Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methadone is a synthetic opioid with potent analgesic effects. Although it is associated commonly with the treatment of opioid addiction, it may be prescribed by licensed family physicians for analgesia. Methadone's unique pharmacokinetics and pharmacodynamics make it a valuable option in the management of cancer pain and other chronic pain, including neuropathic pain states. It may be an appropriate replacement for opioids when side effects have limited further dosage escalation. Metabolism of and response to methadone varies with each patient. Transition to methadone and dosage titration should be completed slowly and with frequent monitoring. Conversion should be based on the current daily oral morphine equivalent dosage. After starting methadone therapy or increasing the dosage, systemic toxicity may not become apparent for several days. Some medications alter the absorption or metabolism of methadone, and their concurrent use may require dosing adjustments. Methadone is less expensive than other sustained-release opioid formulations.
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PMID:Methadone treatment for pain states. 1583 38

Cannabinoids produce a variety of pharmacological effects very similar to those elicited by opioids. Direct and indirect interactions with opioid system have been proposed to explain some cannabinoid effects such as analgesia and attenuation of opioid-withdrawal syndrome, and evidence has been provided in support to the notion that rewarding properties of cannabinoids and opioids might be functionally linked. In particular, a growing body of studies points to an important role of the endogenous cannabinoid system in the modulation of opioid rewarding and addictive effects. The current review examines progresses in the past few years in the elucidation of cannabinoid-opioid interactions in drug abuse and dependence, focusing on recent findings from behavioural studies using different animal models of addiction. Specifically, here we review data on the behavioural aspects (i.e., drug abuse, dependence, tolerance, sensitization, relapse and drug vulnerability) of the specific, often reciprocal, cross-talk between cannabinoids and opioids with particular reference to the role of the endocannabinoid system in opioid addiction. The potential biochemical mechanisms involved in these pharmacological interactions are discussed together with possible therapeutic implications in the pharmacotherapy of opioid dependence. However, individuation of the precise anatomical substrates and molecular mechanisms of such interaction still remains a complex and challenging field for future research.
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PMID:Endocannabinoid system and opioid addiction: behavioural aspects. 1593 59

Opioid receptor, is classified into three subtypes, mu, kappa and delta, with the mu-type receptor plays important roles in opioid analgesia and opioid addiction. The cDNA encoding mu-type receptor was obtained by RT-PCR from human brain RNA and was cloned into pcDNA3.1(+). The resultant recombinant plasmid pcDNAMORs were transfected into CHO cells by liposome. After PCR identification, the positive clone were treated with agonist and antiagonist were tested for their competence of signal transduction. CHO cells that contained mu-opioid receptor in the expression vector pcDNA3.1(+) acquired naloxone-blockable high-affinity specific binding of morphine and DAMGO. The concentration of cAMP in CHO cells transfected with pcDNAMOR was reduced after binding to morphine and DAMGO, and increased after binding naloxone. These results indicate that the mu-type receptor expreesd on the CHO cell has similar biological property as the nature receptor. The availability of these specific cell lines will facilitate the drug development and promote our understanding the mechanism underlying opiate addiction.
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PMID:[Expression of human mu-opioid receptor cDNA in CHO cell]. 1597 8

Contemporary standard pharmacological care for the treatment of noncancer pain includes the use of opioid medications. The responsiveness of neuropathic pain to opioids has long been an area of controversy. Evidence from multiple randomized controlled trials indicates that opioids can relieve pain in a variety of neuropathic pain syndromes. Opioids are typically reserved for moderate to severe pain that cannot be relieved by the nonsteroidal anti-inflammatory drugs (NSAIDs). Opioids are often used in combination with other adjuvants or other analgesic agents. The advantage of opioids is the lack of a ceiling effect of the pure mu opioid agonists. The disadvantages of these drugs are a series of mechanism-based opioids-related side effects (e.g., nausea, drowsiness, constipation) and the potential issue of their abuse and misuse. Each patient needs to undergo a comprehensive evaluation and receive education on the treatment. The physician must be well conversant with the differential diagnosis and definitions of physical dependence, tolerance, pseudotolerance, aberrant behaviors, addiction, and pseudoaddiction. No specific opioid drug is intrinsically ''better'' than the others. Opioid rotation refers to the switch from one opioid to another when the degree of analgesia obtained is limited by the persistence of adverse effects or the occurrence of clinically relevant tolerance. This approach is based on the observation that a patient's response varies from opioid to opioid. At present, after 1) appropriate selection of patients and 2) longitudinal patient care with routine assessment of degree of analgesia, functional daily activities, adverse events and aberrant behaviors is carried out, opioid therapy can be the safest and most effective treatment measure for quality of life improvement in the chronic pain patient.
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PMID:Opioid therapy for chronic noncancer pain: practice guidelines for initiation and maintenance of therapy. 1601 15

The aim of this investigation was to study the effect of the doping steroid nandrolone on metamizol and morphine-induced analgesia and tolerance/dependence in rats. Nandrolone per se did not change the basal nociceptive thresholds in both sexes. It diminished the analgesic effect of metamizol in females, revealed by tail flick test, and males, revealed by paw pressure and hot plate tests. In general, the action of nandrolone was to decrease the morphine-induced analgesia in female and male rats. This was strongly manifested by paw pressure and tail flick tests in male, and tail flick tests in female animals. Nandrolone slowed the development of opioid tolerance/dependence. It aggravated the withdrawal syndrome in the females and invigorated aggression in the males. The data provide evidence that anabolic steroid nandrolone might decrease the analgesic action of metamizol or morphine. The doping steroid could modulate opioid tolerance/dependence and the aggressive behavior in a gender dependent manner. The action of nandrolone is most likely due to profound long-term effects on the central nervous system and might be a gateway to addiction of other drugs of abuse.
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PMID:Nandrolone modulates the non-opioid and opioid analgesia and tolerance/dependence: role of sexual dimorphism. 1602 30

