Advancements in the Clinical Use of Antidepressants for Adolescent Depression
-
摘要: 青少年抑郁症患者相较于成年抑郁症患者,具有更高的发病率、较差的生活质量和治疗效果。国际指南普遍推荐轻度青少年抑郁症优先考虑心理治疗,对于中重度患者,抗抑郁药物联合心理治疗是1种可行的选择,如何选择适合的抗抑郁药物仍然是待解决的难题。抗抑郁药物存在一系列副作用,包括睡眠障碍、锥体外系反应和消化道反应等,为了减轻这些副作用并提高临床疗效,个体化的治疗方案至关重要。总结了青少年抑郁症的发病机制、抗抑郁药物的药代动力学和副作用,以及2013~2023年针对青少年抑郁症患者的用药指南,并针对青少年抑郁症患者药物治疗方案提出科学建议。Abstract: Compared with adult patients with depression, adolescents with depression have a higher incidence rate, poorer quality of life and poorer treatment effects. International guidelines generally recommend giving priority to psychological treatment for mild adolescent depression. For moderate to severe patients, antidepressant drugs combined with psychotherapy are a feasible option. How to choose suitable antidepressant drugs is still a problem to be solved. Antidepressant drugs have a series of side effects, including sleep disorders, extrapyramidal reactions, and gastrointestinal reactions. In order to reduce these side effects and improve clinical efficacy, individualized treatment plans are crucial. This article summarizes the pathogenesis of adolescent depression, the pharmacokinetics and side effects of antidepressant drugs, as well as the medication guidelines for adolescent patients with depression from 2013 to 2023, and provides scientific suggestions for drug treatment options for adolescent patients with depression.
-
Key words:
- Adolescent /
- Depression /
- Antidepressive agents /
- Pharmacokinetics /
- Efficacy /
- Side effects
-
生殖道沙眼衣原体(chlamydia trachomatis,CT)感染是我国重点监测的性传播疾病,也是全球最常见的性传播疾病,全世界每年新增病例超过1.3亿例[1]。云南省的生殖道沙眼衣原体发病率也呈逐年上升趋势,2012年至2017年生殖道沙眼衣原体感染发病率年均增长率25.35%,且感染者也主要集中在15~44岁年龄组[2-3]。生殖道沙眼衣原体感染可引发眼结膜、咽部、直肠等多器官感染,若治疗不及时,还可导致女性盆腔炎、异位妊娠、不孕不育等并发症[4]。同时,由于感染引发的生殖器部位炎症或溃疡,也使HIV的易感性和传播风险大大增加[5-6]。研究表明[7-10],沙眼衣原体感染可无任何局部或全身症状,导致感染者未能接受到有效治疗,增加了二次感染其他病原体包括HIV的可能性,同时HIV感染也会增加CT持续感染及全身散播的危险,其中HIV阳性女性中感染沙眼衣原体的流行率为9.7%~16.2%。婚检人群包含了一般适婚人群和主要的性活跃人群,对该人群进行性传播疾病的监测有助于评估普通人群的感染状况。为此,本研究对云南省2019年部分州(市)婚检人群开展了生殖道沙眼衣原体感染调查,为制定疾病控制措施和分析防控效果提供依据。
1. 资料与方法
1.1 调查地点
云南省按照其地理位置可分为滇南、滇西、滇东以及滇中地区,本次研究根据地理位置,结合云南省各州市近3 a暗娼人群HIV平均感染率在全省的排序情况将全省各州市分为高中低3个流行水平,分别选取高流行地区(红河州和临沧市)、中流行地区(德宏州和西双版纳州)和低流行地区(保山市和普洱市)共6个州市作为调查现场。
1.2 调查对象
采用固定场所连续抽样方式,招募前往所选取的6个调查州市当地医疗保健机构进行婚前检查,并愿意参加调查并签署知情同意书者作为调查对象。本次调查共纳入1671人,其中红河州343人(20.5%),临沧市315人(18.9%),德宏州301人(18.0%),西双版纳州69人(4.1%),保山市316人(18.9%),普洱市327人(19.6%)。其中,男性841人(50.3%),女性830人(49.7%),年龄为18~57岁,平均(27.74±6.317)岁;以汉族为主,占61.6%(1030/1671),文化程度主要以初中为主,占46.2%(772/1671);以云南省为主,占96.0%(1604/1671),职业主要为农民,占56.9%(951/1671),月平均收入主要在2000~3000元之间,占39.6%(662/1671)。
1.3 调查内容与方法
采用通过专家咨询、KMO和巴特利特检验(KMO = 0.691,P < 0.001)等方法确保效度和信度达到要求的问卷收集调查对象的一般人口学信息、性行为情况、是否感染性病和就医情况等信息。问卷调查结束后,采集调查对象尿液样本,对于已有性行为的女性,同时采集宫颈分泌物标本,用于生殖道沙眼衣原体核酸检测。
1.4 实验室检测
生殖道沙眼衣原体核酸检测使用罗氏核酸检测试剂盒,检测原理为PCR荧光探针法。使用Cobas x480自动核酸提取仪从罗氏配套的尿液和宫颈拭子保存管中直接提取核酸,Cobas z480荧光定量PCR仪扩增核酸并判定结果。采用试剂盒配套的阳性对照、阴性对照和内参标准品对扩增检测进行全面过程质控,所有操作均按照说明书严格执行。
1.5 统计学处理
使用EpiData3.1软件建立数据库,SPSS19.0软件进行数据统计学分析。计数资料以例数或百分比[n(%)]表示。一般人口学特征和性行为特征、性病感染和就医等情况比较采用单因素Logistic回归进行分析,以是否感染CT作为因变量(是 = 1,否 = 0),以相关因素作为自变量。将单因素分析中P < 0.1的变量进行多因素Logistic回归分析,计算各因素校正后的比值比(AOR)及95%的可信区间(95%CI),检验水准为α = 0.05,P < 0.05为差异有统计学意义。
2. 结果
2.1 研究对象中CT感染情况
