Controlled clinical trials in cancer pain. How controlled should they be? A qualitative systematic review

Bell, Rae Frances; Wisløff, Torbjørn; Eccleston, Christopher; Kalso, Eija

doi:10.1038/sj.bjc.6603162

Cited by 21 publications

(21 citation statements)

References 48 publications

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“…Opioids represent the basis of analgesic therapy of CIBP [14][15][16][17][18] despite the lack of controlled clinical trials on the effectiveness of opioids in pain due to bone metastases [19]. There is a large interindividual variability in opioid efficacy.…”

Section: Introductionmentioning

confidence: 99%

Clinical and Genetic Factors Related to Cancer-Induced Bone Pain and Bone Pain Relief

Scarpi

Calistri

Klepstad³

et al. 2014

The Oncologist

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Objective. The study objective was to evaluate whether there are clinical or genetic differences between patients with cancer-induced bone pain (CIBP) and patients with non-CIBP, and, in the CIBP group, in those with good versus poor opioid response. Materials and Methods. A total of 2,294 adult patients with cancer who were receiving opioids for moderate or severe pain were included in the European Pharmacogenetic Opioid Study. Pain intensity and pain relief were measured using the Brief Pain Inventory. Linkage disequilibrium of 112 single nucleotide polymorphisms was evaluated in 25 candidate genes, and 43 haplotypes were assessed. Correlations among demographical factors, disease-related factors, genetic factors, CIBP, and pain relief were analyzed by logistic regression models corrected for multiple testing. Patients with bone metastases and bone/soft tissue pain were defined as having prevalent bone pain (CIBP population).This population was compared with patients who had other types of cancer pain (non-CIBP). Results. A total of 577 patients (26.2%) had CIBP, and 1,624 patients (73.8%) had non-CIBP. Patients with CIBP had more breakthrough cancer pain episodes (64.2% vs. 56.4%, p 5 .001), had significantly higher pain interference in"walkingability in the past 24 hours" (p , .0001), used more adjuvant drugs (84.1% vs. 78.3%, p 5 .003), and had a higher, albeit nonsignificant, median overall survival (3.8 vs. 2.9 months, p 5 .716) than patients with non-CIBP. None of the examined haplotypes exceeded p values corrected for multiple testing for the investigated outcomes. Conclusion. Patients with CIBP who were taking opioids had a clinical profile slightly different from that of the non-CIBP group. However, no specific genetic pattern emerged for CIBP versus non-CIBP or for responsive versus nonresponsive patients with CIBP.

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Section: Introductionmentioning

confidence: 99%

Clinical and Genetic Factors Related to Cancer-Induced Bone Pain and Bone Pain Relief

Scarpi

Calistri

Klepstad³

et al. 2014

The Oncologist

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“…In a methodologic review of trials investigating oral opioids for cancer pain, only one trial had a placebo control, while another trial had a placebo control in the pilot phase of the study [19]. In the first of these trials which investigated the effect of a loading dose of morphine elixir added to the first dose of slow-release morphine tablets, a total of 9 patients were treated with a single dose of placebo, the study duration being 12 hours [20].…”

Section: Opioidsmentioning

confidence: 99%

“…In the second study which was also a cross-over study and included 15 patients, venlafaxine 75 mg gave some pain relief and no significance in adverse effects compared to placebo [37]. [24] and Bell [19]. In addition, searches were performed on PubMed with limits "randomized controlled trial" and search terms "fentanyl AND placebo and cancer" / "methadone AND placebo AND cancer.…”

Section: Antidepressants For Neuropathic Pain With Special Referencementioning

confidence: 99%

Cancer Pain: Analgesics and Co‐Analgesics

Bell

2010

Evidence‐Based Chronic Pain Management

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“…Opioid ligands including morphine are potent analgesics that are widely used for the treatment of severe pain, e.g., cancer progression (1,2). In addition to other serious adverse effects such as respiratory depression and constipation, tolerance and dependence may also disturb the continuation of opioid therapy (3).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of morphine tolerance is mediated by painful stimuli via central mechanisms

et al. 2012

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Tolerance to morphine analgesia following repeated administration disturbs the continuation of opioid therapy for severe pain. Emerging evidence suggests that the development of morphine tolerance may be antagonized by painful stimuli. To clarify the detailed mechanisms of these phenomena, we examined the effects of several pain stimuli on morphine-induced tolerance. Subcutaneous (s.c.) injection of morphine (10 mg/kg) produced an analgesic effect, which was evaluated by tail-pinch test. Morphine-induced analgesia was diminished by repeated administration of morphine (10 mg/kg, s.c.) once a day for 5 days, demonstrating the development of tolerance. Morphine analgesic tolerance was suppressed by nerve injury-induced neuropathic pain and formalin-or carrageenaninduced inflammatory pain. Tolerance to serum corticosterone elevation by morphine (10 mg/kg), which was evaluated by fluorometric assay, was also suppressed by formalin-induced inflammatory pain. Moreover, morphine analgesia induced by intracerebroventricular (10 nmol) or intrathecal (5 nmol) injection was diminished by repeated administration of morphine s.c., and this was also suppressed by carrageenan-induced inflammatory pain. These results suggest that morphine tolerance is inhibited by several pain stimuli, including neuropathic and inflammatory pain, through central mechanisms.

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Controlled clinical trials in cancer pain. How controlled should they be? A qualitative systematic review

Cited by 21 publications

References 48 publications

Clinical and Genetic Factors Related to Cancer-Induced Bone Pain and Bone Pain Relief

Clinical and Genetic Factors Related to Cancer-Induced Bone Pain and Bone Pain Relief

Cancer Pain: Analgesics and Co‐Analgesics

Inhibition of morphine tolerance is mediated by painful stimuli via central mechanisms

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