Relevant bibliographies by topics / Opioid activity

Academic literature on the topic 'Opioid activity'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Opioid activity"

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Yang, Junzhi, Bianca Reilly, Thomas Davis, and Patrick Ronaldson. "Modulation of Opioid Transport at the Blood-Brain Barrier by Altered ATP-Binding Cassette (ABC) Transporter Expression and Activity." Pharmaceutics 10, no. 4 (October 18, 2018): 192. http://dx.doi.org/10.3390/pharmaceutics10040192.

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Opioids are highly effective analgesics that have a serious potential for adverse drug reactions and for development of addiction and tolerance. Since the use of opioids has escalated in recent years, it is increasingly important to understand biological mechanisms that can increase the probability of opioid-associated adverse events occurring in patient populations. This is emphasized by the current opioid epidemic in the United States where opioid analgesics are frequently abused and misused. It has been established that the effectiveness of opioids is maximized when these drugs readily access opioid receptors in the central nervous system (CNS). Indeed, opioid delivery to the brain is significantly influenced by the blood-brain barrier (BBB). In particular, ATP-binding cassette (ABC) transporters that are endogenously expressed at the BBB are critical determinants of CNS opioid penetration. In this review, we will discuss current knowledge on the transport of opioid analgesic drugs by ABC transporters at the BBB. We will also examine how expression and trafficking of ABC transporters can be modified by pain and/or opioid pharmacotherapy, a novel mechanism that can promote opioid-associated adverse drug events and development of addiction and tolerance.
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Sehgal, Nalini. "Peripherally Acting Opioids and Clinical Implications for Pain Control." Pain Physician 3;14, no. 3;5 (May 14, 2011): 249–58. http://dx.doi.org/10.36076/ppj.2011/14/249.

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Opioid receptors are widely expressed in the central and peripheral nervous system and in the non-neuronal tissues. Data from animal and human clinical studies support the involvement of peripheral opioid receptors in analgesia, especially in the presence of inflammation. Inflammation has been shown to increase the synthesis of opioid receptors in the dorsal root ganglion neurons and enhance transport and accumulation of opioid receptors in the peripheral terminals of sensory neurons. Under the influence of chemokines and adhesion molecules, opioid peptide-containing immune cells extravasate and accumulate in the injured tissues. Stress, chemokines, cytokines, and other releasing factors in inflamed tissues stimulate these granulocytes to release opioid peptides. Once secreted, opioid peptides bind to and activate peripheral opioid receptors on sensory nerve fibers and produce analgesia by decreasing the excitability of sensory nerves and/or inhibiting release of pro-inflammatory neuropeptides. Research has revealed that local application of exogenous opioid agonists produces a potent analgesic effect by activating peripheral opioid receptors in inflamed tissues. The analgesic activity occurs without activation of opioid receptors in the central nervous system (CNS), and therefore centrally mediated side effects, such as respiratory depression, mental clouding, altered consciousness, or addiction, are not associated with peripheral opioid activity. This discovery has stimulated research on developing peripherally restricted opioid agonists that lack CNS effects. In addition, it has been recognized that opioid receptors modulate inflammation, and that opioids have antiinflammatory effects. The anti-inflammatory actions of opioids are not well known or understood. Conflicting reports on mu-opioids suggest both anti-inflammatory and pro-inflammatory effects. This article will present the basis for peripheral opioid analgesia and describe current research directed at developing novel treatments for pain with improved side effect profiles. Key words: Opioids, opioid receptors, opioid agonists, peripheral nervous system, peripheral opioid receptors
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Hellman, Kevin M., Thaddeus S. Brink, and Peggy Mason. "Activity of Murine Raphe Magnus Cells Predicts Tachypnea and On-Going Nociceptive Responsiveness." Journal of Neurophysiology 98, no. 6 (December 2007): 3121–33. http://dx.doi.org/10.1152/jn.00904.2007.

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In rats, opioids produce analgesia in large part by their effects on two cell populations in the medullary raphe magnus (RM). To extend our mechanistic understanding of opioid analgesia to the genetically tractable mouse, we characterized behavioral reactions and RM neural responses to opioid administration. d-Ala2, N-Me-Phe4-Gly5ol-enkephalin, a mu-opioid receptor agonist, microinjected into the murine RM produced cardiorespiratory depression and reduced slow wave electroencephalographic activity as well as increased the noxious heat-evoked withdrawal latencies. As in rat, RM cell types that were excited and inhibited by noxious stimuli, termed on and off cells, respectively, were observed in mice. However, in contrast to findings in rat, opioid doses that suppressed withdrawals did not alter the background discharge rate of murine on and off cells, suggesting that the cellular mechanisms by which the murine RM generates opioid analgesia are substantially different from those in rats. Murine on cell discharge did not predict the latency or magnitude of an ensuing withdrawal but did correlate to the magnitude and latency of concurrent withdrawals. Although opioids failed to alter the background discharge of on and off cells, they reduced the responses of RM neurons to noxious stimulation, further evidence that RM modulates on-going withdrawals. In characterizing the role of RM in respiratory modulation, we found that on cells burst and off cells paused during tachypneic events. The effects of opioids in the murine RM on homeostasis and the association of on and off cell discharge with tachypnea corroborate roles for opioid signaling in RM beyond analgesia.
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Peterson, P. K., B. Sharp, G. Gekker, C. Brummitt, and W. F. Keane. "Opioid-mediated suppression of cultured peripheral blood mononuclear cell respiratory burst activity." Journal of Immunology 138, no. 11 (June 1, 1987): 3907–12. http://dx.doi.org/10.4049/jimmunol.138.11.3907.

