Different Profiles of the Triad of Lysophosphatidylcholine, Lysophosphatidic Acid, and Autotaxin in Patients with Neuropathic Pain Diseases: a Preliminary Observational Study.
Cerebrospinal fluids
Lysophosphatidylcholines
Lysophospholipids
Neuralgia
Journal
Pain and therapy
ISSN: 2193-8237
Titre abrégé: Pain Ther
Pays: New Zealand
ID NLM: 101634491
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
11
08
2022
accepted:
22
09
2022
pubmed:
8
10
2022
medline:
8
10
2022
entrez:
7
10
2022
Statut:
ppublish
Résumé
The mechanisms underlying neuropathic pain remain unclear. Lysophosphatidic acid (LPA) is a bioactive phospholipid derived mainly from lysophosphatidylcholine (LPC) by extracellular autotaxin (ATX), and has attracted attention as a candidate biomarker of neuropathic pain. We aimed to investigate the levels of LPA, LPC, and ATX in patients with lumbar spinal canal stenosis (LSCS) or other neuropathic pain diseases, and to distinguish the underlying mechanism of LSCS from other neuropathic pain conditions. Furthermore, the levels of phosphorylated neurofilament heavy chain (pNF-H), an objective surrogate marker of axonal damage, were also measured. Cerebrospinal fluid (CSF) samples were obtained from 56 patients with LSCS (n = 31) and various etiologies other than LSCS (n = 25). Patients with LSCS complained of pain intensity comparable to that of patients without LSCS. The LPA levels were significantly higher in patients with LSCS than in non-LSCS patients, while the ATX levels were significantly lower. However, the differences in LPC and pNF-H levels between the two patient groups were not significant. The LPA/LPC ratio was significantly higher in the LSCS group. Notably, the difference in LPA between the two groups diminished in the analysis of covariance (ANCOVA) with ATX as a covariate. Thus, it helped to reveal that LPA synthesis in patients with LSCS depends more efficiently on ATX than in non-LSCS neuropathic pain patients with other etiologies. Our findings further suggest that the triad of LPA, LPC, and ATX in LSCS may contribute to the development and maintenance of neuropathic pain in a manner different from non-LSCS neuropathic conditions.
Identifiants
pubmed: 36205847
doi: 10.1007/s40122-022-00445-2
pii: 10.1007/s40122-022-00445-2
pmc: PMC9633889
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1439-1449Subventions
Organisme : Core Research for Evolutional Science and Technology
ID : 17gm0710001h0105
Organisme : Japan Agency for Medical Research and Development
ID : 17gm0710001h0105
Organisme : Japan Agency for Medical Research and Development
ID : 17gm0010004s0101
Organisme : Japan Agency for Medical Research and Development
ID : 22ek0610028h0001
Organisme : Japan Society for the Promotion of Science
ID : 15H05906
Informations de copyright
© 2022. The Author(s).
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