NEW YORK (Reuters Health) - Researchers have identified three variants of the catecholamine-O-methyltransferase (COMT) gene that influence pain sensitivity and the risk of developing a chronic pain condition. These findings could ultimately lead to tailored pain control strategies and to new therapeutic targets.
In the study, the presence of a low pain sensitivity COMT variant greatly reduced the risk of developing myogenous temporomandibular joint disorder (TMD), but the authors believe that this finding will apply to other chronic pain conditions as well.
“This is the first demonstration that a genetic variation influences both human pain perception and the risk for developing a chronic pain condition,” lead author Dr. Luda Diatchenko, from the University of North Carolina at Chapel Hill, said in a statement.
The study, which is reported in the January issue of Human Molecular Genetics, involved an analysis of COMT variants and pain sensitivity in 202 healthy female volunteers. The subjects were followed for 3 years to assess the development of TMD.
The researchers identified low, average, and high pain sensitivity haplotypes of the COMT gene. These three haplotypes accounted for nearly 96% of all COMT haplotypes observed in the study. Moreover, five combinations of these haplotypes were strongly predictive of sensitivity to experimental pain (p = 0.0004).
The COMT variant influenced the risk of TMD. The presence of just one low pain sensitivity haplotype reduced this risk by as much as 2.3-fold, the investigators report.
“The findings suggest that pain sensitivity is more trait-like -- it is not as subjective as we once thought,” senior author Dr. William Maixner told Reuters Health. Moreover, “there is a genetic basis for that trait and one of the key components relates to genetic variations in COMT.”
“By determining the genetic variants present in an individual with a chronic pain condition, it is going to help us tailor the drug treatments,” Dr. Maixner noted. “Such testing may even help us tailor behavioral therapy.”
Source: Hum Mol Genet 2005;14:1-9. [ Google search on this article ]
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