纤维肌痛综合征

纤维肌痛综合征(fibromyalgia syndromc,FS)是一种以骨骼肌肉慢性弥散性疼痛、僵硬和特定部位压痛点,以及睡眠障碍、疲劳等为特点的综合征。本综合征无明显的滑膜炎或肌炎表现,也无明显实验室或放射学检查异常。80％～90％病例为女性,30～50岁为发病高峰年龄。     

纤维肌痛综合征的中医治疗

纤维肌痛综合征是一种以广泛的肌肉骨骼疼痛为主证的非关节性风湿病,是一种特发性疾病,可继发于外伤、各种风湿病等,本病属中医痹证范畴。其病理生理至今不明,因此对它的治疗方法也不多。目前西医的治疗主要致力于改善睡眠状态、减低痛觉感受器的敏感性、改善肌肉血流等。应用中医理论指导,采用内外治法,临床疗效确切,显示出越来越明显的优势,现将近年来笔者关于本病的中医治疗体会总结如下。     

治疗纤维肌痛的建议

受美国疼痛协会委托，美国的研究者从文献综述中总结发现，药物治疗和非药物治疗的联合应用是治疗纤维肌痛的最佳疗法。     

关键词：纤维肌痛综合征

礼来公司称，美国FDA近日已经批准该公司的重磅炸弹抗抑郁药Cymbalta（duloxetine hydrochloride）用于纤维肌痛综合征的治疗。FDA早先已批准Cymbalta用于抑郁、焦虑及糖尿病性神经痛的治疗，此次批准该药用于纤维肌痛综合征的治疗主要基于两项涉及874名患者，为期3个月的关键性临床研究结果。这些研究结果显示，以BPI24d,时平均疼痛评分量表进行评价，与安慰剂组相比，在研究终点，Cymbalta能够显著减轻患者的疼痛。     

Pfizer公司的Lyrica成为首个获准的纤维肌痛治疗药物

美国FDA批准Pfizer公司的Lyrica（pregabalin）（Ⅰ）用于治疗纤维肌痛，使之成为迄今为止唯一一种治疗这种疼痛障碍的获批药物。     

米那普伦治疗纤维肌痛综合征有效

据美国的研究人员报道，米那普伦（milnacipran）（I）治疗纤维肌痛综合征的“多维症状”有效。     

纤维肌痛：医学专家和患者的完整指南

纤维肌痛是一种严重肌肉骨骼疼痛的疲劳综合征，它困扰了近3～6万的美国人。本书由各行各业保健医生集体共同结晶。而作者Sharon Ostalecki汇集整理各行业医师人员不同观点和视角，从激励个人案例到中肯忠告面面俱到。本书提供了权威性临床咨询和问题解答以帮助患者及家属全面理解处理纤维肌痛的方方面面。作者Ostalecki博士个人专长营养领域，恰恰提醒我们，     

普瑞巴林治疗纤维肌痛综合征的临床疗效研究

目的:探究通过普瑞巴林治疗纤维肌痛综合征的临床应用效果。方法:选取某院收治的确诊为纤维肌痛综合症的患者53名,按照随机原则将其分为两组,即应用塞来昔布及安慰剂治疗的对照组26例与在此基础上加用普瑞巴林的实验组27例。评价两组患者的不良反应发生率、VAS评分、治疗有效率。结果:治疗组通过加用普瑞巴林后在VAS评分、疼痛点数及治疗有效率(24/27,88.92%)方面上明显高于对照组(13/26,50.00%),且经统计学检验,差异明显(P0.05)。结论:临床上应用普瑞巴林对纤维肌痛综合症进行治疗可得到良好的治疗效果,并显著改变疾病伴随的睡眠障碍、晨僵和乏力状况,值得在临床中推广。     

FDA批准第一个用于治疗纤维肌痛的药物

美国食品与药品管理局(FDA)6月21日批准了第一个用于治疗纤维肌痛的药物Lyrica(prega-balin普瑞巴林)。这项批准是基于包括1800例病人的两个双盲对照临床研究的,该研究支持以每日300mg或450mg的Lyrica治疗纤维肌痛。研究表明Lyrica能减轻一些纤维肌痛患者的疼痛并改善其日常生活。Lyrica的批准被认为是一个重大的进步,但是在临床实验中,还是有一些病人在服用Lyrica后并没有好转。Lyrica最常见的副作用包括轻度到中度的眩晕和困倦。临床实验中也有视力障碍,体重增加,口干,手脚浮肿的报导。这些副作用似乎与剂量相关。Lyrica会削弱驾车能…     

