1 neuronal maturation dendrites doublecortin synaptic maturation newborn neurons neural regeneration nerve regeneration neurodegenerative diseases Alzheimer′s disease transgenic animal models mice epimedium herb milkvetch root kudzuvine root divalent metal transporter 1 ferroportin 1 neural regeneration nerve regeneration microRNA-124 neurogenesis neuronal survival Huntington′s disease SRY-related HMG box transcription factor 9 brain-derived neurotrophic factor peroxisome proliferator-activated receptor gamma coactivator 1-alpha mutant huntingtin nerve regeneration Ras/Raf/Erk1/2 signaling pathway spinal cord injury apoptosis repair regulation inhibition neural regeneration nerve regeneration neurogenic bladder bibliometric analysis Web of Science database visualization analysis CiteSpace III citation analysis neural regeneration nerve regeneration sciatic nerve injury autologous nerve grafting epineurial suturing three-dimensional finite element models load stress displacement neural regeneration nerve regeneration brain injury facial palsy Bell′s palsy comparison methodological quality therapy fixed effect model acupuncture incomplete recovery randomized controlled trials electroacupuncture NSFC grants neural regeneration nerve regeneration peripheral nerve injury thalidomide ankylosing spondylitis adverse reactions peripheral neuropathy treatment dose treatment time age sex neural regeneration Neurology. Diseases of the nervous system RC346-429 prospective study |
| Indexed By | CSCD |
| Language | 英语 |
| Funding Project | [Natural Science Foundation of Liaoning Province of China] |
| CSCD ID | CSCD:5427560 |
| Citation statistics |
Cited Times:1[CSCD]
[CSCD Record]
|
| Document Type | 期刊论文 |
| Identifier | http://ir.imr.ac.cn/handle/321006/146645 |
| Collection | 中国科学院金属研究所 |
| Affiliation | 中国科学院金属研究所 |
| Recommended Citation GB/T 7714 | Xue Hongxia,Fu Wenyi,Cui Huadong,et al. High-dose thalidomide increases the risk of peripheral neuropathy in the treatment of ankylosing spondylitis[J]. Neural Regeneration Research,2015,10(5):814-818. |
| APA | Xue Hongxia,Fu Wenyi,Cui Huadong,Yang Lili,Zhang Ning,&Zhao Lijuan.(2015).High-dose thalidomide increases the risk of peripheral neuropathy in the treatment of ankylosing spondylitis.Neural Regeneration Research,10(5),814-818. |
| MLA | Xue Hongxia,et al."High-dose thalidomide increases the risk of peripheral neuropathy in the treatment of ankylosing spondylitis".Neural Regeneration Research 10.5(2015):814-818. |
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