慢阻肺患者个体化治疗的目标是否能够实现?

2018-08-10 佚名 医师报

近年来,国际指南对慢阻肺的定义、发病机制、评估、个体化治疗、急性加重及合并症等方面均进行了全面修改,其中一些观点尚需在临床上进一步验证,因而引发国内外慢阻肺领域专家学者的广泛讨论。让我们一起聆听国内专家的剖析,共同探讨慢阻肺的国际热议话题。


近年来,国际指南对慢阻肺的定义、发病机制、评估、个体化治疗、急性加重及合并症等方面均进行了全面修改,其中一些观点尚需在临床上进一步验证,因而引发国内外慢阻肺领域专家学者的广泛讨论。让我们一起聆听国内专家的剖析,共同探讨慢阻肺的国际热议话题。

慢阻肺患者个体化治疗的目标 是否能够实现?

在医学向个体化治疗转变的历史时期,慢阻肺个体化治疗目标主要集中于改善症状以及降低预测风险。未来慢阻肺个体化治疗方案很可能依据患者基因型和生物标志物变得更有针对性,以及肺康复的个体化途径。慢阻肺是一个常见且复杂的疾病,在预防和针对不同亚型的个体化治疗上需要更多关注,如何将GOLD诊治策略与中国临床的实践结合起来,针对不同患者的病情进行个体化治疗是我们值得深入探讨的话题。

正方 中国医科大学附属第一医院呼吸与危重症医学科 

尹燕:目前慢阻肺患者实行个体化治疗已经开展

尽管慢阻肺患者均须符合不可逆气流受限的诊断标准,但其在遗传学、生物学、临床表现、预后转归等多方面存在异质性。例如,不同程度肺气肿表型的慢阻肺患者存在单核苷酸多态性的差异。

不同的患者支气管扩张剂疗效不同,非肥胖的女性患者更易从异丙托溴铵的治疗中获益,合并哮喘特征的患者需要应用糖皮质激素治疗;不同的患者对其呼吸困难的感知存在差异,急性加重频发型患者具有更高的Borg评分。此外,慢阻肺病程中易合并/并发肺癌骨质疏松、冠状动脉钙化、骨骼肌功能障碍等疾病。因此,仅仅单纯评估患者病情是否加重或缓解,不加区别地对患者进行雷同治疗无疑是不恰当的,根据患者基础疾病情况制定个体化医疗策略势在必行。

自从2011年GOLD指南中提出根据肺功能、症状、急性加重风险进行综合评估以来,临床医生对慢阻肺的认知已逐渐由从气流受限性疾病转向关注疾病复杂性和异质性,有效的个体化诊疗方案的制定成为近年来研究的热点及难点。不同的临床表型有不同且特异的治疗策略。

2012年,西班牙慢阻肺指南GesEPOC)首次建立了基于临床表型的药物治疗方案。GesEPOC 2017中,原来的病情严重程度分类已被更简单的危险分层(低危或高危)所替代,新的危险分层基于肺功能、呼吸困难等级、急性加重史进行评估,且推荐仅对高危患者确定临床表型,,分为四种:(1)非急性加重表型;(2)哮喘慢阻肺重叠(ACO);(3)急性加重肺气肿型;(4)急性加重慢性支气管炎型。

根据患者的风险分层和临床表型,采取不同的药物治疗,更加倾向于个体化治疗。嗜酸粒细胞(EOS)是新近发现的能够预测慢阻肺急性加重的生物标志物,40%慢阻肺患者具有高EOS表型,即外周血EOS≥2%,而有证据显示高水平的血EOS与慢阻肺急性加重风险增高相关,这种风险可部分地被长期吸入型激素治疗所降低。美泊利单抗是一种人源性的单克隆抗体,能够通过封闭IL-5降低血和组织的嗜酸粒细胞。

METREX研究指出,美泊利单抗可降低慢阻肺患者中重度急性加重的频率。METREO研究指出,100 mg美泊利单抗可降低EOS表型慢阻肺患者中重度急性加重的频率。这是慢阻肺个体化治疗的一个典型案例。

虽然,慢阻肺亚型或表型相关研究已取得一定的进展,但不同研究的聚类结果存在着显着差异,且目前分型尚没有达成共识并缺乏重复性及可持续性。因此,如何聚类分析及识别慢阻肺亚型、建立多维评估和实行精准的个体化治疗将是未来慢阻肺领域研究的主导方向。

