The journal of pain : official journal of the American Pain Society
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The Weill Cornell Medical College Pain Registry database contains patient characteristics, treatments, and outcomes for a prospective cohort of 1,159 chronic pain patients who were seen at the Weill Cornell Medical College Pain Medicine outpatient clinic from July 8, 2011 to December 10, 2014. Patients aged 45 to 64 years comprised 43% followed by age ≥ 65 years at 37%. Fifty-eight percent were female. ⋯ Median daily opioid dose in morphine equivalents was 55 with a range from 2 to 1,145 morphine equivalents. Regression analysis revealed that being male was associated with greater likelihood of an opioid ordered and higher average dosage than being female. The registry can identify patient characteristics and treatments that provide new insights into chronic pain management.
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Hyperalgesic priming, a sexually dimorphic model of transition to chronic pain, is expressed as prolongation of prostaglandin E2-induced hyperalgesia by the activation of an additional pathway including an autocrine mechanism at the plasma membrane. The autocrine mechanism involves the transport of cyclic adenosine monophosphate (AMP) to the extracellular space, and its conversion to AMP and adenosine, by ecto-5'phosphodiesterase and ecto-5'nucleotidase, respectively. The end product, adenosine, activates A1 receptors, producing delayed onset prolongation of prostaglandin E2 hyperalgesia. ⋯ Whereas in rats treated with antisense AMP-induced hyperalgesia was abolished, the A1 receptor agonist N6-cyclopentiladenosine still produced hyperalgesia. Thus, EsRα interacts with this autocrine pathway at the level of ecto-5'nucleotidase. These results demonstrate a sexually dimorphic mechanism for the expression of priming.
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Review Meta Analysis
Analgesic effects of alcohol: A systematic review and meta-analysis of controlled experimental studies in healthy participants.
Despite the long-standing belief in the analgesic properties of alcohol, experimental studies have produced mixed results. This meta-analysis aimed to clarify whether alcohol produces a decrease in experimentally-induced pain and to determine the magnitude of any such effect. PubMed, PsycINFO, and Embase databases were searched from inception until April 21, 2016 for controlled studies examining the effect of quantified dosages of alcohol on pain response to noxious stimulation. Eighteen studies involving 404 participants were identified providing alcohol versus no-alcohol comparisons for 13 tests of pain threshold (n = 212) and 9 tests of pain intensity ratings (n = 192). Random effects meta-analysis of standardized mean difference (SMD) provided robust support for analgesic effects of alcohol. A mean blood alcohol content (BAC) of approximately .08% (3-4 standard drinks) produced a small elevation of pain threshold (SMD [95% CI] = .35 [.17-.54], P = .002), and a moderate to large reduction in pain intensity ratings (SMD [95% CI] = .64 [.37-.91], P < .0001), or equivalently, a mean reduction of 1.25 points on a 0- to 10-point pain rating scale. Furthermore, increasing BAC resulted in increasing analgesia, with each .02% BAC increment producing an increase of SMD = .11 for pain threshold and SMD = .20 for reduced pain intensity. Some evidence of publication bias emerged, but statistical correction methods suggested minimal impact on effect size. Taken together, findings suggest that alcohol is an effective analgesic that delivers clinically-relevant reductions in ratings of pain intensity, which could explain alcohol misuse in those with persistent pain despite its potential consequences for long-term health. Further research is needed to corroborate these findings for clinical pain states. ⋯ This meta-analysis provides robust evidence for the analgesic properties of alcohol, which could potentially contribute to alcohol misuse in pain patients. Strongest analgesia occurs for alcohol levels exceeding World Health Organization guidelines for low-risk drinking and suggests raising awareness of alternative, less harmful pain interventions to vulnerable patients may be beneficial.
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Randomized Controlled Trial
TRPA1 and TRPV1 antagonists do not inhibit human acidosis-induced pain.
Acidosis occurs in a variety of pathophysiological and painful conditions where it is thought to excite or contribute to excitation of nociceptive neurons. Despite potential clinical relevance the principal receptor for sensing acidosis is unclear, but several receptors have been proposed. We investigated the contribution of the acid-sensing ion channels, transient receptor potential vanilloid type 1 (TRPV1) and transient receptor potential ankyrin type 1 (TRPA1) to peripheral pain signaling. ⋯ A continuous intraepidermal injection of pH 4.3 was used to counter the buffering capacity of tissue and generate a prolonged painful stimulation. In this model, addition of A-967079, BCTC or amiloride did not reduce the reported pain. In conclusion, target-validated antagonists, applied locally in human skin, have excluded the main hypothesized targets and the mechanism of the human acidosis-induced pain remains unclear.
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Pain in sickle cell disease (SCD) is associated with increased morbidity, mortality, and high health care costs. Although episodic acute pain is the hallmark of this disorder, there is an increasing awareness that chronic pain is part of the pain experience of many older adolescents and adults. A common set of criteria for classifying chronic pain associated with SCD would enhance SCD pain research efforts in epidemiology, pain mechanisms, and clinical trials of pain management interventions, and ultimately improve clinical assessment and management. ⋯ The working group synthesized available literature to provide evidence for the dimensions of this disease-specific pain taxonomy. A single pain condition labeled chronic SCD pain was derived with 3 modifiers reflecting different clinical features. Future systematic research is needed to evaluate the feasibility, validity, and reliability of these criteria.