Thus, in order to move the issue of the genetic aspects of chronic pain and opioid sensitivity a step forward, we investigated the influence of SNPs in the μ-receptor gene OPRM1, the ABCB1 gene for the drug transporter P-glycoprotein and the calcium channel fragment gene α2δ CACNAD2, as well as the endogenous ligand for the μ-opioid receptor β-endorphin. These three candidate genes, all associated with pain processing and opioid analgesia, were analyzed in blood samples collected from 80 patients with chronic low back pain and 56 healthy controls. We also collected plasma samples for assessment of β-endorphin levels. The patients were classified as high responders (N=16), normal responders (N=44) or non-responders (N= 20) to the opioid remifentanil. All the study participants filled out an EORTC QLQ-30 Quality of Life (QoL) form for pain, function and symptom scoring.
