Wilkes Scott
Centre for Primary and Community Care, School of Health, Natural & Social Sciences, University of Sunderland, Sunderland, UK.
Drugs Today (Barc). 2006 Oct;42(10):671-81. doi: 10.1358/dot.2006.42.10.1025701.
Bupropion was initially developed and licensed for the treatment of major depressive disorder in the United States in 1989. It was licensed as a pharmacotherapy for smoking cessation in the United States in 1997 and in the United Kingdom in 2000, and for the prevention of seasonal major depressive episodes in patients with seasonal affective disorder in the United States in 2006. Its main mechanism of action is believed to be via dopamine and noradrenalin reuptake inhibition. In addition to proven clinical efficacy for the treatment of major depression, the prevention of depressive episodes in patients with seasonal affective disorder, and as an aid to smoking cessation treatment, bupropion has demonstrated efficacy for attenuation of symptoms of attention deficit hyperactivity disorder, and more recently it has shown anti-inflammatory action against proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), which may be implicated in a number of inflammatory diseases such as Crohn's disease. The twice-daily sustained-release formulation has been extensively evaluated for smoking cessation and has shown continuous smoking abstinence rates at one year of the order of 20% across many clinical groups including healthy smokers, and smokers with cardiovascular disease, chronic obstructive airways disease, depression and schizophrenia. Bupropion is well tolerated with side effects including insomnia, headache, dry mouth, dizziness and nausea. Bupropion is a cytochrome p450 2D6 inhibitor and care must be taken when coprescribing with drugs cleared by this enzyme and when coprescribing with drugs that lower seizure threshold. Despite the clinical effectiveness and cost-effectiveness of bupropion as an aid to smoking cessation, its uptake for this indication remains low when compared with nicotine replacement therapy.
安非他酮最初于1989年在美国研发并获批用于治疗重度抑郁症。1997年在美国、2000年在英国获批作为戒烟的药物疗法，2006年在美国获批用于预防季节性情感障碍患者的季节性重度抑郁发作。其主要作用机制据信是通过抑制多巴胺和去甲肾上腺素的再摄取。除了在治疗重度抑郁症、预防季节性情感障碍患者的抑郁发作以及辅助戒烟治疗方面已证实的临床疗效外，安非他酮还在减轻注意力缺陷多动障碍症状方面显示出疗效，最近还表现出对促炎细胞因子如肿瘤坏死因子-α（TNF-α）的抗炎作用，TNF-α可能与包括克罗恩病在内的多种炎症性疾病有关。每日两次的缓释制剂已针对戒烟进行了广泛评估，在包括健康吸烟者、患有心血管疾病、慢性阻塞性气道疾病、抑郁症和精神分裂症的吸烟者在内的许多临床组中，一年的持续戒烟率约为20%。安非他酮耐受性良好，副作用包括失眠、头痛、口干、头晕和恶心。安非他酮是一种细胞色素P450 2D6抑制剂，与经该酶清除的药物合用时以及与降低癫痫阈值的药物合用时必须谨慎。尽管安非他酮作为辅助戒烟药物具有临床有效性和成本效益，但与尼古丁替代疗法相比，其在这一适应症上的使用率仍然较低。
