Dataset Information

Independent association of tobacco use with opioid use disorder in patients of European ancestry with chronic non-cancer pain.

ABSTRACT:

Background

The harms associated with prescription opioid abuse have become a public health crisis. There is a need for evidence-based objective markers of the risk of opioid use disorder (OUD) in patients with pain receiving opioid treatment. The objective of this study was to evaluate the independent association of tobacco use and OUD in patients with chronic non-cancer pain.

Methods

This cross-sectional naturalistic study evaluated 798 adults ≥ 18 years with chronic non-cancer pain treated with long-term opioid therapy (≥ 6 months) who either developed an OUD (cases, n = 216) or displayed no evidence of an OUD (controls, n = 582). The primary outcome was presence of OUD. In addition to current self-reported tobacco use (primary predictor), covariates included demographics, pain severity, and psychiatric history. Data were collected between November 2012 and September 2018.

Results

Current tobacco use independently was strongly associated with OUD [odds ratio (OR) 14.0, 95 % confidence interval (CI) 9.5-20.6, p < 0.001], and this association remained significant after adjusting for other risk factors [adjusted odds ratio (aOR) 7.6, 95 % CI 4.8-12.2, p < 0.001]. Other factors associated independently with development of OUD included age, marital status, financial status, education and pain severity.

Conclusions and relevance

Current tobacco use is significantly associated with OUD in patients with chronic pain receiving long-term opioid therapy.

SUBMITTER: Cheatle MD

PROVIDER: S-EPMC7219106 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Despite the large toll of opioid use disorder (OUD), genome-wide association studies (GWAS) of OUD to date have yielded few susceptibility loci. We performed a large-scale GWAS of OUD in individuals of European (EUR) and African (AFR) ancestry, optimizing genetic informativeness by performing MTAG (Multi-trait analysis of GWAS) with genetically correlated substance use disorders (SUDs). Meta-analysis included seven cohorts: the Million Veteran Program, Psychiatric Genomics Consortium, iPSYCH, FinnGen, Partners Biobank, BioVU, and Yale-Penn 3, resulting in a total N = 639,063 (Ncases = 20,686;Neffective = 77,026) across ancestries. OUD cases were defined as having a lifetime OUD diagnosis, and controls as anyone not known to meet OUD criteria. We estimated SNP-heritability (h2SNP) and genetic correlations (rg). Based on genetic correlation, we performed MTAG on OUD, alcohol use disorder (AUD), and cannabis use disorder (CanUD). A leave-one-out polygenic risk score (PRS) analysis was performed to compare OUD and OUD-MTAG PRS as predictors of OUD case status in Yale-Penn 3. The EUR meta-analysis identified three genome-wide significant (GWS; p ≤ 5 × 10-8) lead SNPs-one at FURIN (rs11372849; p = 9.54 × 10-10) and two OPRM1 variants (rs1799971, p = 4.92 × 10-09; rs79704991, p = 1.11 × 10-08; r2 = 0.02). Rs1799971 (p = 4.91 × 10-08) and another OPRM1 variant (rs9478500; p = 1.95 × 10-08; r2 = 0.03) were identified in the cross-ancestry meta-analysis. Estimated h2SNP was 12.75%, with strong rg with CanUD (rg = 0.82; p = 1.14 × 10-47) and AUD (rg = 0.77; p = 6.36 × 10-78). The OUD-MTAG resulted in a GWAS Nequivalent = 128,748 and 18 independent GWS loci, some mapping to genes or gene regions that have previously been associated with psychiatric or addiction phenotypes. The OUD-MTAG PRS accounted for 3.81% of OUD variance (beta = 0.61;s.e. = 0.066; p = 2.00 × 10-16) compared to 2.41% (beta = 0.45; s.e. = 0.058; p = 2.90 × 10-13) explained by the OUD PRS. The current study identified OUD variant associations at OPRM1, single variant associations with FURIN, and 18 GWS associations in the OUD-MTAG. The genetic architecture of OUD is likely influenced by both OUD-specific loci and loci shared across SUDs.