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Abstract Opiate addiction and stress have been associated with altered immune responses. In this study, we evaluated the influence of morphine and the stress responsive opioid peptide beta-endorphin (beta-END) on O-2 and H2O2 production by cultured human peripheral blood mononuclear cells. Exposure of these cells during 48 hr of culture to morphine and beta-END at pharmacologically (10(-8) M) and physiologically (10(-12) M) relevant concentrations, respectively, markedly suppressed peripheral blood mononuclear cell O-2 and H2O2 release in response to the respiratory burst stimuli opsonized zymosan and phorbol myristate acetate. Both opioids also induced a minimal, but statistically significant, increase in resting O-2 and H2O2 generation. The modulatory effects of morphine and beta-END on peripheral blood mononuclear cell oxygen metabolism appeared to involve a classical opioid receptor, because opioid activity was blocked by naloxone and was not observed with N-acetylated-beta-END. Using purified lymphocyte and monocyte preparations, we determined that although opioids directly increase monocyte-resting oxygen metabolism, lymphocytes are the primary target cell in opioid-mediated suppression of monocyte respiratory burst activity. The release of a suppressive product from opioid-triggered lymphocytes was inhibited by cyclosporine. Based on the results of this study, we propose that opioid-mediated suppression of mononuclear phagocyte respiratory burst activity is another factor to be considered in the immunodeficiency of opiate addiction and stress.
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Cannaert, Annelies, Lakshmi Vasudevan, Melissa Friscia, Amanda L. A. Mohr, Sarah M. R. Wille, and Christophe P. Stove. "Activity-Based Concept to Screen Biological Matrices for Opiates and (Synthetic) Opioids." Clinical Chemistry 64, no. 8 (August 1, 2018): 1221–29. http://dx.doi.org/10.1373/clinchem.2018.289496.

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Abstract BACKGROUND Detection of new highly potent synthetic opioids is challenging as new compounds enter the market. Here we present a novel screening method for the detection of opiates and (synthetic) opioids based on their activity. METHODS A cell-based system was set up in which activation of the μ-opioid receptor (MOR) led to recruitment of β-arrestin 2, resulting in functional complementation of a split NanoLuc luciferase and allowing readout via bioluminescence. Assay performance was evaluated on 107 postmortem blood samples. Blood (500 μL) was extracted via solid-phase extraction. Following evaporation and reconstitution in 100 μL of Opti-MEM® I, 20 μL was analyzed in the bioassay. RESULTS In 8 samples containing synthetic opioids, in which no positive signal was obtained in the bioassay, quadrupole time-of-flight mass spectrometry revealed the MOR antagonist naloxone, which can prevent receptor activation. Hence, further evaluation did not include these samples. For U-47700 (74.5–547 ng/mL) and furanyl fentanyl (<1–38.8 ng/mL), detection was 100% (8/8) for U-47700 and 95% (21/22) for furanyl fentanyl. An analytical specificity of 93% (55/59) was obtained for the opioid negatives. From an additional 10 samples found to contain other opioids, 5 were correctly scored positive. Nondetection in 5 cases could be explained by very low concentrations (<1 ng/mL alfentanil/sufentanil) or presence of inactive enantiomers. CONCLUSIONS The MOR reporter assay allows rapid identification of opioid activity in blood. Although the cooccurrence of opioid antagonists is currently a limitation, the bioassay's high detection capability, specificity, and untargeted nature may render it a useful first-line screening tool to investigate potential opioid intoxications.
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Ozdemir, Ercan. "The Role of the Cannabinoid System in Opioid Analgesia and Tolerance." Mini-Reviews in Medicinal Chemistry 20, no. 10 (May 27, 2020): 875–85. http://dx.doi.org/10.2174/1389557520666200313120835.

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Opioid receptor agonist drugs, such as morphine, are very effective for treating chronic and severe pain; but, tolerance can develop with long-term use. Although there is a lot of information about the pathophysiological mechanisms of opioid tolerance, it is still not fully clarified. Suggested mechanisms for opioid tolerance include opioid receptor desensitisation, reduction of sensitivity G-proteins, activation of Mitogen-Activated Protein Kinase (MAPK), altered intracellular signaling pathway including nitric oxide, and activation of mammalian Target of Rapamycin (mTOR). One way to reduce opioid tolerance and increase the analgesic potential is to use low doses. Combination of cannabinoids with opioids has been shown to manifest the reduction of the opioid dose. Experimental studies revealed an interaction of the endocannabinoid system and opioid antinociception. Cannabinoid and opioid receptor systems use common pathways in the formation of analgesic effect and demonstrate their activity via G Protein Coupled Receptors (GPCR). Cannabinoid drugs modulate opioid analgesic activity at a number of distinct levels within the cell, ranging from direct receptor associations to post-receptor interactions through shared signal transduction pathways. This review summarizes the data indicating that with combining cannabinoids and opioids drugs may be able to produce long-term analgesic effects, while preventing the opioid analgesic tolerance.
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Ronström, Joakim W., Natalie L. Johnson, Stephen T. Jones, Sara J. Werner, Hillary A. Wadsworth, James N. Brundage, Valerie Stolp, et al. "Opioid-Induced Reductions in Amygdala Lateral Paracapsular GABA Neuron Circuit Activity." International Journal of Molecular Sciences 24, no. 3 (January 18, 2023): 1929. http://dx.doi.org/10.3390/ijms24031929.

