Genetic susceptibility to postherniotomy pain. The influence of polymorphisms in the Mu opioid receptor, TNF-α, GRIK3, GCH1, BDNF and CACNA2D2 genes

Johannes Gjerstad

doi:10.1016/j.sjpain.2016.02.007

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Genetic susceptibility to postherniotomy pain. The influence of polymorphisms in the Mu opioid receptor, TNF-α, GRIK3, GCH1, BDNF and CACNA2D2 genes

Johannes Gjerstad

Published/Copyright: July 1, 2016

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From the journal Scandinavian Journal of Pain Volume 12 Issue 1

Persistent postoperative pain is a problem affecting almost a third of all patients undergoing surgery. The underlying pathophysiology of postoperative pain comprises prolonged inflammation and nerve damage. In this issue of the Scandinavian Journal of Pain, Kalliomaki and coworkers [1] examine the association between six single nucleotide polymorphisms (SNPs) and development of persistent postherniotomy pain. All the SNPs examined in the study have earlier been suggested to be associated with persistent pain. Patients with persistent postherniotomy pain were found to have a higher frequency of the TNF-α rs1800629 A allele than pain-free patients. Hence, the study shows a significant association between a specific SNP in the promoter of the TNF gene and risk for persistent pain following inguinal hernia surgery.

Earlier studies suggest that the rs1800629 A allele affects the binding of several transcription factors and therefore may be associated with increased expression of TNF-α [2, 3]. Interestingly, the rs1800629 SNP, i.e. the G>A base substitution in position -308, has previously been reported to induce a two-fold greater promoter activity [2]. The increased frequency of this “gain of function” TNF-α SNP [2] supports the hypothesis that the TNF-α A allele promotes inflammation [4] and contributes to development of persistent neuropathic pain following surgical procedures.

The study of Kalliomaki and coworkers may be interesting for clinicians interested in neuropathic pain. The study supports previous data, according to which release of TNF following nerve injury may promote nerve growth and persistent pain [5]. However, whether or not the TNF-α SNP in patients really affects the inflammatory process, and how this relates to the neuropathic mechanisms, remains to be investigated. Moreover, the study was based on a priori hypotheses and one-tailed tests, without correction for multiple testing. Therefore, the findings need to be corroborated by further studies including other groups of patients with neuropathic pain.

DOI of refers to article: http://dx.doi.org/10.1016/j.sjpain.2015.12.006.

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Conflict of interest: None declared.

References

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Published Online: 2016-07-01

Published in Print: 2016-07-01

Articles in the same Issue

https://doi.org/10.1016/j.sjpain.2016.02.007