在调查的1671例研究对象中,共检测出CT核酸阳性111例,其中男性42例,女性通过宫颈检测出29例,尿液54例,指南[11]指出,宫颈和尿液检测中其中任一项为阳性,则判定为阳性,因此女性共检测出69例。总的人群感染率为6.64%(111/1671,95%CI:5.40%~7.80%),男性感染率4.99%(42/841,95%CI:3.50%~6.50%),女性感染率8.31%(69/830,95%CI:6.40%~10.20%)。普洱市和德宏州的感染率较高,分别为8.87%(29/327,95%CI:5.80%~12.00%),8.64%(26/301,95%CI:5.40%~11.80%)。18~20岁的感染率为20.83%(20/96,95%CI:12.60%~29.10%)。文化程度为初中及以下的婚检人群CT的感染率为7.83%(85/1085,95%CI:6.20%~9.40%),见表1。
表 1 婚检人群CT感染影响因素分析Table 1. Analysis of influencing factors of CT infection in premarital examination population变量 合计 感染人数(n) 感染率(%) 单因素分析 多因素分析 P OR(95%CI) P AOR(95%CI) 州市 0.054 0.043* 保山市 316 12 3.80 — 1.000 — 1.000 红河州 343 15 4.37 0.971 0.986(0.468~2.078) 0.556 1.301(0.542~3.119) 西双版纳州 69 4 5.80 0.333 1.685(0.586~4.846) 0.202 2.200(0.655~7.382) 德宏州 301 26 8.64 0.012* 2.317(1.119~4.477) 0.014* 2.649(1.219~5.755) 临沧市 315 25 7.94 0.178 1.612(0.804~3.232) 0.160 1.877(0.780~4.518) 普洱市 327 29 8.87 0.048* 1.954(1.005~3.801) 0.013* 2.708(1.231~5.954) 年龄(岁) < 0.001* < 0.001* ≥41 89 5 5.62 — 1.000 — 1.000 31~40 324 19 5.86 0.930 1.047(0.380~2.886) 0.738 1.192(0.426~3.341) 21~30 1162 67 5.77 0.952 1.029(0.404~2.622) 0.558 1.332(0.510~3.480) 18~20 96 20 20.83 0.005* 4.364(1.562~12.194) 0.007* 4.346(1.468~12.707) 性别 男 841 42 4.99 — 1.000 — 1.000 女 830 69 8.31 0.007* 1.725(1.161~2.564) 0.084 1.446(0.952~2.196) 民族 汉族 1030 61 5.92 — 1.000 其他 641 50 7.80 0.178 1.299(0.888~1.900) 文化程度 高中及以上 586 26 4.44 — 1.000 — 1.000 初中及以下 1085 85 7.83 0.009* 1.831(1.166~2.875) 0.028* 1.854(1.071~3.211) 户籍 本省 1604 106 6.61 — 1.000 非本省 67 5 7.46 0.783 1.140(0.449~2.895) 职业 农民 951 72 7.57 — 1.000 — 1.000 其他 720 39 5.42 0.081 0.699(0.468~1.045) 0.454 1.243(0.703~2.199) 月平均经济收入(元) 0.408 ≥5000 235 12 5.11 — 1.000 3000~5000 461 26 5.64 0.709 1.104(0.657~1.855) 2000~3000 662 51 7.70 0.433 0.791(0.440~1.422) ≤2000 313 22 7.01 0.358 0.712(0.345~1.469) *P < 0.05。 2.2 CT感染的相关因素分析
使用Logistic回归分析感染CT的相关因素,单因素分析后将P < 0.1的因素纳入多因素分析中。多因素分析结果显示,相比保山市,德宏州(AOR = 2.649,95%CI:1.219~5.755)和普洱市(AOR = 2.708,95%CI:1.231~5.954)CT的感染率相对较高;年龄18~20岁(AOR = 4.346,95%CI:1.468~12.707)和文化程度为初中及以下的(AOR = 1.854,95%CI:1.071~3.211)更可能感染CT,见表1。
3. 讨论
本研究对云南省婚检人群中CT感染情况进行了调查,婚检人群在一定程度上可以代表一般人群,从而对评估一个地区的性传播疾病的水平具有参考价值。根据以往的调查,云南省暗娼人群中CT的感染率为14.43%[12],而男男性行为人群(men who have sex with men,MSM)中CT感染率为18.2%[13]。本调查显示,云南省婚检人群中CT的感染率为6.64%,低于重点人群暗娼和MSM中CT的感染率,但与青年学生中CT的感染率8.52%(68/798)差异无统计学意义(χ2 = 2.150,P = 0.084)[14]。女性CT的感染率高于男性,这与以往病例报告的情况相一致[3]。该结果可能是与本次研究中女性阳性感染者首次性行为平均年龄(20.23±3.077)岁,低于男性阳性患者的首次性行为平均年龄(21.44±3.095)岁有关,由于女性首次发生性行为的年龄较小,可能会导致在发生性行为时缺少相应的保护措施,从而进一步增加了女性感染CT的可能性,与本文的研究结果也呈现出一致性。
调查的结果显示,不同州(市)的CT感染率存在显著的差异。与保山市相比,德宏州和普洱市婚检人群CT感染率相对较高,虽然没有统计学差异,但临沧市的CT感染率也达到了7.94%,反应了这些地区具有较高的性病传播风险。对云南省2010年至2017年淋病的时空聚集分析也显示,云南省的西南地区是一个一类聚集地区,包括了普洱市、德宏州和临沧市的大部分县(市、区)[15],这在一定程度上也反应了这些地区性病传播处于较高的水平。但根据2012~2017年生殖道沙眼衣原体病例报告的情况来看,报告发病率前3位的是昆明市、西双版纳州和德宏州,而普洱市和临沧市的报告发病率只有1.44%和0.83%[3],这可能与不同州(市)医疗机构衣原体检测能力和主动筛查意识及力度存在差异有关,提示在全省还需要进一步加强性病的检测能力,加大筛查力度和动员检测,尽可能地发现传染源,并进行规范化的治疗。
本次研究调查中,相比于文化程度为高中及以上的人群而言,文化程度为初中及以下的人群属于婚检人群CT感染的危险因素。研究结果显示[16-17],由于该人群文化程度较低,对于性病的传播和防治知识了解较少,缺少自我保护意识,更加易发生高危行为。因此需要针对该人群的特点,加强性病防治知识的健康教育,提高自我保护意识,减少高危性行为的发生,从而减少CT等相关性病的感染和传播。
