Genetic discovery: the prescription for chronic pain.
Ontology highlight
ABSTRACT:
SUBMITTER: Zheng M
PROVIDER: S-EPMC3016624 | biostudies-literature | 2010
REPOSITORIES: biostudies-literature
Publications
Genetic discovery: the prescription for chronic pain.
Genome medicine 20101115 11
A recent publication that combined rat gene expression data and a human genetic association study has identified the first genetic risk factor for chronic pain in humans. In four of the five cohorts studied, there was a significant association of an allele within a gene (KCNS1) encoding a potassium channel (Kv9.1) with an increased risk for chronic pain. Identification of genetic risk factors for chronic pain could catalyze new advances in this difficult clinical area that has become a major pub ...[more]
Similar Datasets
Project description:BACKGROUND:Patients with prescription opioid use disorder commonly report relief of chronic pain as the chief reason for first opioid use; indeed, the prevalence of chronic pain is high in this population. Understanding the association between pain severity and subsequent opioid use is crucial for understanding how to manage these conditions simultaneously and has not been examined in this population. The aim of this analysis was to examine the proximal effect of pain severity on opioid use during 12 weeks of buprenorphine-naloxone therapy for patients with chronic pain and prescription opioid use disorder. METHODS:This study is a secondary analysis of a national, randomized, controlled trial of buprenorphine-naloxone plus counseling for prescription opioid dependent patients. The association between past-week pain severity and opioid use in the subsequent week was examined in 148 patients presenting with chronic pain at baseline. RESULTS:Results from a multivariable logistic regression model showed that greater pain severity in a given week was significantly associated with increased odds of opioid use in the following week over the 12-week treatment, even after adjusting for covariates associated with opioid use (aOR=1.15, p<0.001). CONCLUSIONS:Despite previous reports of no association between baseline pain and subsequent opioid use, our findings suggest that patients who experience flare-ups of pain during treatment are prone to relapse to opioid use. Future studies may identify those who are at risk to use opioids by carefully monitoring patterns of their pain intensity over time.
| S-EPMC4880512 | biostudies-literature
Project description:BackgroundChronic opiate use leads to a sensitized behavioral response to acute pain, which in turn, leads to escalating doses of opiates. This study was designed to test the hypothesis that chronic opiate usage is also associated with a sensitized neurobiological response to acute pain in individuals that have used prescription opiates for 6 or more months.MethodsFourteen patients with non-alcoholic chronic pancreatitis that have been taking prescription opiates for 6 or more months and 14 gender matched, non-opiate using controls were enrolled. Functional neuroimaging data was acquired while participants received blocks of thermal stimulation to their wrist (individually-tailored to their pain threshold).ResultsSelf-reported pain was significantly greater in opiate using patients (3.4 ± 3.4) than controls (0.2 ± 0.8: Brief Pain Inventory p < 0.005), however no significant difference between groups was observed in the individually-tailored pain thresholds. Opiate using patients evidenced a significantly greater response to pain than controls in two established nodes of the "Pain Matrix": somatosensory cortex (pFWE≤0.001) and anterior cingulate cortex (p ≤ 0.01). This response was positively correlated with prescribed morphine equivalent dosages (average: 133.5 ± 94.8 mg/day).ConclusionThe findings suggest that in chronic pancreatitis patients, a dose of opiates that normalizes their behavioral response to acute pain is associated with an amplified neural response to acute pain. Further longitudinal studies are needed to determine if this neural sensitization hastens a behavioral tolerance to opiates or the development of an opioid use disorder.
