Transient receptor potential channel polymorphisms are associated with the somatosensory function in neuropathic pain patients.

Transient receptor potential channels are important mediators of
thermal and mechanical stimuli and play an important role in
neuropathic pain. The contribution of hereditary variants in the
genes of transient receptor potential channels to neuropathic pain
is unknown. We investigated the frequency of transient receptor
potential ankyrin 1, transient receptor potential melastin 8 and
transient receptor potential vanilloid 1 single nucleotide
polymorphisms and their impact on somatosensory abnormalities in
neuropathic pain patients. Within the German Research Network on
Neuropathic Pain (Deutscher Forscbungsverbund Neuropathischer
Schmerz) 371 neuropathic pain patients were phenotypically
characterized using standardized quantitative sensory testing.
Pyrosequencing was employed to determine a total of eleven single
nucleotide polymorphisms in transient receptor potential channel
genes of the neuropathic pain patients and a cohort of 253 German
healthy volunteers. Associations of quantitative sensory testing
parameters and single nucleotide polymorphisms between and within
groups and subgroups, based on sensory phenotypes, were analyzed.
Single nucleotide polymorphisms frequencies did not differ between
both the cohorts. However, in neuropathic pain patients transient
receptor potential ankyrin 1 710G>A (rs920829, E179K) was
associated with the presence of paradoxical heat sensation
(p = 0.03), and transient receptor potential vanilloid 1 1911A>G
(rs8065080, I585V) with cold hypoalgesia (p = 0.0035). Two main
subgroups characterized by preserved (1) and impaired (2) sensory
function were identified. In subgroup 1 transient receptor
potential vanilloid 1 1911A>G led to significantly less heat
hyperalgesia, pinprick hyperalgesia and mechanical hypaesthesia
(p = 0.006, p = 0.005 and pG (rs222747, M315I) to cold
hypaesthesia (p = 0.002), but there was absence of associations in
subgroup 2. In this study we found no evidence that genetic
variants of transient receptor potential channels are involved in
the expression of neuropathic pain, but transient receptor
potential channel polymorphisms contributed significantly to the
somatosensory abnormalities of neuropathic pain patients.