2015~2019年我国生殖道沙眼衣原体发病率年均增长10.45%[18],同时部分重点监测的性病低年龄段发病率也在呈逐年上升的趋势[14]。本次调查结果显示,相比于年龄在41岁及其以上人群而言,18~20岁人群是婚检人群CT感染的危险因素,这与珠海市的研究[19]结果相符,同时也与美国、日本等国家的感染情况相一致[20]。本次研究中年龄≤20岁人群,由于缺乏相关的性病防治知识,导致发生首次性行为年龄均在20岁之前(96/96),且近87.5%(84/96)的青少年不能坚持使用安全套,由此可以看出,大多青少年发生首次性行为的年龄较小,且不能坚持使用安全套,这与岑平等[21]的研究结果相一致,这可能与20岁以下人群属于性活跃人群有关。因此应加强对青少年的相关性病防治知识的健康教育,扩大生殖道沙眼衣原体检测的范围。由于CT感染是导致女性生殖感染的常见病原体以及导致女性不孕不育的主要因素之一[22],还会导致男性出现尿道炎、附睾炎、前列腺炎、性功能减退及不育[11],从而影响到生育。目前早发现、早诊断、早治疗是性病防控的最有效措施[12],应加强对婚检人群,尤其是性活跃人群的性病感染情况进行监测,联合各级相关部门,采取多种手段为该人群提供疾病检测,尽可能减少CT的感染与传播,进一步促进优生优育。
由于本次调查是根据云南省暗娼人群HIV平均感染率,在高、中、低流行区中各任意选取了2个州市的部分县区进行样本的采集,虽然同属于性传播疾病,但两者有各自的传播特点,对样本的代表性可能有潜在的影响,但本研究首次在云南省对婚检人群进行CT感染率的调查,为进一步深入研究CT的流行,制定防治措施提供了基础数据。
-
表 1 各类青少年抑郁症患者抗抑郁药物治疗相关指南
Table 1. Guidelines for antidepressant medication treatment in adolescents with various types of depression
机构 年份 SSRIs SNRIs 建议 参考文献 用药依据 指南依据的文献 CSBM 2022 SSRIs类(首选) — 遵循抗抑郁药与心理治疗并重的原则 [33] SSRIs类疗效及安全
性有循证医学证据支持[34] APA 2021 氟西汀 — 建议联合心理治疗 [30] 伦理原则和行为准则 [35] RANZCP 2021 氟西汀 — 心理治疗为一线治疗 [32] 有抗抑郁药物(氟西汀)对青少年患者有效的一级证据 [36] KSAD、KCNP 2021 艾司西酞普兰(首选)、氟西汀、舍曲林 — 用于轻中度抑郁发作的青少年 [25] 氟西汀和舍曲林疗效显著 [37] JSCNP(未特别提及青少年抑郁症) 2020 艾司西酞普兰、舍曲林 度洛西汀、文拉法辛 若SSRIs无效,一线治疗切换为SNRIs/或米氮平;而若SNRIs无效,推荐改用米氮平,反之亦然(若米氮平无效,改用SNRIs)。 [26] 对于轻度抑郁症,SSRIs被选为一线治疗,SNRIs被选为二线治疗,对于米氮平没有达成共识 [28,38−39] AFPBN
(未特别提及
青少年抑郁症)2019 SSRIs类 SNRIs 无论临床严重程度如何,SSRIs及SNRIs均被认为是一线治疗药物 [27] 三环类抗抑郁药、米氮平或米安色林可增强SRRIs
疗效[40−41] NICE 2019 氟西汀 — 轻度抑郁症不应使用抗抑郁药物,中重度抑郁症,如果在4~6个疗程的心理治疗无效后,可以给予氟西汀治疗 [31] 如表现出严重自我伤害,应遵循良好的自我伤害指导立即处理 — CANMAT 2016 SSRIs类 — SSRIs会增加青少年自杀风险,建议谨慎使用并密切监测 [28] 氟西汀、文拉法辛与安慰剂相比自杀风险无差别;帕罗西汀的风险较安慰剂低。 [42−43] GLAD-PC 2015 氟西汀(FDA批准)、艾司西酞普兰(FDA批准)、西酞普兰、氟伏沙明、帕罗西汀、舍曲林 — 除氟西汀外,所有SSRIs在停用时都应缓慢减量,因为存在停药的风险 [22] 根据青少年患者的临床表现、医生的处方偏好 [44] WFSBP 2015 氟西汀、舍曲林 文拉法辛 — [24] 有效缓解儿童和青少年抑郁症状,具有预防新抑郁发作的潜力。 [45−47] SSRIs:选择性5-羟色胺再摄取抑制剂;SNRIs:选择性5-羟色胺和去甲肾上腺素再摄取抑制剂;FDA:美国食品药品管理局;CSBM:中华医学会行为医学分会;APA:美国心理学协会;RANZCP:澳大利亚与新西兰皇家精神科医师学会;KSAD:韩国情感障碍学会;KCNP:韩国神经精神药理学学院;JSCNP:日本临床神经精神药理学学会;AFPBN:法国生物精神病学和神经精神药理学协会;NICE:英国国家卫生与临床优化研究所;CANMAT:加拿大情绪和焦虑治疗网络;GLAD-PC:美国青少年抑郁症初级护理指南;WFSBP:世界生物精神病学学会联合会。 表 2 FDA批准可用于青少年患者的抗抑郁药物汇总
Table 2. Summary of FDA-approved antidepressant medications for adolescent patients
药物名称 达峰
时间/h[48]半衰期[48] 主要
代谢酶[49]年龄范围
/岁[50]适应症[23] 目标剂量[50] 药物的相对受体结合亲和力[51] SET DAT NET α1 M1 H1 氟西汀(SSRI) 6~8 2~3 d CYP2C9 、CYP2C19、CYP2D6 8~17 抑郁症、
强迫症40 mg/d 1 >1000 545 >1000 638 >1000 艾司西酞普兰(SSRI) 4 27~33 h CYP3A4、CYP2C19、CYP2D6 12~17 抑郁症 >10 mg/d 1 >10000 >1000 >1000 >1000 257 舍曲林(SSRI) 6~8 26 h
CYP2C19、
CYP3A46~17 强迫症 150 mg/d 1 220 >1000 >1000 >1000 >100000 氟伏沙明(SSRI) 5 22 h CYP2D6 8~17 强迫症 40 mg/d 1 >1000 620 560 >5000 >5000 度洛西汀(SNRI) 6 8~17 h CYP1A2 7~17 广泛性
焦虑障碍60~90 mg/d 1 504 7.5 >1000 >1000 >1000 FDA:美国食品药品管理局;SSRI:选择性5-羟色胺再摄取抑制剂;SNRI:选择性5-羟色胺和去甲肾上腺素再摄取抑制剂;SET:5-羟色胺转运体;DAT:多巴胺转运体;NET:去甲肾上腺素转运体;M:毒蕈碱受体;H:组胺受体;α1:α1-肾上腺素受体。相对受体结合亲和力是指药物与每个受体相对于药物最高亲和力部位的结合亲和力,数值越大,与药物下一个潜在靶点结合所需的浓度就越高。 -
