1813 01 REUMA3 Editoriale - ME/CFS Australia

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52 P. Sarzi-Puttini et al.A larger RCT (n=69) reported decreased visualanalogue pain scores, improved pain relief and decreasedpain threshold after tramadol treatment.Another study compared a combination of 37.5 mgtramadol/325 mg acetaminophen tablets withplacebo in 315 patients with FM. Pain and physicalfunctioning improved significantly in the tramadol/acetaminophen-treatedsubjects. The averagedose of tramadol/acetaminophen was 4.0±1.8tablets per day with an attrition rate of 19% (n=29)due to adverse events. The attrition rate in theplacebo-treated subjects was 12% (n=18). Thisstudy suggested that the combination of tramadol/acetaminophenwas effective in treating FMpatients’ pain without causing serious adverseevents (17).Bennett et al. (18) examined efficacy data to comparethe impact of tramadol/acetaminophen versusplacebo on quality of life; the authors concluded thatmoderate-to-severe fibromyalgia pain significantlyimpairs health-related quality of life (HRQOL) inplacebo-treated patients.A recent study has demonstrated that transdermalbuprenorphine, a strong opioid, has beneficial effectson severe widespread pain (VAS >6/10), butit is less effective on other symptoms that are typicalof the disease (19).FM that is diagnosed according to the ACR criteriaseems to include patients with different painprocessing mechanisms. Screening for disordersthat may initiate or exacerbate symptoms of FM iscritical; if comorbid disorders are not identifiedearly and treated appropriately, therapies that targetFM, only, may be ineffective.In fact, there is a subset of FM patients that do notrespond to opioids, while other patients, who mayhave overlapping conditions such as diabetes,chronic myofascial pain, temporomandibular jointdisorder, arthritis, degenerative disc disease andother diseases, may benefit quite significantly fromopioids (8, 18).Physicians should obtain a careful medical and psychologicalprofile of the patient before prescribingopioids (17, 18). Therapy with these drugs shouldbe initiated after an adequate trial of acetaminophenfor nociceptive pain and of tricyclic antidepressantsor anticonvulsants.To obtain a synergistic effect on analgesia, somepatients may be prescribed combinations of differentpain relievers (multimodal analgesia) with differenteffects on pain pathways, but not for managingside effects. Patients should be asked to giveinformed consent for treatment; even though it isnot necessary for legal purposes, it would help toeducate patients and give them a sense of responsibility(18).It is appropriate to increase doses of immediate-releaseopioids slowly until pain reduction isachieved and then switch patients to controlled-releaseopioids, considering that most patients withchronic, non-malignant pain can be managed with
Fibromyalgia syndrome: the pharmacological treatment options 53be considered as a systemic disease that is relatednot only to neurotransmission imbalance, but alsoto other neurotrophic, neurosteroidal, CNS hormonalmodifications and diffuse, autonomic, immunologic,and metabolic somatic changes (8, 21).According to this hypothesis, antidepressants restoreneurotransmitter levels and modulate receptorexpression in the hypothalamus, which normalizeshyperactivity of the hypothalamic-pituitary-adrenal(HPA) axis (18, 1). An over-activationof the HPA axis is observed in depression and inchronic stress, both of which are frequently presentin patients with long-term pain disorders. Conversely,the response to stress is considered to playa crucial role in the pathogenesis of several syndromes,such as FM, chronic fatigue syndrome andirritable bowel syndrome (22, 23). Similarly, autonomicsystem alterations, such as sympatheticoveractivity, are present in both depression and FM(21). Finally, pro-inflammatory cytokines withinthe CNS play a role in the pathophysiology ofmood disorders (and pain), and modulating thesecytokines via chronic antidepressant treatment contributeto improve depression (and pain) (24).Several studies reported high frequency of mooddisorders in FM patients (25, 26) compared to controls(27). Short-term clinical studies have shownefficacy for antidepressants in the treatment of FM(28).Abnormalities in central monoaminergic neurotransmissionthat are observed in depression mightplay a role in FM pathophysiology because dysfunctionof 5-HT– and NE-mediated descendingpain-inhibitory pathways is an important mechanismrelated to the pain experienced by FM patients.Antidepressants that increase 5-HT and NEmediatedneurotransmission are commonly used totreat FM and other chronic pain conditions, particularlyneuropathic pain. Inhibition of both the 5-HTand NE reuptake transporters using tricyclic antidepressants(TCA) or SNRIs (serotonergic and noradrenergicreuptake inhibitors), seems more effectivein treating pain, and FM, in general, than inhibitionof either transporter alone using selectiveserotonergic (SSRIs) or noradrenergic (NARIs) reuptakeinhibitors (29-31).However, the efficacy of TCAs is counterbalancedby side effects (32, 33), while the better-toleratedSSRIs demonstrate less effectiveness in treating fibromyalgia(34-37).Antidepressants acting both on NE and 5HT inducea contextual increase of the endogenous opioidsystem response that raises the pain thresholdat the periacqueductal level and increases the gatecontrol of nociception at the spinal cord level (38).Antidepressants usually produce a fast, direct analgesiceffect (on opioid, enkephalinergic, substanceP) that is independent of mood state; it first appearsafter a few hours and can be achieved withlow doses.After a longer period of 2-3 weeks, a more robustanalgesic effect develops when antidepressantshave a more profound influence on mood and anxiety,and the affective and cognitive components ofpain become regulated. This effect can only be producedwith full doses that are easier to achieve withthe new generation of antidepressants, such as SS-RIs and SNRIs (39, 40).Concerning the use of antidepressants in fibromyalgia,Perrot and colleagues (41) identifiedforty-nine publications on the use of antidepressantsto treat painful rheumatologic conditions (including37 studies and 12 meta-analyses) that wereconsidered valid and used to develop the followingconsiderations: the analgesic effect is higher forTCAs than SSRIs; clear evidence concerning doseresponsedoes not exist; the onset of action occurswithin a week; the route of administration is oral;and side effects are more prevalent in TCAs thanSSRIs. Unfortunately, this review included studiesTable I - Summary of the controlled studies of dual reuptake inhibitors (SNRI).Authors References Drug N. Pts Weeks Dose Outc. ResultsArnold, 2004 43 DUL vs PLA 207 12 120 FIQ DUL > PLARussell, 2008 44 DUL vs PLA 520 24 20-120 BPIPGIDUL > PLAVitton et al., 2005 45 MIL vs PLA 125 4 200 PGIFIQMIL > PLAArnold, 2005 46 DUL > PLA 354 12 60-120 BPI DUL > PLAVLF = venlafaxine; DUL = duloxetine; MIL = milnacipran; dose in mg/day; outc. = outcome measures: VAS = Visual Analog Scale; FIQ = Fibromyalgia Impact Questionnaire;
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