| S-EPMC6914256 | biostudies-literature
Project description:Patients receiving long-term opioid therapy for chronic pain and interested in tapering their opioid dose were randomly assigned to a 22-week taper support intervention (psychiatric consultation, opioid dose tapering, and 18 weekly meetings with a physician assistant to explore motivation for tapering and learn pain self-management skills) or usual care (N = 35). Assessments were conducted at baseline and 22 and 34 weeks after randomization. Using an intention to treat approach, we constructed linear regression models to compare groups at each follow-up. At 22 weeks, adjusted mean daily morphine-equivalent opioid dose in the past week (primary outcome) was lower in the taper support group, but this difference was not statistically significant (adjusted mean difference = -42.9 mg; 95% confidence interval, -92.42 to 6.62; P = .09). Pain severity ratings (0-10 numeric rating scale) decreased in both groups at 22 weeks, with no significant difference between groups (adjusted mean difference = -.68; 95% confidence interval, -2.01 to .64; P = .30). The taper support group improved significantly more than the usual care group in self-reported pain interference, pain self-efficacy, and prescription opioid problems at 22 weeks (all P-values < .05). This taper support intervention is feasible and shows promise in reducing opioid dose while not increasing pain severity or interference.PerspectiveIn a pilot randomized trial comparing a prescription opioid taper support intervention to usual care, lower opioid doses and pain severity ratings were observed at 22 weeks in both groups. The groups did not differ significantly at 22 weeks in opioid dose or pain severity, but the taper support group improved significantly more in pain interference, pain self-efficacy, and perceived opioid problems. These results support the feasibility and promise of this opioid taper support intervention.
| S-EPMC5337146 | biostudies-literature
Project description:ImportanceLong-acting opioids increase the risk of unintentional overdose deaths but also may increase mortality from cardiorespiratory and other causes.ObjectiveTo compare all-cause mortality for patients with chronic noncancer pain who were prescribed either long-acting opioids or alternative medications for moderate to severe chronic pain.Design, setting, and participantsRetrospective cohort study between 1999 and 2012 of Tennessee Medicaid patients with chronic noncancer pain and no evidence of palliative or end-of-life care.ExposuresPropensity score-matched new episodes of prescribed therapy for long-acting opioids or either analgesic anticonvulsants or low-dose cyclic antidepressants (control medications).Main outcomes and measuresTotal and cause-specific mortality as determined from death certificates. Adjusted hazard ratios (HRs) and risk differences (difference in incidence of death) were calculated for long-acting opioid therapy vs control medication.ResultsThere were 22,912 new episodes of prescribed therapy for both long-acting opioids and control medications (mean [SD] age, 48 [11] years; 60% women). The long-acting opioid group was followed up for a mean 176 days and had 185 deaths and the control treatment group was followed up for a mean 128 days and had 87 deaths. The HR for total mortality was 1.64 (95% CI, 1.26-2.12) with a risk difference of 68.5 excess deaths (95% CI, 28.2-120.7) per 10,000 person-years. Increased risk was due to out-of-hospital deaths (154 long-acting opioid, 60 control deaths; HR, 1.90; 95% CI, 1.40-2.58; risk difference, 67.1; 95% CI, 30.1-117.3) excess deaths per 10,000 person-years. For out-of-hospital deaths other than unintentional overdose (120 long-acting opioid, 53 control deaths), the HR was 1.72 (95% CI, 1.24-2.39) with a risk difference of 47.4 excess deaths (95% CI, 15.7-91.4) per 10,000 person-years. The HR for cardiovascular deaths (79 long-acting opioid, 36 control deaths) was 1.65 (95% CI, 1.10-2.46) with a risk difference of 28.9 excess deaths (95% CI, 4.6-65.3) per 10,000 person-years. The HR during the first 30 days of therapy (53 long-acting opioid, 13 control deaths) was 4.16 (95% CI, 2.27-7.63) with a risk difference of 200 excess deaths (95% CI, 80-420) per 10,000 person-years.Conclusions and relevancePrescription of long-acting opioids for chronic noncancer pain, compared with anticonvulsants or cyclic antidepressants, was associated with a significantly increased risk of all-cause mortality, including deaths from causes other than overdose, with a modest absolute risk difference. These findings should be considered when evaluating harms and benefits of treatment.