[1] Liu W,Li G,Wang C,et al. Efficacy of sertraline combined with cognitive behavioral therapy for adolescent depression: A systematic review and meta-analysis[J]. Comput Math Methods Med,2021,2021:5309588. [2] Shorey S,Ng E D,Wong C. Global prevalence of depression and elevated depressive symptoms among adolescents: A systematic review and meta-analysis[J]. Br J Clin Psychol,2022,61(2):287-305. doi: 10.1111/bjc.12333 [3] Avenevoli S,Swendsen J,He J P,et al. Major depression in the national comorbidity survey-adolescent supplement: Prevalence,correlates,and treatment[J]. J Am Acad Child Adolesc Psychiatry,2015,54(1): 37-44. e2. [4] Johnson D,Dupuis G,Piche J,et al. Adult mental health outcomes of adolescent depression: A systematic review[J]. Depress Anxiety,2018,35(8):700-716. doi: 10.1002/da.22777 [5] Lee K H,Shin J,Lee J,et al. Measures of connectivity and dorsolateral prefrontal cortex volumes and depressive symptoms following treatment with selective serotonin reuptake inhibitors in adolescents[J]. JAMA Netw Open,2023,6(8):e2327331. doi: 10.1001/jamanetworkopen.2023.27331 [6] Li C,Xu P,Huang Y,et al. RNA methylations in depression,from pathological mechanism to therapeutic potential[J]. Biochem Pharmacol,2023,215:115750. doi: 10.1016/j.bcp.2023.115750 [7] Shao S L,Liu D Q,Zhang B,et al. Inflammatory response,a key pathophysiological mechanism of obesity-induced depression[J]. Mediators Inflamm,2020,2020:8893892. [8] Egeland M,Zunszain P A,Pariante C M. Molecular mechanisms in the regulation of adult neurogenesis during stress[J]. Nat Rev Neurosci,2015,16(4):189-200. doi: 10.1038/nrn3855 [9] Jesulola E,Micalos P,Baguley I J. Understanding the pathophysiology of depression: From monoamines to the neurogenesis hypothesis model - are we there yet?[J]. Behav Brain Res,2018,341:79-90. doi: 10.1016/j.bbr.2017.12.025 [10] Liu Y,Wu Z,Cheng L,et al. The role of the intestinal microbiota in the pathogenesis of host depression and mechanism of TPs relieving depression[J]. Food Funct,2021,12(17):7651-7663. doi: 10.1039/D1FO01091C [11] Barnett R. Depression[J]. Lancet,2019,393(10186):2113. doi: 10.1016/S0140-6736(19)31151-1 [12] Lu J,Xu X,Huang Y,et al. Prevalence of depressive disorders and treatment in China: A cross-sectional epidemiological study[J]. Lancet Psychiatry,2021,8(11):981-990. doi: 10.1016/S2215-0366(21)00251-0 [13] LeMoult J,Chen M C,Foland-Ross L C,et al. Concordance of mother-daughter diurnal cortisol production: Understanding the intergenerational transmission of risk for depression[J]. Biol Psychol,2015,108:98-104. doi: 10.1016/j.biopsycho.2015.03.019 [14] Asarnow L D. Depression and sleep: What has the treatment research revealed and could the HPA axis be a potential mechanism?[J]. Curr Opin Psychol,2020,34:112-116. doi: 10.1016/j.copsyc.2019.12.002 [15] Sałaciak K,Pytka K. Revisiting the sigma-1 receptor as a biological target to treat affective and cognitive disorders[J]. Neurosci Biobehav Rev,2022,132:1114-1136. doi: 10.1016/j.neubiorev.2021.10.037 [16] Colich N L,McLaughlin K A. Accelerated pubertal development as a mechanism linking trauma exposure with depression and anxiety in adolescence[J]. Curr Opin Psychol,2022,46:101338. doi: 10.1016/j.copsyc.2022.101338 [17] Rodman A M,Vidal Bustamante C M,Dennison M J,et al. A year in the social life of a teenager: Within-person fluctuations in stress,phone communication,and anxiety and depression[J]. Clin Psychol Sci,2021,9(5):791-809. doi: 10.1177/2167702621991804 [18] Cheng Z,Su J,Zhang K,et al. Epigenetic mechanism of early life stress-induced depression: Focus on the