The journal of pain : official journal of the American Pain Society
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The Opioid Risk Tool (ORT) is a commonly used measure of risk of aberrant drug-related behaviors in patients with chronic pain prescribed opioid therapy. In this study, the discriminant predictive validity of the ORT was evaluated in a unique cohort of patients with chronic nonmalignant pain (CNMP) on long-term opioid therapy who displayed no evidence of developing an opioid use disorder (OUD) and a sample of patients with CNMP who developed an OUD after commencing opioid therapy. Results revealed that the original ORT was able to discriminate between patients with and without OUDs (odds ratio = 1.624; 95% confidence interval [CI] = 1.539-1.715, P < .001). ⋯ A revised unweighted ORT removing the history of preadolescent sexual abuse item was notably superior in predicting the development of OUD in patients with CNMP on long-term opioid therapy (odds ratio = 3.085; 95% CI = 2.725-3.493; P < .001) with high specificity (.851; 95% CI = .811-.885), sensitivity (.854; 95% CI = .799-.898), positive predictive value (.757; 95% CI = .709-.799), and negative predictive value (.914; 95% CI = .885-.937). Perspective: The revised ORT is the first tool developed on a unique cohort to predict the risk of developing an OUD in patients with CNMP receiving opioid therapy, as opposed to aberrant drug-related behaviors that can reflect a number of other issues. The revised ORT has clinical usefulness in providing clinicians a simple, validated method to rapidly screen for the risk of developing OUD in patients on or being considered for opioid therapy.
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Observational Study
Enrichment of genomic pathways based on differential DNA methylation associated with chronic postsurgical pain and anxiety in children - a prospective, pilot study.
We have reported child anxiety sensitivity (Child Anxiety Sensitivity Index [CASI]) predicts chronic postsurgical pain (CPSP). Herein, we evaluated DNA methylation profiles to understand the gene-environment interactions underlying CPSP and CASI, to identify shared, enriched, genomic pathways. In 73 prospectively recruited adolescents undergoing spine fusion, preoperative CASI and pain data over 12 months after surgery were collected. ⋯ This pilot study provides new epigenetic insights into the pathophysiology of CPSP and a basis for future studies in biomarker development and targetable interventions. PERSPECTIVE: Differential DNA methylation in regulatory genomic regions enriching shared neural pathways were associated with CPSP and CASI in adolescents undergoing spine surgery. Our findings support GABA hypofunction and the roles of the dopamine-DARPP32 pathway in emotion/reward contributing to behavioral maintenance of pain 10 to 12 months after surgery.
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Acute pain episodes are the most common complication in patients with sickle cell disease (SCD). Classically attributed to vaso-occlusion, recent insights suggest that chronic pain may also contribute to the pathogenesis of acute pain episodes, which adds complexity to their diagnosis and management. A taxonomy, or classification system, for acute pain in patients with SCD would aid research efforts and enhance clinical care. ⋯ As part of this, a set of 4 diagnostic criteria, with 2 modifiers to account for the influence of chronic pain, are proposed to define the types of acute pain observed in patients with SCD. PERSPECTIVE: This article presents a taxonomy for acute pain in patients with SCD. This taxonomy could help to standardize definitions of acute pain in clinical studies of patients with SCD.
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Sensory neuron nicotinic acetylcholine receptors (nAChRs) contribute to pain associated with tissue injury. However, there are marked differences between rats and mice with respect to both the properties and distribution of nAChR currents in sensory neurons. Because both species are used to understand pain signaling in humans, we sought to determine whether the currents present in either species was reflective of those present in human sensory neurons. ⋯ These results suggest that there are not only species differences in the sensory neuron distribution of nAChR currents between rodent and human, but that the subunit composition of the channel underlying human nAChR currents may be different from those in the mouse or rat. PERSPECTIVE: The properties and distribution of nicotine evoked currents in human sensory neurons were markedly different from those previously observed in mice and rats. These observations add additional support to the suggestion that human sensory neurons may be an essential screening tool for those considering moving novel therapeutics targeting primary afferents into clinical trials.