Journal of pain and symptom management
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Oxycodone has been in clinical use since 1917. Parenteral oxycodone was used mainly for the treatment of acute postoperative pain whereas combinations, for example, oxycodone and acetaminophen, were used for moderate pain. Since the introduction of controlled-release oxycodone, it has been used to manage cancer-related pain and chronic non-cancer-related pain problems. ⋯ The pharmacodynamic effects of oxycodone are typical of a mu-opioid agonist. Oxycodone closely resembles morphine but it has some distinct differences, particularly in its pharmacokinetic profile. Being an old drug, the basic pharmacology of oxycodone has been a neglected field of research.
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J Pain Symptom Manage · May 2005
ReviewCancer pain assessment in clinical trials. A review of the literature (1999-2002).
The aim of this review was to evaluate the methods of pain measurement in controlled clinical trials in oncology published between 1999 and 2002. An electronic literature search strategy was used according to established criteria applied to the Medline database and PubMed search engine. Articles were selected to include only studies that had chronic cancer pain as the primary or secondary objective of a controlled clinical trial. ⋯ Statistical techniques were seldom appropriate to the type of data collected and often inadequate to describe the pain variable under study. It is clear from this review that most authors were aware of the need of valid pain measurement tools to be used in clinical trials. However, too often these tools were not appropriately used in the trial, or at least their use was not described with sufficient accuracy in the trial methods.
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The metabolism of opioids closely relates to their chemical structure. Opioids are subject to O-dealkylation, N-dealkylation, ketoreduction, or deacetylation leading to phase-I metabolites. By glucuronidation or sulfatation, phase-II metabolites are formed. ⋯ By this, it may play an important role in the clinical effects of morphine. Several other opioids, such as meperidine and perhaps also morphine and hydromorphone, produce metabolites with neuroexcitatory effects. In sum, the evidence suggests that the metabolites of several opioids account for an important part of the clinical effects that must be considered in clinical practice.
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Hydromorphone is a semi-synthetic opioid that has been used widely for acute pain, chronic cancer pain and to a lesser extent, in chronic nonmalignant pain. Its pharmacokinetics and pharmacodynamics have been well studied, including immediate release oral preparations, a variety of slow release oral preparations, as well as administration through intravenous, subcutaneous, epidural, intrathecal and other routes. ⋯ There is no evidence that hydromorphone has any greater abuse liability than other opioids. Further research is needed to address remaining areas of uncertainty: equianalgesic ratios; relative risk of toxicity compared with other opioids, its use in nonmalignant pain, and the role of specific hydromorophone metabolites in the development of toxicity, particularly in association with organ failure.
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Pain is the cancer-related event that is most disruptive to the cancer patient's quality of life. Although bone cancer pain is one of the most severe and common of the chronic pains that accompany breast, prostate, and lung cancers, relatively little is known about the mechanisms that generate and maintain this pain. Recently, we developed a mouse model of bone cancer pain. ⋯ Humans suffering from bone cancer pain generally require significantly higher doses of morphine as compared to individuals with inflammatory pain and in the mouse model the doses of morphine required to block bone cancer pain-related behaviors were 10 times that required to block peak inflammatory pain behaviors of comparable magnitude induced by hindpaw injection of complete Freund's adjuvant (CFA; 1-3 mg/kg). As these animals were treated acutely, there was not time for morphine tolerance to develop and the rightward shift in analgesic efficacy observed in bone cancer pain versus inflammatory pain suggests a fundamental difference in the underlying mechanisms that generate bone cancer versus inflammatory pain. These results indicate that this model will be useful in defining drug therapies that are targeted for complex bone cancer pain syndromes.