Exercise and cognitive-behavioural treatment in fibromyalgia syndrome

Fibromyalgia syndrome is a nonarticular rheumatic disorder characterised by diffuse musculoskeletal pain, stiffness, fatigue, disturbed sleep and tender points. The pathophysiology is not well understood and treatment remains a challenge. Although pharmacological therapy is still the primary treatment choice, a long-term effective intervention has not been demonstrated yet. Thus, besides pharmacotherapy, other multimodal interventions are often used. Exercise and cognitive-behavioural treatments which exist in the multimodal approach and encompass largely self-managed strategy, are reviewed in this article. Although, there is a great number of exercise studies, the large diversity of outcome measures and measurement instruments that have been used in studies, varying intensity and types of exercises, small sample sizes, high attrition rates, large variability in baseline function, symptom severity and psychosocial status limit to come to a conclusion about the efficacy of exercise in the treatment of fibromyalgia syndrome. There are also inconclusive results about the efficacy of cognitive-behavioural treatment because of limited number of studies with small sample sizes of patients with fibromyalgia syndrome. However, the results of the trials overall demonstrate the beneficial effects of both different types of exercise and cognitive-behavioural treatment, on the other hand, there is still a need for larger, more systematic and randomised controlled trials to evaluate the effectiveness.     

Pirlindole in the treatment of depression and fibromyalgia syndrome

Depression and fibromyalgia syndrome are debilitating chronic conditions that impose a significant burden on individuals, families and society. Both depression and fibromyalgia have many overlapping symptoms, and antidepressants of several classes are among recommended treatment options for patients with fibromyalgia syndrome. Pirlindole is a selective and reversible inhibitor of monoamine oxidase (MAO) subtype A (MAO-A) that is approved in some European and non-European countries for the treatment of depression. The antidepressant efficacy and safety of pirlindole have been demonstrated in a number of placebo- and active comparator-controlled studies and are supported by many years of clinical experience in the treatment of depression. The drug's efficacy and safety have also been demonstrated, more recently, in the treatment of fibromyalgia syndrome. Pirlindole has a favourable tolerability profile, with no deleterious effect on cardiovascular dynamics. The effect of pirlindole on sensorimotor performance relevant to driving a motor vehicle is similar to that of placebo, as pirlindole appears to have an activating rather than a sedating antidepressant profile. Because of its specific and reversible inhibition of MAO-A and relatively short elimination half-life, no tyramine or 'cheese' effect is likely after short- or long-term administration. The available evidence supports pirlindole as a safe and effective treatment option for the management of depression and fibromyalgia syndrome.     

Pregabalin for the treatment of fibromyalgia

Introduction: Fibromyalgia (FM) is the most common cause of chronic widespread body pain in humans. Co-morbidities include sleep disturbance, fatigue, impaired physical functioning, altered mood and negative effects on health-related quality of life. Pregabalin inhibits presynaptic release of pronociceptive neurotransmitters in the CNS; this likely underpins its therapeutic benefit in patients with FM.

Areas covered: This review addresses pregabalin pharmacokinetics, efficacy and adverse event (AE) profiles from randomized controlled trials and open-label extension studies in patients with FM. These effects are compared with those of the serotonin norepinephrine reuptake inhibitors, duloxetine and milnacipran that also have FDA approval for the treatment of fibromyalgia.

Expert opinion: At the approved dosages, oral pregabalin has at most a moderate therapeutic benefit above placebo with tolerable side-effects, in no more than 50% of patients with FM. Durability of clinically meaningful (≥ 30%) pain relief in pregabalin-responders has been demonstrated for at least 6-months, but longer-term studies are required as most patients have symptoms for decades. Exclusion of patients with common co-morbidities from the pregabalin RCTs in FM raises questions on the generalizability of the RCT findings to the typical patient seen in clinical practice and so additional investigation is required.     