| S-EPMC5030814 | biostudies-literature
Project description:ObjectiveThis study assessed associations between severity of, and prescription medication use for, chronic low back pain (CLBP) and health-related quality of life, health status, work productivity, and healthcare resource utilization.MethodsThis cross-sectional study utilized SF-12, EQ-5D-5L, and work productivity and activity impairment (WPAI) questionnaires, and visits to healthcare providers among adults with self-reported CLBP participating in the National Health and Wellness Survey in Germany, France, UK, Italy, and Spain. Respondents were stratified into four groups according to pain severity (mild or moderate/severe) and prescription medication use (Rx-treated or Rx-untreated). Differences between groups were estimated using generalized linear models controlling for sociodemographics and health characteristics.ResultsOf 2086 respondents with CLBP, 683 had mild pain (276 Rx-untreated, 407 Rx-treated) and 1403 had moderate/severe pain (781 Rx-untreated, 622 Rx-treated). Respondents with moderate/severe pain had significantly worse health-related quality of life (SF-12v2 physical component summary), health status (EQ-5D-5L), and both absenteeism and presenteeism compared with those with mild pain, including Rx-untreated (moderate/severe pain Rx-untreated vs. mild pain Rx-untreated, p ≤ 0.05) and Rx-treated (moderate/severe pain Rx-treated vs. mild pain Rx-treated, p ≤ 0.05) groups. Significantly more visits to healthcare providers in the last 6 months were reported for moderate/severe pain compared with mild pain for Rx-treated (least squares mean 13.01 vs. 10.93, p = 0.012) but not Rx-untreated (8.72 vs. 7.61, p = 0.072) groups. Health-related quality of life (SF-12v2 physical component summary) and health status (EQ-5D-5L), as well as absenteeism and presenteeism, were significantly worse, and healthcare utilization was significantly higher, in the moderate/severe pain Rx-treated group compared with all other groups (all p ≤ 0.05).ConclusionGreater severity of CLBP was associated with worse health-related quality of life, health status, and absenteeism and presenteeism, irrespective of prescription medication use. Greater severity of CLBP was associated with increased healthcare utilization in prescription medication users.
| S-EPMC9298715 | biostudies-literature
Project description:The study pursued dual goals: To advance mRNA-seq bioinformatics towards unbiased transcriptome capture and to demonstrate its potential for discovery in neuroscience by applying the approach to an in vivo model of neurological disease. We found that 12.4% of known genes were induced and 7% were suppressed in the dysfunctional (but anatomically intact) L4 dorsal root ganglion (DRG) 2 weeks after L5 spinal Nerve Ligation (SNL). A new algorithm for agnostic mapping of pre-mRNA splice junctions (SJ) achieved a precision of 97%.
2010-05-02 | GSE20895 | GEO
Project description:BACKGROUND AND AIMS:Buprenorphine-naloxone (BUP-NLX) can be used to manage prescription opioid addiction among persons with chronic pain, but post-treatment relapse is common and difficult to predict. This study estimated whether changes in pain over time and pain volatility during BUP-NLX maintenance would predict opioid use during the taper BUP-NLX taper. DESIGN:Secondary analysis of a multi-site clinical trial for prescription opioid addiction, using data obtained during a 12-week BUP-NLX stabilization and 4-week BUP-NLX taper. SETTING:Community clinics affiliated with a national clinical trials network in 10 US cities. PARTICIPANTS:Subjects with chronic pain who entered the BUP-NLX taper phase (n = 125) with enrollment occurring from June 2006 to July 2009 (52% male, 88% Caucasian, 31% married). MEASUREMENTS:Outcomes were weekly biologically verified and self-reported opioid use from the 4-week taper phase. Predictors were estimates of baseline severity, rate of change and volatility in pain from weekly self-reports during the 12-week maintenance phase. FINDINGS:Controlling for baseline pain and treatment condition, increased pain [odds ratio (OR) = 2.38, P = 0.02] and greater pain volatility (OR = 2.43, P = 0.04) predicted greater odds of positive opioid urine screen during BUP-NLX taper. Increased pain (IRR = 1.40, P = 0.04) and greater pain volatility [incidence-rate ratio (IRR) = 1.66, P = 0.009] also predicted greater frequency of self-reported opioid use. CONCLUSIONS:Adults with chronic pain receiving out-patient treatment with buprenorphine-naloxone (BUP-NLX) for prescription opioid addiction have an elevated risk for opioid use when tapering off maintenance treatment. Those with relative persistence in pain over time and greater volatility in pain during treatment are less likely to sustain abstinence during BUP-NLX taper.