Pain treatment of patients with opioid addiction and tolerance may be challenging due to their unexpectedly higher pain sensitivities and opioid requirements. It has been reported that the N-methyl-D-aspartate receptor is involved in mechanisms of tolerance to opioid analgesics. Recently enhancement of morphine induced analgesia by low dose ketamine addition to the treatment regimen has been reported. We report a cancer patient with meperidine tolerance and psychological dependency to the agent who was afterwards successfully treated with morphine-ketamine combination.
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PMID:Ketamine combined with morphine for the management of cancer pain in a patient with meperidine tolerance and addiction. 1615 42

Pain may become intractable as tolerance develops to opioids and the opioids, paradoxically, induce pain. We examined the hypothesis that the analgesia produced by the novel analgesic and high-efficacy 5-hydroxytryptamine (5-HT)(1A) receptor agonist (3-chloro-4-fluoro-phenyl)-[4-fluoro-4-[[(5-methyl-pyridin-2-ylmethyl)-amino]methyl]piperidin-1-yl]methanone, fumaric acid salt (F 13640) may counteract opioid-induced pain. In studies of the somatosensory quality of pain in infraorbital nerve-injured rats, morphine infusion (5 mg/day) by means of osmotic pumps initially caused analgesia (i.e., decreased the behavioral response to von Frey filament stimulation), followed by hyperallodynia and analgesic tolerance. Infusion of F 13640 (0.63 mg/day) prevented the development of opioid hyperallodynia and reversed opioid hyperallodynia once established. In studies of the affective/motivational quality of pain, F 13640 both prevented and reversed the conditioned place aversion induced by naloxone (0.04 mg/kg i.p.) in morphine-infused rats; F 13640 also prevented and reversed the conditioned place preference induced by morphine injections (7.5 mg/kg i.p.). The data confirm that opioids produce bidirectional hypo- and proalgesic actions, and offer initial evidence that high-efficacy 5-HT(1A) receptor activation counteracts both the sensory and the affective/motivational qualities of opioid-induced pain. The data also indicate that F 13640 may be effective with opioid-resistant pain. It further is suggested that opioid addiction may represent self-therapy of opioid-induced pathological pain.
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PMID:High-efficacy 5-hydroxytryptamine 1A receptor activation counteracts opioid hyperallodynia and affective conditioning. 1625 31

A substantial number of patients with cancer suffer considerable pain at some point during their disease, and approximately 25% of cancer patients die in pain. Providing effective pain management for patients with severe pain that impacts quality of life can present the oncologist or palliative care specialist with complex clinical challenges that often require multifaceted therapeutic measures. This paper presents multidisciplinary consensus-based recommendations for the treatment of intractable cancer pain using intrathecal drug delivery systems, which offer rapid and effective pain relief with less toxicity relative to oral or parenteral administration. Intrathecal drug delivery systems can be highly effective in a variety of patient settings, including cases of refractory pain, diminished performance status, poor tolerability of oral medications, polyanalgesia for complex pain, and inadequate dosing due to addiction concerns. The use of implantable or external systems is discussed, as well as implantation procedures, drug titration recommendations, and management of potential side effects. The authors offer a newly developed algorithm for delivering intraspinal analgesia in patients with cancer. The intent is that increased understanding of available options for truly effective pain management in the oncology and palliative care arena and the benefits of multidisciplinary cooperation will translate into genuine improvements in patient quality of life and a measurable decrease in the number of patients who suffer needlessly in their final days.
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PMID:Intrathecal drug delivery for the management of cancer pain: a multidisciplinary consensus of best clinical practices. 1635 Apr 26

More patients with opioid addiction are receiving opioid agonist therapy (OAT) with methadone and buprenorphine. As a result, physicians will more frequently encounter patients receiving OAT who develop acutely painful conditions, requiring effective treatment strategies. Undertreatment of acute pain is suboptimal medical treatment, and patients receiving long-term OAT are at particular risk. This paper acknowledges the complex interplay among addictive disease, OAT, and acute pain management and describes 4 common misconceptions resulting in suboptimal treatment of acute pain. Clinical recommendations for providing analgesia for patients with acute pain who are receiving OAT are presented. Although challenging, acute pain in patients receiving this type of therapy can effectively be managed.
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PMID:Acute pain management for patients receiving maintenance methadone or buprenorphine therapy. 1641 12

Patients requiring acute pain management may be opioid dependent as a result of either recreational or therapeutic opioid use, including those in opioid addiction programmes. Pain in these patients is often under-estimated and under-treated. In addiction, drug-seeking behaviour differentiates it from simple dependence. With few randomised controlled trials, current evidence predominantly consists of guidelines based on case reports, retrospective studies and expert opinion. Consensus recommendations include maintaining regular provision of the patient's pre-existing opioid requirement, with additional analgesia, ideally multimodal, in appropriate combinations of short-acting opioid (as required), local anaesthesia, and adjuvant anti-inflammatory analgesics and paracetamol. Patient controlled analgesia with higher bolus doses and shorter lock-out intervals is a recommended strategy. Transdermal opioid patches and implantable pumps will continue to deliver opioid, to which non-opioid and short-acting opioids may be added. Re-exposure to opioid is ideally avoided in previously addicted patients, but if not feasible, opioid therapy should be prescribed.
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PMID:Acute pain management for opioid dependent patients. 1692 67


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