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Opioid use and withdrawal evokes behavioral adaptations such as drug seeking and anxiety, though the underlying neurocircuitry changes are unknown. The basolateral amygdala (BLA) regulates these behaviors through principal neuron activation. Excitatory BLA pyramidal neuron activity is controlled by feedforward inhibition provided, in part, by lateral paracapsular (LPC) GABAergic inhibitory neurons, residing along the BLA/external capsule border. LPC neurons express µ-opioid receptors (MORs) and are potential targets of opioids in the etiology of opioid-use disorders and anxiety-like behaviors. Here, we investigated the effects of opioid exposure on LPC neuron activity using immunohistochemical and electrophysiological approaches. We show that LPC neurons, and other nearby BLA GABA and non-GABA neurons, express MORs and δ-opioid receptors. Additionally, DAMGO, a selective MOR agonist, reduced GABA but not glutamate-mediated spontaneous postsynaptic currents in LPC neurons. Furthermore, in LPC neurons, abstinence from repeated morphine-exposure in vivo (10 mg/kg/day, 5 days, 2 days off) decrease the intrinsic membrane excitability, with a ~75% increase in afterhyperpolarization and ~40–50% enhanced adenylyl cyclase-dependent activity in LPC neurons. These data show that MORs in the BLA are a highly sensitive targets for opioid-induced inhibition and that repeated opioid exposure results in impaired LPC neuron excitability.
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Bril, Silviu, Yoav Shoham, and Jeremy Marcus. "The ‘Mystery’ of Opioid-Induced Diarrhea." Pain Research and Management 16, no. 3 (2011): 197–99. http://dx.doi.org/10.1155/2011/309685.

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Bowel dysfunction, mainly constipation, is a well-known and anticipated side effect of opioids. The physician prescribing an opioid frequently confronts the challenge of preventing and treating bowel dysfunction. Different strategies have emerged for managing opioid-induced constipation. These strategies include physical activity, maintaining adequate fluid intake, adhering to regular daily bowel habits, using laxatives and other anticonstipation medications and, recently, using a peripheral opioid antagonist, either as a separate drug or in the form of an opioid agonist-antagonist combination pill. What options exist for the physician when a patient receiving opioids complains of diarrhea, cramps and bloating, rather than the expected constipation? The present article describes a possible cause of opioid-induced diarrhea and strategies for management.
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Kaczyńska, Katarzyna, and Piotr Wojciechowski. "Non-Opioid Peptides Targeting Opioid Effects." International Journal of Molecular Sciences 22, no. 24 (December 19, 2021): 13619. http://dx.doi.org/10.3390/ijms222413619.

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Opioids are the most potent widely used analgesics, primarily, but not exclusively, in palliative care. However, they are associated with numerous side effects, such as tolerance, addiction, respiratory depression, and cardiovascular events. This, in turn, can result in their overuse in cases of addiction, the need for dose escalation in cases of developing tolerance, and the emergence of dose-related opioid toxicity, resulting in respiratory depression or cardiovascular problems that can even lead to unintentional death. Therefore, a very important challenge for researchers is to look for ways to counteract the side effects of opioids. The use of peptides and their related compounds, which have been shown to modulate the effects of opioids, may provide such an opportunity. This short review is a compendium of knowledge about the most important and recent findings regarding selected peptides and their modulatory effects on various opioid actions, including cardiovascular and respiratory responses. In addition to the peptides more commonly reported in the literature in the context of their pro- and/or anti-opioid activity—such as neuropeptide FF (NPFF), cholecystokinin (CCK), and melanocyte inhibiting factor (MIF)—we also included in the review nociceptin/orphanin (N/OFQ), ghrelin, oxytocin, endothelin, and venom peptides.
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Michaud, Veronique, Ravil Bikmetov, Matt K. Smith, Pamela Dow, Lucy I. Darakjian, Malavika Deodhar, Brian Cicali, Kevin T. Bain, and Jacques Turgeon. "Use of Drug Claims Data and a Medication Risk Score to Assess the Impact of CYP2D6 Drug Interactions among Opioid Users on Healthcare Costs." Journal of Personalized Medicine 11, no. 11 (November 10, 2021): 1174. http://dx.doi.org/10.3390/jpm11111174.

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Cytochrome P450 2D6 (CYP2D6) activity is highly variable due to several factors, including genetic polymorphisms and drug-drug-gene interactions. Hydrocodone, oxycodone, codeine, and tramadol the most commonly prescribed CYP2D6-activated opioids for pain. However, the co-administration of CYP2D6 interacting drugs can modulate CYP2D6-medicated activation of these opioids, affecting drug analgesia, effectiveness, and safety, and can impact healthcare costs. A retrospective, observational cohort analysis was performed in a large (n = 50,843) adult population. This study used drug claims data to derive medication risk scores and matching propensity scores to estimate the effects of opioid use and drug-drug interactions (DDIs) on medical expenditures. 4088 individuals were identified as opioid users; 95% of those were prescribed CYP2D6-activated opioids. Among those, 15% were identified as being at risk for DDIs. Opioid users had a significant increase in yearly medical expenditure compared to non-opioid users ($2457 vs. $1210). In matched individuals, average healthcare expenditures were higher for opioid users with DDIs compared to those without DDIs ($7841 vs. $5625). The derived medication risk score was higher in CYP2D6 opioid users with interacting drug(s) compared to no DDI (15 vs. 12). Higher costs associated with CYP2D6 opioid use under DDI conditions suggest inadequate CYP2D6 opioid prescribing practices. Efforts to improve chronic opioid use in adults should reduce interacting drug combinations, especially among patients using CYP2D6 activated opioids.
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Dissertations / Theses on the topic "Opioid activity"

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McFadyen, Iain James. "Structure-activity relationships of opioid ligands." Thesis, Loughborough University, 1999. https://dspace.lboro.ac.uk/2134/33189.

