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Chronic Opioid Therapy for Non-Cancer Pain: An Evidence Based Look at the IssueJane C. Ballantyne, M.D. Boston, Massachusetts
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Introduction
Our question is whether the evidence available in the medical literature supports long-term opioid therapy for thetreatment of non-cancer or non-terminal pain. Is the therapy efficacious, and does its efficacy outweigh itsliabilities? A real difficulty is the lack of agreement in the medical profession and society at large as to what are thedesired outcomes – good pain control, improved function or improved quality of life; and what liabilities areacceptable – particularly whether the risk of addiction is acceptable.
Efficacy
Short-term analgesic efficacy
Randomized trials (RCTs) have been conducted to test the analgesic efficacy of opioids for various chronic painconditions, including the arthritides and various neuropathic pain conditions. Table 1 lists these trials andsummarizes their results.
1-18
 
Measured pain scales from the RCTs show a statistically significant improvementacross all the studies, both in case of painful arthritides and neuropathic pain. The question underlying the trials waswhether chronic pain conditions, particularly neuropathic pain conditions, are opioid responsive. (There had been atraditionally held view that neuropathic pain is not opioid responsive). The randomized studies make it clear thatcontrary to this traditional belief, neuropathic pain is indeed opioid responsive, although larger doses are requiredthan those needed to treat nociceptive pain.
7,11,14-19
It must be noted that these trials are conducted only over theshort term (usually weeks, although one trial reached 32 weeks),
5,20
and that doses used in these trials are generallymoderate (up to 180 mg morphine or morphine equivalent per day).
 Long-term analgesic efficacy
The real question, however, when embarking on a course of opioid treatment for chronic pain, is whether analgesicefficacy is maintained over time. Here we need to turn to less rigorous forms of evidence, since it is not feasible toconduct RCTs over prolonged periods. The only knowledge of long-term analgesic efficacy comes from surveys,case series and open-label follow-up studies in association with some RCTs.
20-22
These report satisfactory analgesiafor all patients who stay on the treatment. A review of the open-label follow-up studies, however, has shown that56% of patients abandon the treatment because of lack of efficacy or side-effects.
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Moreover, many opioid trialsutilize enrichment in their protocols (patients who do not respond are selected out during a pre-trial phase), and thereis an unusually high drop-out rate across opioid trials during enrichment, likely reducing the internal validity of thetrials.
23
Overall, the evidence supporting long-term analgesic efficacy is weak.Treatment in the long-term studies has been based on the traditional premise that dosage should be titrated upwardsto overcome pharmacological tolerance, this being an inevitable consequence of long-term opioid treatment. In fact,the majority of patients are able to reach a stable, non-escalating effective dose, and analgesic tolerance seems tostabilize over time. Some patients, however, fail dose escalation, reporting no change or a worsening of their pain,despite high doses of opioids.
24,25
Some report actual improvement in pain once opioid treatment is discontinued.
26,27
The putative mechanisms for failed opioid analgesia may be related to rampant tolerance or opioid-inducedhyperalgesia.
24
Advances in basic science help understand these phenomena and their clinical relevance, but itremains unclear exactly what aspects of treatment – drug choice, dose or timing – cause these phenomena tocompromise opioid efficacy. The premise that tolerance can always be overcome by dose escalation is nowquestioned.
20
 
 Function and quality of life
Whether long-term opioid treatment can improve patients’ function or quality of life (QOL) is clearly a broader issue than whether opioids can reduce a pain score. Surprisingly, only a few of the existing opioid studies havefocused on this issue, and there are few available data. Several case series report on function, and these consistentlyreport improvement, although the quality of this type of evidence must be questioned.
28
Epidemiological studies areless positive, and report failure of opioids to improve QOL in chronic pain patients.
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The RCTs provide mixedresults on function (Table 1); some find improvement, others do not. The focus of the functional testing in studiesvaries with the primary interest of the investigators – for example, physical function, joint tenderness, activity levelsand grip strength for arthritis patients, sleep, anxiety, psychomotor function and disability scores for back pain patients. This variability precludes an overall assessment. Moreover, RCTs are only able to assess short-termfunctional achievements. Studies specifically assessing cognitive function, including the ability to drive and operatemachinery, find that cognitive function, manual dexterity and reaction times are maintained provided a stable dose
 
