Responders and nonresponders to topical capsaicin display distinct temporal summation of pain profiles

Wong, Felyx; Reddy, Aditi; Rho, Yeanuk; Vollert, Jan; Strutton, Paul H.; Hughes, Sam

doi:10.1097/pr9.0000000000001071

Cited by 2 publications

(2 citation statements)

References 31 publications

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“…One third of healthy individuals reports no pain response to topical capsaicin (1%) challenge [ 166 ]. There is increasing evidence that a TRPV1 gene polymorphism is responsible for individual differences in human sensitivity to capsaicin [ 167 , 168 ].…”

Section: Conclusion and Future Research Directionsmentioning

confidence: 99%

“…There is increasing evidence that a TRPV1 gene polymorphism is responsible for individual differences in human sensitivity to capsaicin [ 167 , 168 ]. Therefore, the one-size-fits all approach may not be applicable to capsaicin desensitization: depending on their genotype, some patients may show excellent therapeutic response to capsaicin, whereas others (the “non-responders” [ 166 ]) may not. Furthermore, animal experiments suggest that TRPV1 expression may be decreased in some patients, for example those with diabetic polyneuropathy [ 169 ].…”

Section: Conclusion and Future Research Directionsmentioning

confidence: 99%

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Targeting TRPV1 for Cancer Pain Relief: Can It Work?

Szallasi

2024

Cancers

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Chronic intractable pain affects a large proportion of cancer patients, especially those with metastatic bone disease. Blocking sensory afferents for cancer pain relief represents an attractive alternative to opioids and other drugs acting in the CNS in that sensory nerve blockers are not addictive and do not affect the mental state of the patient. A distinct subpopulation of sensory afferents expresses the capsaicin receptor TRPV1. Intrathecal resiniferatoxin, an ultrapotent capsaicin analog, ablates TRPV1-expressing nerve endings exposed to the cerebrospinal fluid, resulting in permanent analgesia in women with cervical cancer metastasis to the pelvic bone. High-dose capsaicin patches are effective pain killers in patients with chemotherapy-induced peripheral neuropathic pain. However, large gaps remain in our knowledge since the mechanisms by which cancer activates TRPV1 are essentially unknown. Most important, it is not clear whether or not sensory denervation mediated by TRPV1 agonists affects cancer progression. In a murine model of breast cancer, capsaicin desensitization was reported to accelerate progression. By contrast, desensitization mediated by resiniferatoxin was found to block melanoma growth. These observations imply that TRPV1 blockade for pain relief may be indicated for some cancers and contraindicated for others. In this review, we explore the current state of this field and compare the analgesic potential of TRPV1 antagonism and sensory afferent desensitization in cancer patients.

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Section: Conclusion and Future Research Directionsmentioning

confidence: 99%