Pregabalin for the treatment of fibromyalgia

INTRODUCTION: Fibromyalgia (FM) is the most common cause of chronic widespread body pain in humans. Co-morbidities include sleep disturbance, fatigue, impaired physical functioning, altered mood and negative effects on health-related quality of life. Pregabalin inhibits presynaptic release of pronociceptive neurotransmitters in the CNS; this likely underpins its therapeutic benefit in patients with FM. AREAS COVERED: This review addresses pregabalin pharmacokinetics, efficacy and adverse event (AE) profiles from randomized controlled trials and open-label extension studies in patients with FM. These effects are compared with those of the serotonin norepinephrine reuptake inhibitors, duloxetine and milnacipran that also have FDA approval for the treatment of fibromyalgia. EXPERT OPINION: At the approved dosages, oral pregabalin has at most a moderate therapeutic benefit above placebo with tolerable side-effects, in no more than 50% of patients with FM. Durability of clinically meaningful (≥ 30%) pain relief in pregabalin-responders has been demonstrated for at least 6-months, but longer-term studies are required as most patients have symptoms for decades. Exclusion of patients with common co-morbidities from the pregabalin RCTs in FM raises questions on the generalizability of the RCT findings to the typical patient seen in clinical practice and so additional investigation is required.     

Understanding the fibromyalgia syndrome

The fibromyalgia syndrome (FMS) is the most frequent cause of chronic, widespread pain. This review, which is targeted at the psychiatry and psychopharmacology communities, summarizes the state-of-the-art as it relates to both the pathophysiology and treatment of FMS. Toward this end, the anatomy and physiology of pain pathways are summarized, followed by a review of the altered biology of pain processing, neurotransmitter function, and neuroendocrine systems in FMS. The categories of current drugs employed to treat the disorder are detailed, along with a critical review of the literature supporting such use.     

The genetics of fibromyalgia syndrome

Fibromyalgia syndrome (FMS) is a common chronic widespread pain syndrome mainly affecting women. Although the etiology of FMS is not completely understood, varieties of neuroendocrine disturbances, as well as abnormalities of autonomic function, have been implicated in its pathogenesis. The exposure of a genetically predisposed individual to a host of environmental stressors is presumed to lead to the development of FMS. Fibromyalgia overlaps with several related syndromes, collectively compromising the spectrum of the functional somatic disorder. FMS is characterized by a strong familial aggregation. Recent evidence suggests a role for polymorphisms of genes in the serotoninergic, dopaminergic and catecholaminergic systems in the etiopathogenesis of FMS. These polymorphisms are not specific for FMS and are similarly associated with additional comorbid conditions. The mode of inheritance in FMS is unknown, but it is most probably polygenic. Recognition of these gene polymorphisms may help to better subgroup FMS patients and to guide a more rational pharmacological approach. Future genetic studies conducted in larger cohorts of FMS patients and matched control groups may further illuminate the role of genetics in FMS.     

心肾综合征病理生理学机制及临床治疗进展

心肾综合征(CRS)以心肾衰竭、肾功能恶化及利尿剂抵抗为临床特征性表现,但其发病机制至今尚未阐明.本文聚焦肾灌注压降低、神经激素过度激活、一氧化氮(NO)与活性氧族(ROS)之间的失衡,以及管-球反馈异常等,综述近年血管加压素受体拮抗剂及选择性腺苷A1受体拮抗剂等新制剂的临床治疗策略.     