neurotransmitter systems[J]. Front Cell Dev Biol,2022,10:929732. doi: 10.3389/fcell.2022.929732 [19] Kang B,Li Y,Zhao X,et al. Negative parenting style and depression in adolescents: A moderated mediation of self-esteem and perceived social support[J]. J Affect Disord,2024,345:149-156. doi: 10.1016/j.jad.2023.10.132 [20] O'Callaghan G,Stringaris A. Reward processing in adolescent depression across neuroimaging modalities[J]. Z Kinder Jugendpsychiatr Psychother,2019,47(6):535-541. doi: 10.1024/1422-4917/a000663 [21] Mao N,Che K,Chu T,et al. Aberrant resting-state brain function in adolescent depression[J]. Front Psychol,2020,11:1784. doi: 10.3389/fpsyg.2020.01784 [22] Cheung A H,Zuckerbrot R A,Jensen P S,et al. Guidelines for adolescent depression in primary care (GLAD-PC): II. Treatment and ongoing management[J]. Pediatrics,2007,120(5):e1313-1326. doi: 10.1542/peds.2006-1395 [23] Safer D J,Zito J M. Short- and long-term antidepressant clinical trials for major depressive disorder in youth: Findings and concerns[J]. Front Psychiatry,2019,10:705. [24] Bauer M,Severus E,Köhler S,et al. World federation of societies of biological psychiatry (WFSBP) guidelines for biological treatment of unipolar depressive disorders. part 2: Maintenance treatment of major depressive disorder-update 2015[J]. World J Biol Psychiatry,2015,16(2):76-95. doi: 10.3109/15622975.2014.1001786 [25] Seo J S,Bahk W M,Woo Y S,et al. Korean medication algorithm for depressive disorder 2021,fourth revision: An executive summary[J]. Clin Psychopharmacol Neurosci,2021,19(4):751-772. doi: 10.9758/cpn.2021.19.4.751 [26] Sakurai H,Uchida H,Kato M,et al. Pharmacological management of depression: Japanese expert consensus[J]. J Affect Disord,2020,266:626-632. doi: 10.1016/j.jad.2020.01.149 [27] Bennabi D,Charpeaud T,Yrondi A,et al. Clinical guidelines for the management of treatment-resistant depression: French recommendations from experts,the French Association for Biological Psychiatry and Neuropsychopharmacology and the fondation FondaMental[J]. BMC Psychiatry,2019,19(1):262. doi: 10.1186/s12888-019-2237-x [28] Kennedy S H,Lam R W,McIntyre R S,et al. Canadian network for mood and anxiety treatments (CANMAT) 2016 clinical guidelines for the management of adults with major depressive disorder: Section 3. Pharmacological treatments[J]. Can J Psychiatry,2016,61(9):540-560. doi: 10.1177/0706743716659417 [29] Meyer A E,Curry J F. Moderators of treatment for adolescent depression[J]. J Clin Child Adolesc Psychol,2021,50(4):486-497. doi: 10.1080/15374416.2020.1796683 [30] Summary of the clinical practice guideline for the treatment of depression across three age cohorts[J]. Am Psychol,2022,77(6): 770-780. [31] Luxton R,Kyriakopoulos M. Depression in children and young people: identification and management NICE guidelines[J]. Arch Dis Child Educ Pract Ed,2022,107(1):36-38. [32] Malhi G S,Bell E,Bassett D,et al. The 2020 royal australian and new zealand college of psychiatrists clinical practice guidelines for mood disorders[J]. Aust N Z J Psychiatry,2021,55(1):7-117. doi: 10.1177/0004867420979353 [33] 中华医学会行为医学分会,中华医学会行为医学分会认知应对治疗学组. 抑郁症治疗与管理的专家推荐意见(2022年)[J]. 