 315Page 2of opioid is used.
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This is not true when the dosing is irregular or escalates.
30,35,36
This becomes an importantissue if the goal of treatment is to return to work and to full functioning.
Table 1 Controlled Studies: Summary of results
CR = controlled release. Study drugs not labeled CR were immediate-release preparations.A plus sign denotes a statistically significant positive difference, and 0 no statistically significant difference.Where two numbers are given, the first is the number of patients in the experimental group, the second is the number in the control group.Parentheses link treatment with outcome when more than two treatment groups are included in the study.
 
Reference StudytypeType of pain n/N Drug Daily dose(mg)Follow-upPainRelief Level of Function
Kjaersgaard-Andersen 90RCT Osteoarthritis of the hip, in elderly patients83/75 Codeine withacetaminophen vs.acetaminophen180 4weeks+Moran 91 RCT,crossover Rheumatoidarthritis20 CR morphine vs. placeboup to 120 10weeks+ 0Arkinstall 95 RCT Musculoskeletal inmost patients46 CR codeine vs. placebo 200-400 1 week + +Moulin 96 RCT,crossover Musculoskeletal or soft tissue46 CR morphine vs. active placebo (benztropine)up to 120 11weeks+ 0Jamison 98 RCT Back pain 24/12 Oxycodone or CR morphine plusoxycodone vs. naproxenUp to 130(morphineequivalent)16-32weeks+ +Sheather-Reid 98RCT,crossover Cervicobrachialsyndrome,fibromylagia6 Codeine vs. ibuprofenor placebo120 12weeks0 0Watson 98 RCT,crossover Postherpeticneuralgia38 CR oxycodone vs. placebo28-62 8weeks+ +Caldwell 99 RCT Osteoarthritis 71/36 CR oxycodone or oxycodone withacetaminophen vs. placeboup to 60 8weeks+ +Peloso 00 RCT Osteoarthritis hipand knee31/35 CR codeine vs. placebo up to 400 4weeks+ +Roth 00 RCT Osteoarthritis 44/(44)/45 CR oxycodone, highdose (or low dose) vs. placeboup to 40 14weeks+ (0) + (0)Huse 01 RCT,crossover Phantom limb pain 12/12 CR morphine vs. placebo70-160 (300 inone patient)4weeks+ 0Caldwell 02 RCT Osteoarthritis 73/73/76/73CR morphine (24 hr) or CR morphine (12 hr) vs. placebo30 4weeks+ 0Maier 02 RCT,crossover Mixed 49 CR morphine vs. placeboup to 180 2weeks+ +Raja 02 RCT,crossover Postherpeticneuralgia76/44 CR morphine or methadone vs. placebo(or tricyclicantidepressant)15-225morphine, 40-140 methadone8-24weeks+ (0) 0Gimbel 03 RCT Diabeticneuropathy63/52 CR oxycodone vs. placebo20-120 6weeks+ +Morley 03 RCT,crossover Mixed neuropathic 11/(18) Methadone high dose(or low dose) vs. placebo20 (10) 20 days + (0)Rowbotham03RCT Peripheral andcentralneuropathic pain43/38 High-dose levorphanolvs. low-doselevorphanolup to 11.8(approximately60 morphineequivalent)8weeks+ 0Watson 03 RCT,crossover Diabeticneuropathy35/36 CR oxycodone vs.active placebo(benztropine)10-40 4weeks+ +
 
