Articles: opioid.
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The Opioid Risk Tool (ORT) is a screening instrument for assessing the risk of opioid-related aberrant behavior in chronic noncancer pain (CNCP) patients. ⋯ Significant differences existed between this study population and the patient sample from which the ORT was derived. Limitations of this study are discussed. We concur with the authors of the original study that the ORT may not be applicable in different pain populations and settings. Based on our findings, we encourage caution in interpreting the ORT in general CNCP settings until further studies are performed.
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Painful diabetic neuropathy is a disease of the peripheral sensory neuron with impaired opioid responsiveness. Since μ-opioid receptor (MOR) activation can inhibit the transient receptor potential vanilloid 1 (TRPV1) activity in peripherally sensory neurons, this study investigated the mechanisms of impaired opioid inhibitory effects on capsaicin-induced TRPV1 activity in painful diabetic neuropathy. Intravenous injection of streptozotocin (STZ, 45 mg/kg) in Wistar rats led to a degeneration of insulin producing pancreatic β-cells, elevated blood glucose, and mechanical hypersensitivity (allodynia). ⋯ Intrathecal delivery of nerve growth factor in diabetic animals normalized sensory neuron MOR and subsequently rescued morphine's inhibitory effects on capsaicin-induced TRPV1 activity in vivo and in vitro. These findings identify a loss in functional MOR on sensory neurons as a contributing factor for the impaired opioid inhibitory effects on capsaicin-induced TRPV1 activity during advanced STZ-induced diabetes. Moreover, they support growing evidence of a distinct regulation of opioid responsiveness during various painful states of disease (e.g. arthritis, cancer, neuropathy) and may give novel therapeutic incentives.
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Opioid analgesics are commonly and increasingly prescribed by physicians for the management of chronic pain. However, strong evidence supports the need for strategies that reduce opioid use. The objective of this review is to outline limitations associated with opioid use and discuss therapeutic techniques that can be adopted to optimize the use of opioids in the management of chronic nonmalignant pain. ⋯ Appropriate patient selection through identification of risk factors, urine drug testing, and access to prescription monitoring programs has been shown to effectively improve care. Structured opioid therapy in a multimodal platform, including use of a low initial dose, prescription of alternative non-opioid analgesics including non-steroidal anti-inflammatory drugs and acetaminophen, as well as development of written care agreements to individualize and guide therapy has also been shown to improve patient outcomes. Implementation of opioid allocation strategies has the potential to encourage appropriate opioid use and improve patient care.
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A growing number of studies have shown that opioid craving (i.e., the perceived need or desire to consume opioids) is one of the strongest determinants of prescription opioid misuse in patients with chronic pain prescribed opioid therapy. To date, however, the factors that are associated with craving in patients with pain remain largely unexplored. Based on previous research, there is reason to believe that catastrophizing might be associated with heightened opioid craving. ⋯ Our preliminary findings provide valuable new insights into the determinants of craving in patients with pain. The finding that catastrophizing was associated with craving even after controlling for a host of demographic, psychological, medical, and medication regimen variables is particularly striking, and raises questions concerning the factors that underlie the association between catastrophizing and craving in patients prescribed opioid therapy.
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Neurogastroenterol. Motil. · Oct 2014
ReviewSite and mechanism of morphine tolerance in the gastrointestinal tract.
Opioid-induced constipation is a major clinical problem. The effects of morphine, and other narcotics, on the gastrointestinal tract persist over long-term use thus limiting the clinical benefit of these excellent pain relievers. The effects of opioids in the gut, including morphine, are largely mediated by the μ-opioid receptors at the soma and nerve terminals of enteric neurons. ⋯ Here, we review the mechanisms by which tolerance develops in the small but not the large intestine. The regional differences lie in the signaling and regulation of the μ-opioid receptor in the various segments of the gastrointestinal tract. The differential role of β-arrestin2 in tolerance development between central and enteric neurons defines the potential for therapeutic approaches in developing ligands with analgesic properties and minimal constipating effects.