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There are three different types of opioid receptor, namely mu, delta and kappa. Morphine and related clinically useful analgesics exert their actions through the mu opioid receptor. Such compounds represent a huge structural diversity, including both peptides and alkaloids. Nevertheless, there exists a common pharmacophore comprising two critical features, namely an amine nitrogen and an aromatic ring, usually with a hydroxyl substituent; the spatial relationship between them is also vital.
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Cavagnero, Silvia 1962. "Structure-activity studies of delta-selective opioid analogues." Thesis, The University of Arizona, 1990. http://hdl.handle.net/10150/278183.

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The two structurally different peptides DPDPE and Dermenkephalin show a similar remarkably high affinity and selectivity for the delta opioid receptor subtype. An effort has been made to gain some insight into the factors responsible for the recognition ability of these two molecules by synthesizing some DPDPE-Dermenkephalin peptide hybrids and some conformationally restricted Dermenkephalin analogues. The results of the binding and the in-vitro bioassays have been compared with those of the parent peptides. A general decrease in receptor affinity has been observed in the peptide hybrids while the dermenkephalin analogues have shown a wider range of affinities and selectivities. The above findings contribute to the understanding of the structural requirements of the delta receptor, provide information about the sensitivity of Dermenkephalin to enzymatic degradation, and indicate directions for future research.
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Oakley, Sarah M. "The influence of G-protein coupling of the #delta#-opioid receptor on the activity of #delta#-opioid receptor ligands." Thesis, University of Surrey, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326816.

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Mathes, Wendy Foulds. "Running wheel activity attenuates the effects of exogenous opiates : implications for the endogenous opioid system /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2000.

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Thesis (Ph.D)--Tufts University, 2000.
Adviser: Robin B. Kanarek. Submitted to the Dept. of Psychology. Includes bibliographical references (leaves 109-134). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
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Wheeler, Carly. "Understanding physical activity among individuals receiving opioid substitution treatment : a mixed methods study." Thesis, Oxford Brookes University, 2015. https://radar.brookes.ac.uk/radar/items/2a36dac0-b5ad-40ea-b821-e10a95fb5222/1/.

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This thesis explores the physical activity (PA) practices and experiences of a group of drug users receiving opioid substitution treatment (OST). Opioid Substitution treatment is the most widely used form of treatment for individuals with opioid dependence. Existing research in this group (and drug users in general) has tended to focus on harmful behaviours, as opposed to their everyday lives. Additionally, a recent shift in UK drugs policy has places an increased emphasis on the wider aspects of recovery from drug use, including the improvement of health, well-being and re- integration into society. Despite the numerous benefits associated with PA, little research has explored PA among individuals receiving OST. The use of a social-ecological approach to guide and understand the research findings was utilized, with both quantitative and qualitative data collected. Self- reported quantitative data was first collected on demographic information, PA participation, perceived benefits and barriers to PA and health-related quality of life from 100 participants. Objective PA data was also collected from a smaller sub- sample of participants through the use of pedometers. Secondly, semi-structured interviews were conducted with 30 participants, to gain further understanding of PA in this group, with the qualitative data analyzed using the Framework approach. Both quantitative and qualitative findings indicate that much of this population is physically active, largely through walking as a form of active transport, with participant in structured sport and exercise occurring less frequently. However, nearly all participants reported previous participation in structured PA prior to drug use and an a desire to resume participation. The benefits of PA participation were unanimously recognized, with perceived barriers to participation highlighted at multiple levels of influence in line with the social-ecological approach used to theoretically underpin the study. While many individuals receiving OST appear to be physically active through unstructured PA, increased participation in structured PA is often desired, yet prohibited through the presence of multiple barriers, some similar to the general population and others specific to this group. Participation in structured PA may yield additional benefits beyond those gained from unstructured activity, contributing to the wider aspects of individuals’ recovery from opioid dependence in line with current UK policy. However, strategies to increase participation may need to consider the multiple needs of this group in addressing barriers to participation.
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GERHARD, GWENYTH GRAVLIN. "THE RELATIONSHIPS AMONG HABITUAL PHYSICAL ACTIVITY, ENDOGENOUS OPIOID LEVELS, AND SUBSEQUENT ACUTE SURGICAL PAIN EXPERIENCES (ENDORPHIN, VISUAL ANALOG SCALING)." Diss., The University of Arizona, 1985. http://hdl.handle.net/10150/188048.