反方 复旦大学附属中山医院呼吸与危重症医学科

张静:慢阻肺稳定期个体化药物治疗的时代还为时过早

实现稳定期慢阻肺个体化药物治疗是我们努力的方向。学界已经公认,慢阻肺是一个高度异质性的疾病,体现在四个层面:(1)基因层面的疾病易感性多种多样;(2)致病因素层面,包含吸烟、生物燃料、大气污染、生长发育等等;(3)生物学网络层面,即“内型”,多可由某个或某些生物标志物反映;(4)临床表型,如症状、急性加重、对治疗的反应、疾病进展速度等等。不同的慢阻肺患者对治疗措施的反应存在差异,因此个体化治疗是有必要的。

但是,目前所掌握的慢阻肺疾病知识和病情评估的技术手段还远未能实施真正的慢阻肺个体化治疗。从基因层面,唯一确认可检测并且由治疗手段的为α1-胰蛋白酶缺乏,然而这种情况仅见于少部分慢阻肺,而绝大部分慢阻肺的发病牵涉到多个分子及其基因多态性,是否能找到单一有效的基因靶点目前还不明确。不同暴露因素所致的慢阻肺是否存在特定的可治疗因素还不明确。近年来,在生物标志物方面有了些进展,但是能够预测药物治疗反应的指标并不多,仅有EOS计数升高预示患者更能从长期吸入糖皮质激素治疗获益。在临床表型方面,已有临床证据提示合并哮喘、呼吸困难等症状水平、既往急性加重次数及其严重程度等可以帮助我们选择药物种类,但是对于和疾病发生发展密切相关的小气道功能、气道炎症反应类型等方面,仍缺乏可靠、简便、重复性好、经大样本研究验证的检测方法,也没有针对性强的治疗药物。

可见,现阶段所谓的“个体化治疗”更多的是根据个别疾病特征在有限的几类药物中加以选择、组合,而缺乏直击发病机制的检测手段和药物。况且,值得注意的是,上述有限的几个疾病特征很难做到准确评估,例如EOS计数的影响因素很多,是否合并哮喘对于病史不清楚、症状不典型的患者难以厘清,呼吸困难除了慢阻肺之外原因多种多样(心脏疾病、贫血等都可以引起呼吸困难),既往急性加重次数更是依赖于患者的体认和报告。

综上所述,现在奢谈慢阻肺的个体化治疗还为时过早,尚有待更多研究证据以及更敏感、客观、重复性好的检测技术。

点评

北京大学第三医院呼吸与危重症医学科  陈亚红:

在现代医学中,技术正让个体化诊疗的实现成为可能。而个体化,正是“4P”医学模式(4P medical model)所倡导的元素之一。近年来,随着基因技术和健康理念的发展,医学模式正逐渐走向“4P”医学模式(4p medical model):预防性(Preemptive)、预测性(Predictive)、个体化(Personalized)和参与性(participatory)。可以看到,从生物-心理-社会模式到4P医学模式,现代医学更以人为主体,强调人的主动性。4P医学模式是以解决慢性病问题为首要目标。慢阻肺作为一种常见而重要的慢性呼吸系统疾病,新近发表的全国慢阻肺流行病学调查发现40岁以上患病率为13.7%,与“高血压糖尿病”患病人数等量齐观,应该采取4P医学模式。

尹燕教授指出国内外慢阻肺指南基于循证医学研究的证据,已经开始基于临床表型给予个体化治疗,而张静教授则指出现阶段针对慢阻肺的临床表型和治疗方法仍然不全面,应该继续深入挖掘其内型,明确其发病机制和潜在的个体化治疗靶点。在过去的几十年,我们对于慢阻肺的认识已经发生了翻天覆地的变化。过去,我们仅依据FEV1来判断慢阻肺的严重程度;如今,我们根据表型分类采取不同的药物治疗。临床表型的提出是慢阻肺个体化治疗的一大进步,但无论是GOLD、GesEPOC还是中国指南,已知的临床表型都具有局限性,不能完全包括所有慢阻肺患者,也不能显示慢阻肺合并症,对未来急性加重的判断也不精确。未来,结合环境因素、营养因素、临床表型、生物标志物、微生物组学、蛋白质组学、代谢组学、基因组学、大数据、物联网技术的发展,以及更多循证医学证据的加入,会有更多新的临床表型被发现,将真正实现对每个慢阻肺患者的个体化治疗。

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    2020-06-25 云艳归真520

    学习了,谢谢

    0

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    2018-08-11 liumin1987

    慢阻肺的个体化治疗。

    0

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    2018-08-10 王秀

    学习了,涨知识了!

    0

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    2018-08-10 天地飞扬

    了解一下,谢谢分享!

    0

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