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Liabilities
 Hormonal and immune effects
Long-term opioid therapy results in clinically relevant suppression of both hypothalamopituitary -adrenal and -gonadal axes with suppression in testosterone, estrogen, and cortisol, resulting in male and female infertility,decreased libido, aggression and drive, and galactorrhea. These effects have been demonstrated in past addictstreated with methadone maintenance,
37
as well as in opioid-treated chronic pain patients.
38
Clinically, testosteronedeficiency is the most frequently manifest of the deficiencies, and male patients can benefit from testosteronereplacement.
39,40
The effects are exaggerated when opioids are delivered intrathecally.
40-42
 Preclinical research convincingly demonstrates that opioids alter the development, differentiation and function of immune cells.
43,44
Immune modulation is complex, and pain as well as opioids can suppress immune function.
45
 Whether or not opioids have a deleterious effect on immune function, and in what circumstances is unclear, although prolonged exposure and abrupt withdrawal have both been implicated in animal studies.
46
 
 Addiction
Perhaps it is not surprising that we currently have no satisfactory definition or criteria for addiction arising in patients receiving therapeutic opioids, considering that the currently accepted definition of 
 substance dependence
(or 
drug addiction)
was arrived at only after decades of debate.
47
This lack of a widely accepted definition makes it hardto determine rates of iatrogenic addiction.The criteria for substance abuse listed in the DSM-IV manual include tolerance, physical dependence and 5 further criteria that are behaviors associated with illicit drug use, and not relevant in the case of therapeutic opioid use.Behaviors that are considered typical of “problematic opioid use” are nuisance behaviors that annoy the prescribing physician and clinic staff (eg repeated lost prescriptions), but because they are not associated with illicit drug use, donot appear similar to DSM-IV criteria. These “nuisance” behaviors could be the result of a chaotic lifestyle,uncontrolled pain or fear of withdrawal, and have never formally been accepted as signs of addiction. To makematters worse, tolerance (a pharmacological phenomenon resulting in the need for dose escalation to achieve thesame effect) and physical dependence (a state of adaptation that results in a withdrawal when drug is stopped) areinevitable consequences of chronic opioid use, and therefore not considered criteria for abuse or addiction duringopioid therapy. A consensus document from American pain and addiction societies lists the following addictioncriteria: impaired control over drug use, compulsive use, continued use despite harm, and craving.
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Yet in theclinic setting, these are likely to be manifest as the “nuisance” behaviors described above, and hard to distinguishfrom other factors driving such behaviors. All in all, we are faced with real difficulties both defining andrecognizing addiction in opioid treated patients, and in assessing risk.At the start of the movement towards broadening opioid therapy to reach those with chronic non-cancer and non-terminal pain, addiction rates were considered to be very low. A key paper reporting hospital rates of addiction wastaken out of context and widely used to support an extremely low rate of addiction (0.03%).
49
More realistically,Portenoy and Foley, in a sentinel paper describing opioid therapy for non-cancer pain, reported rates of addiction of 5%.
50
Rates of this order were widely accepted, despite the weak level of evidence. Controlled studies made noattempt to evaluate addiction. After a decade or more of acceptance that therapeutic opioid use was unlikely toresult in addiction, the medical community began to question the supposed low rates of addiction because of a perceived increase in the number of problematic patients, and because of the documented increase in prescriptiondrug abuse.
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A systematic review published in 1992 reporting addiction rates of up to 18.9%,
52
failed to penetratethe vast number of educational materials that were used during the 1990s to persuade the medical community thataddiction was extremely rare during the treatment of pain. Yet today, when we are justifiably more concerned, thishigher rate has become widely accepted. Whatever figure we believe or accept, the true incidence of addiction inopioid treated chronic pain patients is unknown.
Summary of the evidence
Despite the existence of several RCTs assessing opioid therapy for chronic non-cancer and non-terminal pain,research questions regarding the therapy remain unanswered. The RCTs do not assess the use of high doses (higher than 180 mg morphine per day), or the use of prolonged treatment (extending beyond 32 weeks). Moreover, patientsin RCTs are likely to be a biased sample, not reflecting the normal population of patients seeking opioid treatment of  pain, many of whom will not accept possible randomization to a placebo. We can claim that opioids provide goodshort-term efficacy for chronic non-cancer pain, including neuropathic pain. Although many physician-reporters
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