| S-EPMC5461207 | biostudies-literature
Project description: Not available
| S-EPMC11210295 | biostudies-literature
Project description:Chronic widespread pain (CWP) has complex aetiology and forms part of the fibromyalgia syndrome. Recent evidence suggests a higher frequency of neuropathic pain features in those with CWP than previously thought. The aim of this study was to determine the prevalence of neuropathic pain features in individuals with CWP and to estimate the influence of genetic and environmental factors on neuropathic pain in CWP. Validated questionnaires (the London Fibromyalgia Screening Study questionnaire and PainDETECT questionnaire) were used to classify twins as having CWP and neuropathic pain, respectively. The prevalence of CWP was 14.7% (n = 4324), and of the 1357 twins invited to complete neuropathic pain screening, 15.9% of those having CWP demonstrated features of neuropathic pain. Neuropathic pain was found to be heritable (A = 37%; 95% confidence interval [CI]: 23%-50%) with unique environmental factors accounting for 63% (95% CI: 49%-79%) of the variance. Heritability of neuropathic pain and CWP were found to be correlated, 0.54 (95% CI: 0.42-0.65). Increasing age, raised body mass index, female gender, and smoking were all risk factors for neuropathic pain (P < 0.05), and CWP (P < 0.05). High socioeconomic status showed negative correlation with neuropathic pain (P = 0.003) and CWP (P = 0.001). Bivariate analysis of the 2 pain traits revealed that genetic predisposition to neuropathic pain is shared with that for CWP. This is the first study to provide formal heritability estimates for neuropathic pain in CWP. The findings suggest that at least some of the genetic factors underlying the development of neuropathic pain and CWP are the same.
| S-EPMC4770357 | biostudies-literature
Project description:OBJECTIVE:Prescribed opioids for chronic pain management contribute significantly to the opioid crisis. There is a need to understand the real-world benefits that, despite risks, lead chronic pain patients to persist in opioid use. Negative reinforcement models of addiction posit that individuals use substances to reduce aversive states but have seldom been applied to prescribed opioids. Using ecological momentary assessment, we examined reciprocal associations between opioid use and physical pain, for which opioids are prescribed, and negative affect (NA), for which they are not. METHOD:Chronic low back pain patients on long-term opioid therapy (n = 34) without significant past-year opioid misuse reported multiple times daily via smartphone over 2 weeks (nobservations = 2,285). We hypothesized that pain and NA would be positively associated with subsequent opioid use, and that use would be negatively associated with subsequent pain and NA. RESULTS:Time-lagged multilevel models indicated that participants were more likely to use opioids and in larger doses following elevated pain and NA. There was also an interaction of concurrent pain and NA on opioid dose. In turn, participants reported reduced pain and NA following larger doses. Additionally, individuals at high risk for opioid misuse, compared with low risk, took larger doses following pain, but also experienced smaller subsequent pain and NA reductions. CONCLUSIONS:Opioid use was bidirectionally associated with pain and NA. Findings fit negative reinforcement models associated with risk of developing opioid use disorder. Educating patients and providers about negative reinforcement may help reduce opioid use and opioid-associated risks. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
| S-EPMC6764518 | biostudies-literature