中华行为医学与脑科学杂志,2023,32(3):193-202. doi: 10.3760/cma.j.cn371468-20220921-00563 [34] Murphy S E,Capitão L P,Giles S,et al. The knowns and unknowns of SSRI treatment in young people with depression and anxiety: Efficacy,predictors,and mechanisms of action[J]. Lancet Psychiatry,2021,8(9):824-835. doi: 10.1016/S2215-0366(21)00154-1 [35] Ethical principles of psychologists and code of conduct[J]. Am Psychol,2002,57(12): 1060-1073. [36] Zhou X,Teng T,Zhang Y,et al. Comparative efficacy and acceptability of antidepressants,psychotherapies,and their combination for acute treatment of children and adolescents with depressive disorder: A systematic review and network meta-analysis[J]. Lancet Psychiatry,2020,7(7):581-601. doi: 10.1016/S2215-0366(20)30137-1 [37] Hetrick S E,McKenzie J E,Cox G R,et al. Newer generation antidepressants for depressive disorders in children and adolescents[J]. Cochrane Database Syst Rev,2012,11(11):CD004851. [38] Practice guideline for the treatment of patients with major depressive disorder (revision). American Psychiatric Association[J]. Am J Psychiatry,2000,157(4 Suppl): 1-45. [39] Millan M J. Multi-target strategies for the improved treatment of depressive states: Conceptual foundations and neuronal substrates,drug discovery and therapeutic application[J]. Pharmacol Ther,2006,110(2):135-370. doi: 10.1016/j.pharmthera.2005.11.006 [40] Rojo J E,Ros S,Agüera L,et al. Combined antidepressants: clinical experience[J]. Acta Psychiatr Scand Suppl,2005(428):25-31,36. [41] Blier P,Gobbi G,Turcotte J E,et al. Mirtazapine and paroxetine in major depression: a comparison of monotherapy versus their combination from treatment initiation[J]. Eur Neuropsychopharmacol,2009,19(7):457-465. doi: 10.1016/j.euroneuro.2009.01.015 [42] Gibbons R D,Brown C H,Hur K,et al. Suicidal thoughts and behavior with antidepressant treatment: Reanalysis of the randomized placebo-controlled studies of fluoxetine and venlafaxine[J]. Arch Gen Psychiatry,2012,69(6):580-587. doi: 10.1001/archgenpsychiatry.2011.2048 [43] Carpenter D J,Fong R,Kraus J E,et al. Meta-analysis of efficacy and treatment-emergent suicidality in adults by psychiatric indication and age subgroup following initiation of paroxetine therapy: A complete set of randomized placebo-controlled trials[J]. J Clin Psychiatry,2011,72(11):1503-1514. doi: 10.4088/JCP.08m04927blu [44] Rushton J L,Clark S J,Freed G L. Pediatrician and family physician prescription of selective serotonin reuptake inhibitors[J]. Pediatrics,2000,105(6):E82. doi: 10.1542/peds.105.6.e82 [45] Brent D,Emslie G,Clarke G,et al. Switching to another SSRI or to venlafaxine with or without cognitive behavioral therapy for adolescents with SSRI-resistant depression: The TORDIA randomized controlled trial[J]. JAMA,2008,299(8):901-913. doi: 10.1001/jama.299.8.901 [46] Cheung A,Kusumakar V,Kutcher S,et al. Maintenance study for adolescent depression[J]. J Child Adolesc Psychopharmacol,2008,18(4):389-394. doi: 10.1089/cap.2008.0001 [47] Emslie G J,Kennard B D,Mayes T L,et al. Fluoxetine versus placebo in preventing relapse of major depression in children and adolescents[J]. Am J Psychiatry,2008,165(4):459-467. doi: 10.1176/appi.ajp.2007.07091453 [48] Wyska E. Pharmacokinetic considerations for current state-of-the-art antidepressants[J]. Expert Opin Drug Metab Toxicol,2019,15(10):831-847. doi: 10.1080/17425255.2019.1669560 [49] Bousman C A,Stevenson J M,Ramsey L B,et al. Clinical pharmacogenetics implementation consortium (CPIC) guideline for CYP2D6,CYP2C19,CYP2B6,SLC6A4,and HTR2A genotypes and serotonin reuptake inhibitor antidepressants[J]. Clin Pharmacol Ther,2023,114(1):51-68. doi: 10.1002/cpt.2903 [50] 喻东山,葛茂宏. 