The impact of genetic polymorphism in pain mechanisms

Abstract

Background:Variations in genes codifying target structures in the nociceptive pathway can result in pain attenuation or increase.Objective:Investigate the genetic polymorphism influence in the individual pain threshold. Methods: Search on PubMed with the terms “genetic”, “pain” and its synonyms published in the last 10 years. Results:The subjective and individual mechanisms of pain aren’t completely understood, but genetic susceptibility is one of the hypothesis to explain these differences.The KCNK18 gene influences the synaptic transmission by producing potassium channel protein that equalizes resting membrane potential, calcineurin activated and inhibited by arachidonic acid. This gene was found more frequently in migraine individuals. The COMT gene increase the sensibility to pain by met-enkephalins reduction and/or catecholamine elevation. Its activity’s reduced in fibromyalgia patients. However, the OPRM1 gene, an opioid receptor, was found in individuals with a higher pain threshold.Furthermore, studies with human cell culture shows the analgesic role of the gene A118G, by its greater binding affinity for β-endorphin.It is associated with more effective endorphinergic endogenous pain inhibition. Conclusion:Researches indicates a striking participation of genetic polymorphism in pain mechanisms. The knowledge about genetic variables on pain perception can contribute to the development of individualized analgesic protocols and therapeutic strategies, accordantly to the patient genetic profile. This evolution becomes fundamental in a population that tend to the indiscriminate use of analgesics.