Dataset Information

Opioid receptor mu 1 (OPRM1) A118G polymorphism (rs1799971) and postoperative nausea and vomiting.

ABSTRACT: BACKGROUND:OPRM1-A118G polymorphism (A > G, rs1799971) is associated with interindividual variability in both response to postoperative pain and opioid treatment. The aim of this meta-analysis is to identify the predictive strength in the current literature of OPRM1-A118G polymorphism to postoperative anesthetic reactions, including nausea, vomiting, pruritus and dizziness. METHODS:PubMed, EMBASE, Cochrane Library, Web of Knowledge, Google Scholar and CNKI database were searched to find gene-association researches exploring the impacts of OPRM1-A118G polymorphism on postoperative side effects (time: up to July 2016). Odd ratios (ORs) with 95% confidence intervals (95% CIs) were estimated in allele model, homozygote model, heterozygote model, dominant model and recessive model. Sensitivity analysis and potential bias were also assessed. RESULTS:137 articles were retrieved from databases. 17 eligible studies, including 4690 patients were considered in the meta-analysis. The ORs with 95% CIs of postoperative nausea, vomiting, nausea and vomiting (PONV), pruritus and dizziness in the five genetic models mentioned above were determined. Postoperative vomiting was significantly associated with OPRM1-A118G polymorphism in homozygote (OR: 0.422; 95% CI: 0.254, 0.701; P = 0.001), dominant (OR: 0.765; 95% CI: 0.592, 0.987; P = 0.040) and recessive (OR: 0.439; 95% CI: 0.268, 0.717; P = 0.001) models. The 118G allele was associated with a reduced risk of vomiting. No other associations were detected. There was no evidence of publication bias. CONCLUSIONS:OPRM1-A118G polymorphism (A > G) is associated with a reduced risk of postoperative vomiting, but not nausea, pruritus and dizziness. The results should be interpreted with caution due to limited sample and possible heterogeneity between the included studies. Well-designed and large-scale studies are necessary to confirm our results.

SUBMITTER: Kong Y

PROVIDER: S-EPMC6176240 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Opioid receptor mu 1 (OPRM1) A118G polymorphism (rs1799971) and postoperative nausea and vomiting.

Kong Yanguo Y Yan Tao T Gong Shun S Deng Hao H Zhang Guohua G Wang Jingping J

American journal of translational research 20180915 9

<h4>Background</h4>OPRM1-A118G polymorphism (A > G, rs1799971) is associated with interindividual variability in both response to postoperative pain and opioid treatment. The aim of this meta-analysis is to identify the predictive strength in the current literature of OPRM1-A118G polymorphism to postoperative anesthetic reactions, including nausea, vomiting, pruritus and dizziness.<h4>Methods</h4>PubMed, EMBASE, Cochrane Library, Web of Knowledge, Google Scholar and CNKI database were searched t ...[more]

PMID: 30323865

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Project description:Mu-opioid receptors (MOPRs) are critically involved in the modulation of pain and analgesia, and represent a candidate mechanism for the development of biomarkers of pain conditions and their responses to treatment. To further understand the human implications of genetic variation within the opioid system in pain and opioid-mediated placebo responses, we investigated the association between the functional single-nucleotide polymorphism (SNP) in the μ-opioid receptor gene (OPRM1), A118G, and psychophysical responses, personality traits, and neurotransmitter systems (dopamine (DA), opioid) related to pain and placebo analgesia. OPRM1 G carriers, compared with AA homozygotes, showed an overall reduction of baseline μ-opioid receptor availability in regions implicated in pain and affective regulation. In response to a sustained painful stimulus, we found no effect of A118G on pain-induced endogenous opioid release. Instead, AA homozygotes showed a blunted DA response in the nucleus accumbens (NAc) in response to the pain challenge. After placebo administration, G carriers showed more pronounced mood disturbances and lower placebo-induced μ-opioid system activation in the anterior insula (aINS), the amygdala (AMY), the NAc, the thalamus (THA), and the brainstem, as well as lower levels of DA D2/3 activation in the NAc. At a trait level, G carriers reported higher NEO-Neuroticism scores; a personality trait previously associated with increased pain and lower placebo responses, which were negatively correlated with baseline μ-opioid receptor availability in the aINS and subgenual anterior cingulate cortex (sgACC). Our results demonstrate that the A118G OPRM1 polymorphism contributes to interindividual variations in the function of neurotransmitters responsive to pain (endogenous opioid and dopamine), as well as their regulation through cognitive-emotional influences in the context of therapeutic expectations, the so-called placebo effect. These effects are relevant to human vulnerability to disease processes where these neurotransmitters have a role, such as persistent pain, mood, and substance use disorders, and responses to their treatments.

Project description:Background: At ketamine and esketamine doses at which antidepressant doses are achieved, these agents are relatively selective, noncompetitive, N-methyl-D-aspartate receptor antagonists. However, at substantially higher doses, ketamine has shown mu-opioid receptor (MOR-gene symbol: OPRM1) agonist effects. Preliminary clinical studies showed conflicting results on whether naltrexone, a MOR antagonist, blocks the antidepressant action of ketamine. We examined drug-induced or endogenous MOR involvement in the antidepressant and dissociative responses to esketamine by assessing the effects of a functional single nucleotide polymorphism rs1799971 (A118G) of OPRM1, which is known to alter MOR agonist-mediated responses.Methods: Participants with treatment-resistant depression from 2 phase III, double-blind, controlled trials of esketamine (or placebo) nasal spray plus an oral antidepressant were genotyped for rs1799971. Participants received the experimental agents twice weekly for 4 weeks. Antidepressant responses were rated using the change in Montgomery-Åsberg Depression Rating Scale (MADRS) score on days 2 and 28 post-dose initiation, and dissociative side effects were assessed using the Clinician-Administered Dissociative-States Scale at 40 minutes post-dose on days 1 and 25.Results: In the esketamine + antidepressant arm, no significant genotype effect of single nucleotide polymorphism rs1799971 (A118G) on MADRS score reductions was detected on either day 2 or 28. By contrast, in the antidepressant + placebo arm, there was a significant genotype effect on MADRS score reductions on day 2 and a nonsignificant trend on day 28 towards an improvement in depression symptoms in G-allele carriers. No significant genotype effects on dissociative responses were detected.Conclusions: Variation in rs1799971 (A118G) did not affect the antidepressant response to esketamine + antidepressant. Antidepressant response to antidepressant + placebo was increased in G-allele carriers, compatible with previous reports that release of endorphins/enkephalins may play a role in mediating placebo effect.Trial registration: NCT02417064 and NCT02418585; www.clinicaltrials.gov.

Dataset Information

Opioid receptor mu 1 (OPRM1) A118G polymorphism (rs1799971) and postoperative nausea and vomiting.

Publications

Opioid receptor mu 1 (OPRM1) A118G polymorphism (rs1799971) and postoperative nausea and vomiting.

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