精神科合理用药手册(第2版)[M]. 南京:江苏科学技术出版社,2011:132-151. [51] Preskorn S H. Drug-drug interactions (DDIs) in psychiatric practice,part 8: Relative receptor binding affinity as a way of understanding the differential pharmacology of currently available antidepressants[J]. J Psychiatr Pract,2020,26(1):46-51. doi: 10.1097/PRA.0000000000000445 [52] Margolis J M,O'Donnell J P,Mankowski D C,et al. (R)-,(S)-,and racemic fluoxetine N-demethylation by human cytochrome P450 enzymes[J]. Drug Metab Dispos,2000,28(10):1187-1191. [53] Jornil J,Jensen K G,Larsen F,et al. Identification of cytochrome P450 isoforms involved in the metabolism of paroxetine and estimation of their importance for human paroxetine metabolism using a population-based simulator[J]. Drug Metab Dispos,2010,38(3):376-385. doi: 10.1124/dmd.109.030551 [54] Hiemke C,Härtter S. Pharmacokinetics of selective serotonin reuptake inhibitors[J]. Pharmacol Ther,2000,85(1):11-28. doi: 10.1016/S0163-7258(99)00048-0 [55] Mandrioli R,Mercolini L,Raggi M A. Evaluation of the pharmacokinetics,safety and clinical efficacy of sertraline used to treat social anxiety[J]. Expert Opin Drug Metab Toxicol,2013,9(11):1495-1505. doi: 10.1517/17425255.2013.816675 [56] Mrazek D A,Biernacka J M,O'Kane D J,et al. CYP2C19 variation and citalopram response[J]. Pharmacogenet Genomics,2011,21(1):1-9. doi: 10.1097/FPC.0b013e328340bc5a [57] Zastrozhin M,Skryabin V,Smirnov V,et al. Effect of genetic polymorphism of the CYP2D6 gene on the efficacy and safety of fluvoxamine in major depressive disorder[J]. Am J Ther,2021,29(1):e26-e33. [58] Karlsson L,Zackrisson A L,Josefsson M,et al. Influence of CYP2D6 and CYP2C19 genotypes on venlafaxine metabolic ratios and stereoselective metabolism in forensic autopsy cases[J]. Pharmacogenomics J,2015,15(2):165-171. doi: 10.1038/tpj.2014.50 [59] Knadler M P,Lobo E,Chappell J,et al. Duloxetine: Clinical pharmacokinetics and drug interactions[J]. Clin Pharmacokinet,2011,50(5):281-294. doi: 10.2165/11539240-000000000-00000 [60] Hazell P. Antidepressants in adolescence[J]. Aust Prescr,2022,45(2):49-52. doi: 10.18773/austprescr.2022.011 [61] Kloosterboer S M,Vierhout D,Stojanova J,et al. Psychotropic drug concentrations and clinical outcomes in children and adolescents: A systematic review[J]. Expert Opin Drug Saf,2020,19(7):873-890. doi: 10.1080/14740338.2020.1770224 [62] Cipriani A,Zhou X,Del Giovane C,et al. Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: A network meta-analysis[J]. Lancet,2016,388(10047):881-890. doi: 10.1016/S0140-6736(16)30385-3 [63] Foster S,Mohler-Kuo M. Treating a broader range of depressed adolescents with combined therapy[J]. J Affect Disord,2018,241:417-424. doi: 10.1016/j.jad.2018.08.027 [64] Strawn J R,Mills J A,Poweleit E A,et al. Adverse effects of antidepressant medications and their management in children and adolescents[J]. Pharmacotherapy,2023,43(7):675-690. doi: 10.1002/phar.2767 [65] Strawn J R,Dobson E T,Giles L L. Primary pediatric care psychopharmacology: Focus on medications for ADHD,depression,and anxiety[J]. Curr Probl Pediatr Adolesc Health Care,2017,47(1):3-14. doi: 10.1016/j.cppeds.2016.11.008 [66] David D J,Gourion D. Antidepressant and tolerance: Determinants and management of major side effects[J]. Encephale,2016,42(6):553-561. doi: 10.1016/j.encep.2016.05.006 [67] Revet A,Montastruc F,Roussin A,et al. Antidepressants and movement disorders: a postmarketing study in the world pharmacovigilance database[J]. BMC Psychiatry,2020,20(1):308. doi: 10.1186/s12888-020-02711-z [68] Shelton R C. Serotonin and norepinephrine reuptake inhibitors[J]. Handb Exp Pharmacol,2019,250:145-180. [69] Nestler E J,Carlezon W A Jr. The mesolimbic dopamine reward circuit in depression[J]. Biol Psychiatry,2006,59(12):1151-1159. doi: 10.1016/j.biopsych.2005.09.018 [70] Bridge J A,Iyengar S,Salary C B,et al. Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: A meta-analysis of randomized controlled trials[J]. JAMA,2007,297(15):1683-1696. doi: 10.1001/jama.297.15.1683 [71] Ignaszewski M J,Waslick B. Update on randomized placebo-controlled trials in the past decade for treatment of major depressive disorder in child and adolescent patients: A Systematic Review[J]. J Child Adolesc Psychopharmacol,2018,28(10):668-675. doi: 10.1089/cap.2017.0174 [72] Hirschfeld R M. Differential diagnosis of bipolar disorder and major depressive disorder[J]. J Affect Disord,2014,169 (Suppl 1): S12-16. [73] Rochoy M,Zakhem-Stachera C,Béné J,et al. Antidepressive agents and hyponatremia: A literature review and a case/non-case study in the French pharmacovigilance database[J]. Therapie,2018,73(5):389-398. doi: 10.1016/j.therap.2018.02.006 [74] Richa S,Yazbek J C. Ocular adverse effects of common psychotropic agents: A review[J]. CNS Drugs,2010,24(6):501-526. doi: 10.2165/11533180-000000000-00000 [75] Skop B P,Brown T M. Potential vascular and bleeding complications of treatment with selective serotonin reuptake inhibitors[J]. Psychosomatics,1996,37(1):12-16. doi: 10.1016/S0033-3182(96)71592-X [76] Funk K A,Bostwick J R. A comparison of the risk of QT prolongation among SSRIs[J]. Ann Pharmacother,2013,47(10):1330-1341. doi: 10.1177/1060028013501994 [77] Voican C S,Corruble E,Naveau S,et al. Antidepressant-induced liver injury: A review for clinicians[J]. Am J Psychiatry,2014,171(4):404-415. doi: 10.1176/appi.ajp.2013.13050709 [78] Blumberger D M,Vila-Rodriguez F,Wang W,et al. A randomized sham controlled comparison of once vs twice-daily intermittent theta burst stimulation in depression: A Canadian rTMS treatment and biomarker network in depression (CARTBIND) study[J]. Brain Stimul,2021,14(6):1447-1455. doi: 10.1016/j.brs.2021.09.003 [79] Borbély É,Simon M,Fuchs E,et al. Novel drug developmental strategies for treatment-resistant depression[J]. Br J Pharmacol,2022,179(6):1146-1186. doi: 10.1111/bph.15753 期刊类型引用(1)
1. 邓宝清,叶云凤,宁宁,晏瑞琳,温桂春,黄李成,邓勇峥,袁青,蔡于茂,陈祥生. 不孕不育人群生殖道沙眼衣原体感染影响因素分析. 皮肤性病诊疗学杂志. 2024(02): 82-87 . 百度学术
其他类型引用(0)
-