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The purpose of this study was to elucidate relationships among habitual physical activity level, endogenous opioid level, postoperative opioid analgesic, and experiences of acute pain in response to the noxious stimulation of a subsequent orthopedic surgical procedure. Specifically, the study examined (1) the relationship between habitual activity and preoperative level of endogenous opioids in peripheral blood, and (2) whether habitual activity predicts perception of pain intensity or distress in response to a subsequent noxious stimulus. The study utilized a descriptive correlational design with causal modeling methodology to assess a five-stage theory. The convenience sample was comprised of 36 English-speaking adult subjects hospitalized for orthopedic surgeries. The theoretical concepts, acute pain intensity and distress, were indexed three times for each subject by visual analogue scales. Reliability and validity of the scales were assessed by correlation with concurrent pain measurements using randomized verbal descriptor lists. Multiple regression statistical techniques were used to estimate the theory; violations of causal modeling and statistical assumptions were assessed by residual analysis. For this sample, the strongest predictors of postoperative pain were the immediately preceding comparable indices of pain intensity or pain distress. Approximately 31% of the variance on postoperative analgesic was predicted by the combined effects of immediate postoperative pain and habitual activity. Although activity was not significantly related to endogenous opioid level in peripheral plasma, activity directly and positively influenced immediate postoperative pain intensity (Beta = .37), 24-hour pain distress (B = .27), and total opioid analgesic received in the initial 24 postoperative hours (Intensity B = .40; Distress B = .50). Endogenous opioid was significantly related only to immediate postoperative pain distress (B = -.26). More physically active patients reported greater immediate postoperative pain intensity and greater 24-hour pain distress; they received more postoperative exogenous analgesic. Incorporation of information about activity as a potential determinant of operative pain experiences would increase validity of nursing assessments on which pain interventions are based. Patients in acute pain would benefit from this improved scientific basis for pain assessment.
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Corder, Gregory F. "INJURY ESTABLISHES CONSTITUTIVE µ-OPIOID RECEPTOR ACTIVITY LEADING TO LASTING ENDOGENOUS ANALGESIA AND DEPENDENCE." UKnowledge, 2013. http://uknowledge.uky.edu/physiology_etds/10.

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Injury causes increased pain sensation in humans and animals but the mechanisms underlying the emergence of persistent pathological pain states, which arise in the absence of on-going physical damage, are unclear. Therefore, elucidating the physiological regulation of such intractable pain is of exceptional biomedical importance. It is well known that endogenous activation of µ-opioid receptors (MORs) provides relief from acute pain but the consequences of prolonged endogenous opioidergic signaling have not been considered. Here we test the hypothesis that the intrinsic mechanisms of MOR signaling promote pathological sensitization of pain circuits in the spinal cord. We found that tissue inflammation produces agonist-independent MOR signaling in the dorsal horn of the spinal cord, which tonically represses hyperalgesia for months, even after complete recovery from injury and re-established normal pain thresholds. Disruption of this constitutive activity with MOR inverse agonists reinstated pain and precipitated cellular, somatic and aversive signs of physical withdrawal. This phenomenon required N-methyl-D-aspartate receptor activation of calcium-sensitive adenylyl cyclase type 1. Thus, we present a novel mechanism of long-lasting opioid analgesia that regulates the transition from acute to chronic pain while, in parallel, generates physical dependence. In conclusion we propose that the prevalence of chronic pain syndromes may result from a failure in constitutive signaling of spinal MORs and a loss of endogenous analgesic control.
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Custodio, Lilian. "SPINAL KAPPA OPIOID RECEPTOR ACTIVITY INHIBITS ADENYLYL CYCLASE-1 DEPENDENT MECHANISMS OF CHRONIC POSTOPERATIVE PAIN." UKnowledge, 2019. https://uknowledge.uky.edu/physiology_etds/42.

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Chronic postoperative pain impacts millions of individuals worldwide that undergo a variety of surgical procedures. Opioids remain the mainstay analgesics of acute and perioperative pain; however, prolonged opioid therapy may lead to life-threating adverse effects, tolerance, dependence, and addiction. Therefore, unraveling the cellular mechanisms that drive persistent pain states and opposing endogenous analgesia provided by opioid receptor signaling, may lead to novel analgesics. Evidence suggests that tissue injury leads to increased sensitization of the spinal cord nociceptive neurons which increases susceptibility to chronic pain via an N-methyl-D-aspartate (NMDA) receptor activation of calcium-sensitive adenylyl cyclase isoform 1 (AC1). This phenomenon, named latent pain sensitization (LS), is mediated by a compensatory response of endogenous inhibitory systems. In this dissertation, we test the hypothesis that surgical insult promotes prolonged activation of kappa opioid receptors (KOR) which mask LS via attenuation of pro-nociceptive AC1 signaling pathways in both male and female animals. We employed a murine model of chronic postoperative pain that promotes LS in the spinal cord and closely resembles the phenotypic features of postoperative pain in human subjects. When behavioral signs of hyperalgesia resolved, we targeted spinal opioid receptor systems and pronociceptive modulators with intrathecal delivery of selective pharmacological antagonists and assessed behavioral signs of hyperalgesia and spinal nociceptive sensitization. We propose that LS is kept in remission by a long-lasting compensatory response of tonic endogenous KOR signaling that hinders a pronociceptive LS pathway that includes not only AC1 but also two downstream targets: protein kinase A (PKA) and exchange protein activated by cAMP (Epac1/2) - in a sex-dependent manner. Our results propose new therapeutic targets for the management of persistent postoperative pain and underscore the importance of tailoring sex-specific pain management strategies.
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Pettinger, Louisa. "Effects of bradykinin on [delta]-opioid receptor function and voltage-gated calcium channel activity in sensory neurons." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588749.