Sodium oxybate for the treatment of fibromyalgia

INTRODUCTION: Gamma-hydroxybutyrate (GHB) is a short-chain fatty acid that is synthesized within the CNS, mostly from its parent compound gamma amino butyric acid (GABA). GHB acts as a neuromodulator/neurotransmitter to affect neuronal activity of other neurotransmitters and so, stimulate the release of growth hormone. Its sodium salt (sodium oxybate: SXB) was approved by the Food and Drug Administration (FDA) for the treatment of narcolepsy. SXB has shown to improve disrupted sleep and increase NR3 (slow-wave restorative) sleep in patients with narcolepsy. It is rapidly absorbed and has a plasma half-life of 30 - 60 min, necessitating twice-nightly dosing. Most of the observed effects of SXB result from binding to GABA-B receptors. AREAS COVERED: Several randomized, controlled trials demonstrated significantly improved fibromyalgia (FM) symptoms with SXB. As seen in narcolepsy trials, SXB improved sleep of FM patients, increased slow-wave sleep duration as well as delta power, and reduced frequent night-time awakenings. Furthermore, FM pain and fatigue was consistently reduced with nightly SXB over time. Commonly reported adverse events included headache, nausea, dizziness and somnolence. Despite its proven efficacy, SXB did not receive FDA approval for the management of FM in 2010, mostly because of concerns about abuse. EXPERT OPINION: Insomnia, fatigue and pain are important clinical FM symptoms that showed moderate improvements with SXB in several large, well-designed clinical trials. Because of the limited efficacy of currently available FM drugs additional treatment options are needed. In particular, drugs like SXB - which belong to a different drug class than other Food and Drug Administration (FDA)-approved FM medications such as pregabalin, duloxetine and milnacipran - would provide a much-needed addition to presently available treatment options. However, the FDA has set the bar high for future SXB re-submissions, with requirements of superior efficacy and improved risk mitigation strategies. At this time, no future FDA submission of SXB for the fibromyalgia indication is planned.     

Sodium oxybate for the treatment of fibromyalgia

Introduction: Gamma-hydroxybutyrate (GHB) is a short-chain fatty acid that is synthesized within the CNS, mostly from its parent compound gamma amino butyric acid (GABA). GHB acts as a neuromodulator/neurotransmitter to affect neuronal activity of other neurotransmitters and so, stimulate the release of growth hormone. Its sodium salt (sodium oxybate: SXB) was approved by the Food and Drug Administration (FDA) for the treatment of narcolepsy. SXB has shown to improve disrupted sleep and increase NR3 (slow-wave restorative) sleep in patients with narcolepsy. It is rapidly absorbed and has a plasma half-life of 30 – 60 min, necessitating twice-nightly dosing. Most of the observed effects of SXB result from binding to GABA-B receptors.

Areas covered: Several randomized, controlled trials demonstrated significantly improved fibromyalgia (FM) symptoms with SXB. As seen in narcolepsy trials, SXB improved sleep of FM patients, increased slow-wave sleep duration as well as delta power, and reduced frequent night-time awakenings. Furthermore, FM pain and fatigue was consistently reduced with nightly SXB over time. Commonly reported adverse events included headache, nausea, dizziness and somnolence. Despite its proven efficacy, SXB did not receive FDA approval for the management of FM in 2010, mostly because of concerns about abuse.

Expert opinion: Insomnia, fatigue and pain are important clinical FM symptoms that showed moderate improvements with SXB in several large, well-designed clinical trials. Because of the limited efficacy of currently available FM drugs additional treatment options are needed. In particular, drugs like SXB – which belong to a different drug class than other Food and Drug Administration (FDA)-approved FM medications such as pregabalin, duloxetine and milnacipran – would provide a much-needed addition to presently available treatment options. However, the FDA has set the bar high for future SXB re-submissions, with requirements of superior efficacy and improved risk mitigation strategies. At this time, no future FDA submission of SXB for the fibromyalgia indication is planned.     

Pregabalin--a neuromodulator for the treatment of neuropathic pain, generalized anxiety disorders and fibromyalgia syndrome

Synthesized in 1990 as an anticonvulsant agent, pregabalin was designed as a lipophilic gamma-aminobutyric acid (GABA) analog substituted at the 3'-position in order to facilitate diffusion across the blood-brain barrier. It is an alpha2delta1 ligand that binds to, and modulates, voltage-gated calcium channels. This modulation is characterized by a reduction of the excessive neurotransmitter release that is observed in certain neurologic and psychotic disorders. Pregabalin has analgetic, anticonvulsant, and anxiolytic activity and has demonstrated efficacy in the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, and as adjuvant therapy for adult patients with partial onset seizures. Pregabalin was significantly more effective than placebo for the treatment of generalized anxiety disorder as well as of fibromyalgia and was well tolerated by most of the patients.