Pregabalin Is Effective in Reducing Fibromyalgia Pain - Health Resource International West Africa (HRI)

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Wednesday, 24 May 2017

Pregabalin Is Effective in Reducing Fibromyalgia Pain


Charles Argoff
Evid Based Med. 2017;22(2):70-71. 



Context
Anticonvulsants have been widely used in pain management for more than 50 years. Published neuropathic pain treatment
guidelines have suggested their use, especially for neuropathic pain.[1] The review by Derry et al focuses on the use of one such agent, pregabalin, in the treatment of fibromyalgia, an accepted and validated but heterogeneous condition in which diagnosis is made through history, physical examination and the exclusion of other diseases explaining the key symptoms.
Methods
This was a systematic review of randomised, double-blind trials lasting 8 weeks or longer comparing either pregabalin to placebo or an active treatment for the treatment of pain in fibromyalgia. The Cochrane Central Register of Controlled Trials, MEDLINE and EMBASE were search for randomised controlled trials from inception to 16 March 2016 for this update. Reference lists of retrieved studies and reviews were also searched, and online clinical trial registries. Eight studies were included in this review and none of the included studies involved an active comparator. It is important to note that this systematic review and meta-analysis does not comment on how the diagnosis of fibromyalgia was made in the studies included.

Findings
More people using pregabalin 300–600 mg daily compared with placebo achieved either 30% or 50% pain intensity reduction on the Patient Global Impression of Change scale. Nine per cent more patients using pregabalin 300–600 mg/day compared with placebo achieved at least 50% pain reduction and 11% more patients using similar doses of pregabalin achieved at least 30% pain reduction. The majority of participants in each treatment group experienced adverse effects (70–90%), with dizziness (38%), somnolence (23%), weight gain (9%) and peripheral oedema (8%) occurring most frequently. The authors concluded that the magnitude of benefit of pregabalin is similar to minalcipran and duloxetine, two other medications used to treat fibromyalgia.

Comments
The authors note that fibromyalgia is a heterogeneous condition and that the use of pregabalin is associated with a major reduction in pain intensity for only a small proportion of people. There is no attempt in the review to identify subpopulations of patients with fibromyalgia that may be more or less responsive to treatment with pregabalin. While the authors noted that 'recent research points at small fibre pathology in a subgroup of fibromyalgia patients that may be of pathophysiological importance', the authors in the same sentence continue, 'though this is regarded as speculative'. The authors cite two references to support the presence of small fibre pathology in patients previously diagnosed with fibromyalgia according to the 2010 ACR criteria; however, quite shockingly, do not cite any references to support that these findings derived from formal analysis are speculative. In fact, in Oaklander et al's[2]study, 27 patients with fibromyalgia were compared with 30 controls, and 41% of patients fibromyalgia compared with 3% of controls, demonstrated skin biopsy findings (intraepidermal skin fibre density reduction) consistent with the diagnosis of small fibre polyneuropathy (SFPN). In Üçeyler et al's[3] study, more patients with fibromyalgia compared with depressed or control patients had demonstrated SFPN changes based on a number of assessments, including skin biopsy. One should not describe these observations as speculative, and therefore, the authors of this Cochrane review demonstrate bias in using the term speculative when the data suggest otherwise. The authors would have been correct in stating that no reviewed study documented a subgroup analysis based on the presence or absence of skin biopsy findings consistent with SFPN. The published results from two studies that SFPN is prevalent in patients diagnosed with fibromyalgia is not speculative; instead, it should call into question just how appropriate the diagnosis of fibromyalgia is in such patients. That key point is missing from this review and significantly limits its clinical relevance and integrity

Implications for Practice
Evidence-based medicine has been described as the 'conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence-based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research'.[4] This review departs from these foundations of evidence-based medicine not only by relying on population-based studies only in arriving at their conclusions for clinicians, but also by the authors' dismissal of the results noted in studies that they referenced, of a significant prevalence of SFPN in patients previously diagnosed with fibromyalgia. This dismissal is at odds with how they define fibromyalgia in their 'description of the condition'. Such dismissal does not assist those in practice to best understand their patient's condition(s) and could impair their ability to make important treatment decisions about individual patients. Instead, practicing clinicians, academic clinicians and other academicians who conduct clinical trials only should all, in an unbiased manner, integrate the data regarding the prevalence of SFPN in patients who meet the 2010 American College of Rheumatology criteria for fibromyalgia into their assessment, treatment and investigational approaches to the patients who they are evaluating for fibromyalgia. While there is currently a dearth of published meaningful clinical trials regarding the treatment of SFPN, future efforts need to embrace, not hide, the need to precisely define patient populations so that the information gained from the results of future trials can truly be applied to the patients who we treat in our daily practice.

References
1.   O'Connor AB, Dworkin RH. Treatment of neuropathic pain: an overview of recent guidelines. Am J Med 2009;122(Suppl 10):S22–32.
2.   Oaklander AL, Herzog ZD, Downs HM, et al. Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia. Pain 2013;154:2310–6.
3.   Üçeyler N, Zeller D, Kahn AK, et al. Small fibre pathology in patients with fibromyalgia syndrome. Brain 2013;136(Pt 6):1857–67.

4.   Sackett DL, Rosenberg WM, Gray JA, et al. Evidence based medicine: what it is and what it isn't. BMJ 1996;312:71–2.''

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