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The δ-opioid receptor (DOR) shows potential as a therapeutic target for analgesia. DOR-targeting pharmaceutics may lead to fewer side effects than conventional opioid drugs such as morphine due to relatively low expression of DOR in the central nervous system (compared to the main target for morphine, the u-opioid receptor). The analgesic efficacy of DOR agonists increases following inflammation and receptor insertion has been suggested as a possible mechanism for this. Modulation of membrane expression of functional DOR receptors may be useful in the development of analgesic drugs. Currently, expression of functional DOR at the membrane of sensory neurons is controversial. Here, patch-clamp recordings and total internal reflection fluorescence (TIRF) microscopy have been used to study functional expression and trafficking of DOR in sensory neurons from rat trigeminal ganglia (TG). In addition, the role of inflammatory mediator bradykinin (BK) in DOR membrane expression has been investigated. To determine whether neurons express functional DCR, inhibition of voltage-gated Ca2+ channels (VGCC) by DCR agonist [D-Ala2, D- Leu5]-Enkephalin (DADLE) was determined. DADLE inhibited VGCC in 23% of TG neurons by 25.3 ± 5%. Pre-treatment with BK increased the population of DCR-positive neurons to 54%, but did not significantly affect the degree of VGCC inhibition by DADLE. Real-time TIRF microscopy revealed that BK treatment caused robust trafficking of DCR to the plasma membrane in neurons transfected with GFP-tagged DOR. In contrast, DADLE and TRPV1 agonist capsaicin caused a decrease in membrane abundance of DOR, suggesting internalisation of the receptor. In Ca2+ imaging experiments 80% of cultured TG neurons responded to BK, thus, these data suggest that a majority of BK-responsive TG neurons have the potential to become DOR-positive upon inflammation, re-establishing the therapeutic potential of peripheral DOR. In a separate line of investigation, enhancement of T-type VGCC in nociceptive neurons by BK has been discovered.
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Ramos-Colon, Cyf Nadine, and Cyf Nadine Ramos-Colon. "Design, Synthesis, and Biological Evaluation of Novel Peptide Ligands as Kappa Opioid Receptor Antagonists." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/621869.

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Millions of people in the US currently suffer from chronic pain but available therapeutics do not provide effective chronic pain treatment. Opiate therapy is still the gold standard for chronic pain management with detrimental side effects, such as tolerance, addiction, constipation, and respiratory depression that limit their therapeutic potential. Opiates exert their positive and negative effects by activating the μ opioid receptor (MOR). Conversely, the κ opioid receptor (KOR) has been shown to modulate the tolerance and addiction produced by MOR agonists and is also involved in mood modulation (anxiety and depression). Therefore, blocking KOR activation results in positive effects against opiate side effects and stress-related depression. Dynorphin A (Dyn A) is the endogenous opioid peptide for the KOR. Structure-activity relationship (SAR) studies were carried out to develop a KOR selective antagonist based on the Dyn A structure. A minimum Dyn A pharmacophore with improved stability, no cell toxicity, and antagonist activity was discovered. Peptidomimetic enkephalin analogues previously developed in our group as MOR and δ opioid receptor (DOR) agonists have shown multifunctional activity, with MOR/DOR agonist and KOR antagonist activities. To our knowledge, this finding is first of its class for the opioid receptors. Novel design and synthesis of KOR selective ligands based on our multifunctional enkephalin analogues was done. Successful peptide synthesis resulted in analogues with high stability in rat plasma and no cell toxicity.
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Books on the topic "Opioid activity"

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Ahmad, Iftikhar. Pro and anticonvulsant activity of opioid analgesics and their interaction with propofol. Manchester: University of Manchester, 1994.

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Gelbspan, Ross. The heat is on: The high stakes battle over Earth's threatened climate. Reading, Mass: Addison-Wesley Pub. Co., 1997.

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Gelbspan, Ross. The heat is on: The climate crisis, the cover-up, the prescription. Reading, Mass: Perseus Books, 1998.

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4

Kulkarni, Sandhya N. Synthesis and opioid activity of dynorphin analogues with the modifications in the message sequence. 1995.

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McFadyen, Iain James. Structure-activity relationships of opioid ligands. 1999.

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Snyder, Kristin Renee. Synthesis and opioid activity of dynorphin a analogues. 1993.

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Pham, Thien C., Courtney Kominek, Abigail Brooks, and Jeffrey Fudin. Opioid Pharmacotherapies for Chronic Pain (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0014.

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Chronic pain management employing opioids is divided into subtopics, including: risk–benefit balance; a review of the mode of action of opioid analgesics (Chap. 8); the suitability of synthetic opioids for neuropathic pain; endocrinopathy proceeding from opioid use; the use of the morphine-equivalent daily dose as a conversion tool for managing multiple opioids; the place of extended-release and long-acting opioids; current technology in abuse deterrence; and an overview of the challenges entailed in prescribing. This last section details the complex components of a decision to prescribe opioids for chronic pain. A table is provided of the classification of common opioid analgesics and their duration of activity. A text box gives the table of contents of Appendix B, supportive tables and figures therein for this chapter; there is also a text box listing additional resources.
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Sjøgren, Per, Frank Elsner, and Stein Kaasa. Non-opioid analgesics. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0096.

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Non-opioid analgesics encompass the non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol (acetaminophen). The NSAIDs include acetylsalicylic acid (ASA, aspirin), dipyrone (metamizole), and numerous other drugs in diverse classes. The NSAIDs have potent anti-inflammatory, analgesic and antipyretic activity, and are among the most widely used drugs worldwide. In palliative medicine, they represent the first step of the World Health Organization’s analgesic ladder used for mild pain and they are an important supplement to opioids and adjuvant drugs at higher steps of the ladder. The disadvantages of non-opioid analgesics include a ceiling effect for pain relief and the risk of side effects. NSAIDs are also associated with an increased risk of adverse gastrointestinal, renal, and cardiovascular effects and hepatotoxicity can result from overdosing with paracetamol. This chapter describes the clinical pharmacology of NSAIDs, their classification, molecular mechanisms of action and adverse effects, as well as some recent developments aimed at designing effective anti-inflammatory agents with improved safety and tolerability profiles.
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Arttamangkul, Seksiri. Synthesis and opioid activity of conformationally constrained dynorphin A analogues. 1995.

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Nutt, David J., and Liam J. Nestor. The opioid system and addiction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198797746.003.0010.

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The opioid system of the brain is the major target for opiate drugs such as morphine and heroin, and has been implicated in processes such as pain, stress and reward. Many of these effects take place at the mu opioid receptor (mOR), which is distributed throughout the brain. Significantly, genetic polymorphisms at the mOR may confer a greater dopamine response to the reinforcing effects of alcohol, and it has been suggested that addiction per se may be associated with alterations to the opioid system. There is evidence for the potential efficacy of mOR antagonists (e.g. naltrexone) in reducing drug and alcohol relapse, increasing treatment retention and attenuating the subjective effects of substances of abuse. Medications with partial agonist activity at the kappa opioid receptor (e.g. nalmefene) may also confer an additional clinical advantage by reducing binging following relapse.
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Book chapters on the topic "Opioid activity"

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Sheikh, Sureal Ahmad, Pragya Shakti Mishra, Ritam Bandopadhyay, and Awanish Mishra. "Opioid Activity." In Bioactive Peptides from Food, 427–40. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003106524-27.

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Chrubasik, Joachim, Sigrun Chrubasik, and Laurence Mather. "Determinants of Opioid Activity." In Postoperative Epidural Opioids, 9–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78320-3_3.

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Freye, Enno. "New Concepts in Opioid Activity." In Opioid Agonists, Antagonists and Mixed Narcotic Analgesics, 64–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71854-0_5.

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Nosálová, Gabriela, Veronika Sivová, Bimalendu Ray, Soňa Fraňová, Igor Ondrejka, and Dana Flešková. "Antitussive Activity of Withania somnifera and Opioid Receptors." In Advances in Experimental Medicine and Biology, 19–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/5584_2014_79.

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Ting, Pauline, S. Xu, and S. Krumins. "Endogenous Opioid System Activity Following Temporary Focal Cerebral Ischemia." In Brain Edema IX, 253–56. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_67.

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Neubert, K., R. Schmidt, C. Liebmann, M. Schnittler, N. N. Chung, and P. W. Schiller. "Synthesis and opioid activity of cyclic ß-casomorphin analogs." In Peptides 1990, 619–20. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_256.

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Bramnert, M., and B. Hökfelt. "Influence of the Opioid System on Sympathetic Activity and the Renin-Aldosterone System in Healthy Males." In Opioid Peptides and Blood Pressure Control, 71–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73429-8_7.

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Okuyama, Shigeru, Sanae Hashimoto, Hironaka Aihara, William M. Willingham, and John R. J. Sorenson. "Copper Complexes Have Potent Analgesic Activity and They May Activate Opioid Receptors." In Biology of Copper Complexes, 301–13. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4584-1_23.

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Höllt, V., K. Feasey, N. Kley, I. Moneta, and B. Morris. "Gene Expression of Opioid Peptides is Regulated by Electrical Activity." In Neuropsychopharmacology, 458–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74034-3_45.

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Ting, Pauline, P. A. Cushenberry, T. C. Friedman, and Y. P. Loh. "Enhanced Brain Opioid Receptor Activity Precedes Blood-Brain Barrier Disruption." In Brain Edema X, 250–53. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_77.

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Conference papers on the topic "Opioid activity"

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Aldrich, Jane, Dmitry Yakovlev, Nicolette Ross, Shainnel Eans, Heather Stacy, Thomas Murray, and Jay McLaughlin. "Substitution of Aromatic Residues in the Macrocyclic Opioid Peptide [D-Trp]CJ-15,208 Alters the Opioid Activity Profile in vivo." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.061.

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Ramos Colon, Cyf N., Yeon Sun Lee, Sara M. Hall, Josephine Lai, Frank Porreca, and Victor J. Hruby. "Structure-Activity Relationship Studies of Dynorphin A Analogs at the Kappa Opioid Receptor." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.096.

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Fabri, Júlia Campos, Maria Julia Filgueiras Granato, Maria Clara Lopes Rezende, Maria Luiza Franco de Oliveira, and Leandro de Souza Cruz. "The impact of genetic polymorphism in pain mechanisms." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.708.

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Background:Variations in genes codifying target structures in the nociceptive pathway can result in pain attenuation or increase.Objective:Investigate the genetic polymorphism influence in the individual pain threshold. Methods: Search on PubMed with the terms “genetic”, “pain” and its synonyms published in the last 10 years. Results:The subjective and individual mechanisms of pain aren’t completely understood, but genetic susceptibility is one of the hypothesis to explain these differences.The KCNK18 gene influences the synaptic transmission by producing potassium channel protein that equalizes resting membrane potential, calcineurin activated and inhibited by arachidonic acid. This gene was found more frequently in migraine individuals. The COMT gene increase the sensibility to pain by met-enkephalins reduction and/or catecholamine elevation. Its activity’s reduced in fibromyalgia patients. However, the OPRM1 gene, an opioid receptor, was found in individuals with a higher pain threshold.Furthermore, studies with human cell culture shows the analgesic role of the gene A118G, by its greater binding affinity for β-endorphin.It is associated with more effective endorphinergic endogenous pain inhibition. Conclusion:Researches indicates a striking participation of genetic polymorphism in pain mechanisms. The knowledge about genetic variables on pain perception can contribute to the development of individualized analgesic protocols and therapeutic strategies, accordantly to the patient genetic profile. This evolution becomes fundamental in a population that tend to the indiscriminate use of analgesics.
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Reports on the topic "Opioid activity"

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Dy, Sydney M., Arjun Gupta, Julie M. Waldfogel, Ritu Sharma, Allen Zhang, Josephine L. Feliciano, Ramy Sedhom, et al. Interventions for Breathlessness in Patients With Advanced Cancer. Agency for Healthcare Research and Quality (AHRQ), November 2020. http://dx.doi.org/10.23970/ahrqepccer232.

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Objectives. To assess benefits and harms of nonpharmacological and pharmacological interventions for breathlessness in adults with advanced cancer. Data sources. We searched PubMed®, Embase®, CINAHL®, ISI Web of Science, and the Cochrane Central Register of Controlled Trials through early May 2020. Review methods. We included randomized controlled trials (RCTs) and observational studies with a comparison group evaluating benefits and/or harms, and cohort studies reporting harms. Two reviewers independently screened search results, serially abstracted data, assessed risk of bias, and graded strength of evidence (SOE) for key outcomes: breathlessness, anxiety, health-related quality of life, and exercise capacity. We performed meta-analyses when possible and calculated standardized mean differences (SMDs). Results. We included 48 RCTs and 2 retrospective cohort studies (4,029 patients). The most commonly reported cancer types were lung cancer and mesothelioma. The baseline level of breathlessness varied in severity. Several nonpharmacological interventions were effective for breathlessness, including fans (SMD -2.09 [95% confidence interval (CI) -3.81 to -0.37]) (SOE: moderate), bilevel ventilation (estimated slope difference -0.58 [95% CI -0.92 to -0.23]), acupressure/reflexology, and multicomponent nonpharmacological interventions (behavioral/psychoeducational combined with activity/rehabilitation and integrative medicine). For pharmacological interventions, opioids were not more effective than placebo (SOE: moderate) for improving breathlessness (SMD -0.14 [95% CI -0.47 to 0.18]) or exercise capacity (SOE: moderate); most studies were of exertional breathlessness. Different doses or routes of administration of opioids did not differ in effectiveness for breathlessness (SOE: low). Anxiolytics were not more effective than placebo for breathlessness (SOE: low). Evidence for other pharmacological interventions was limited. Opioids, bilevel ventilation, and activity/rehabilitation interventions had some harms compared to usual care. Conclusions. Some nonpharmacological interventions, including fans, acupressure/reflexology, multicomponent interventions, and bilevel ventilation, were effective for breathlessness in advanced cancer. Evidence did not support opioids or other pharmacological interventions within the limits of the identified studies. More research is needed on when the benefits of opioids may exceed harms for broader, longer term outcomes related to breathlessness in this population.
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Skelly, Andrea C., Roger Chou, Joseph R. Dettori, Erika D. Brodt, Andrea Diulio-Nakamura, Kim Mauer, Rongwei Fu, et al. Integrated and Comprehensive Pain Management Programs: Effectiveness and Harms. Agency for Healthcare Research and Quality (AHRQ), October 2021. http://dx.doi.org/10.23970/ahrqepccer251.

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Objectives. To evaluate the effectiveness and harms of pain management programs that are based on the biopsychosocial model of care, particularly in the Medicare population. Data sources. Electronic databases (Ovid® MEDLINE®, PsycINFO®, CINAHL®, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systematic Reviews) from 1989 to May 24, 2021; reference lists; and a Federal Register notice. Review methods. Given lack of consensus on terminology and program definition for pain management, we defined programs as integrated (based in and integrated with primary care) and comprehensive (referral based and separate from primary care) pain management programs (IPMPs and CPMPs). Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) comparing IPMPs and CPMPs with usual care or waitlist, physical activity, pharmacologic therapy, and psychological therapy in patients with complex acute/subacute pain or chronic nonactive cancer pain. Patients needed to have access to medication support/review, psychological support, and physical function support in programs. Meta-analyses were conducted to improve estimate precision. We classified the magnitude of effects as small, moderate, or large based on predefined criteria. Strength of evidence (SOE) was assessed for the primary outcomes of pain, function, and change in opioid use. Results. We included 57 RCTs; 8 evaluated IPMPs and 49 evaluated CPMPs. Compared with usual care or waitlist, IPMPs were associated with small improvements in pain in the short and intermediate term (SOE: low) and in function in the short term (SOE: moderate), but there were no clear differences at other time points. CPMPs were associated with small improvements in pain immediately postintervention (SOE: moderate) but no differences in the short, intermediate, and long term (SOE: low); for function, improvements were moderate immediately postintervention and in the short term; there were no differences in the intermediate or long term (SOE: low at all time points). CPMPs were associated with small to moderate improvements in function and pain versus pharmacologic treatment alone at multiple time frames (SOE: moderate for function intermediate term; low for pain and function at all other times), and with small improvements in function but no improvements in pain in the short term when compared with physical activity alone (SOE: moderate). There were no differences between CPMPs and psychological therapy alone at any time (SOE: low). Serious harms were not reported, although evidence on harms was insufficient. The mean age was 57 years across IPMP RCTs and 45 years across CPMP RCTs. None of the trials specifically enrolled Medicare beneficiaries. Evidence on factors related to program structure, delivery, coordination, and components that may impact outcomes is sparse and there was substantial variability across studies on these factors. Conclusions. IPMPs and CPMPs may provide small to moderate improvements in function and small improvements in pain in patients with chronic pain compared with usual care. Formal pain management programs have not been widely implemented in the United States for general populations or the Medicare population. To the extent that programs are tailored to patients’ needs, our findings are potentially applicable to the Medicare population. Programs that address a range of biopsychosocial aspects of pain, tailor components to patient need, and coordinate care may be of particular importance in this population.
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