Gold 2023: Highlights for primary care
金 2023：初級醫療的重點

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has issued its 2023 annual report¹. Compared with former versions, it has been significantly updated. Here, we summarize the most relevant changes for a Primary Care audience. The complete document can be downloaded for free from the GOLD web page (www.goldcopd.org), together with a “pocket guide” and a “teaching slide set”.
全球慢性阻塞性肺病倡議（GOLD）已發布其 2023 年年報 ¹ 。與以前的版本相比，這次更新顯著。我們在此總結了對初級護理人員最相關的變更。完整文件可以從 GOLD 網頁（www.goldcopd.org）免費下載，還包括“口袋指南”和“教學幻燈片集”。

GOLD 2023 defines COPD as a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnoea, cough, expectoration and/or exacerbations) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction (FEV1/FVC < 0.7)¹. This definition aims at: (1) recognizing that COPD is heterogeneous; and (2) describing explicitly what are the main structural, functional, and clinical manifestations of the disease.
GOLD 2023 將慢性阻塞性肺病（COPD）定義為一種異質性的肺部疾病，其特徵為由於氣道（支氣管炎、細支氣管炎）和/或肺泡（肺氣腫）異常引起的慢性呼吸症狀（呼吸困難、咳嗽、咳痰和/或加重），導致持續的、通常是進行性的氣流阻塞（FEV1/FVC < 0.7） ¹ 。此定義旨在：（1）認識到 COPD 是異質性的；以及（2）明確描述該疾病的主要結構、功能和臨床表現。

Traditionally, COPD has been considered a self-inflicted disease caused by tobacco smoking and occurring primarily in older males². This is a narrow and incomplete view, since COPD is similarly prevalent in men and women, and can be diagnosed in young individuals and even in never smokers¹. In fact, GOLD 2023 proposes that COPD is actually the end-result of a series of dynamic, cumulative and repeated gene (G)–environment (E) interactions over the lifetime (T) that damage the lungs and alter their normal development/aging processes³. Below, we review the evidence supporting the influence of Genes, Environment and Time (GETomics) in the pathogenesis of COPD³.
傳統上，慢性阻塞性肺病（COPD）被認為是一種由吸煙造成的自我傷害疾病，主要發生在年長男性身上 ² 。這是一種狹隘且不完整的觀點，因為 COPD 在男性和女性中同樣普遍，並且可以在年輕人甚至從不吸煙者中診斷出來 ¹ 。事實上，GOLD 2023 提議 COPD 實際上是由一系列動態、累積和重複的基因（G）-環境（E）互動所造成的最終結果，這些互動在整個生命週期（T）中損害肺部並改變其正常的發展/老化過程 ³ 。以下，我們回顧支持基因、環境和時間（GETomics）在 COPD 發病機制中影響的證據 ³ 。

Genes  基因

Mutations in SERPINA1 gene, leading to α-1 antitrypsin deficiency is the most relevant (albeit rare) genetic risk factor for COPD. Many other genetic variants have been recently identified as risk factors for reduced lung function and COPD, but their individual effect size is small⁴. The prevalence of COPD in males and females in developed countries is now very similar⁵ but some studies suggest more harmful effects of smoking among women^1,6. For instance, females report more dyspnoea and cough, have a steeper decline in lung function over time and have worse outcomes than males in terms of hospitalizations, respiratory failure, and death⁷.
SERPINA1 基因的突變導致α-1 抗胰蛋白酶缺乏，是 COPD 最相關（儘管罕見）的遺傳風險因素。最近已識別出許多其他遺傳變異作為肺功能減退和 COPD 的風險因素，但它們的個別效應大小較小 ⁴ 。在發達國家，男性和女性的 COPD 患病率現在非常相似 ⁵ ，但一些研究表明女性吸煙的有害影響更大 ^1,6 。例如，女性報告的呼吸困難和咳嗽更多，隨著時間的推移肺功能下降更陡峭，且在住院、呼吸衰竭和死亡方面的結果比男性更差 ⁷ 。

Environment  環境

Cigarette smoking is a key environmental risk factor for COPD; yet fewer than 50% of heavy smokers develop COPD⁸ and, as discussed below, about a third of patients with COPD have never smoked^9,10. Passive smoking exposure also is a risk factor for COPD¹¹. Smoking during pregnancy poses a risk for the foetus, by altering lung growth and development in utero^3,12. In low- and middle-income countries (LMICs), COPD in non-smokers may be responsible for up to 60–70% of cases¹⁰. Wood, animal dung, crop residues, and coal (i.e., biomass), typically burned in poorly functioning stoves, may lead to very high levels of household air pollution¹³ and increase the risk for COPD. COPD in non-smokers is more common in females of younger age¹. Symptoms and spirometric impairment are similar to those of smoking-induced COPD but emphysema is less prevalent and lung function decline less steep in non-smoking COPD. Research is needed to identify the most appropriate pharmacotherapy for this type of COPD¹⁰. Occupational exposures, including organic and inorganic dusts, chemical agents, and fumes^14,15, and air pollution also increases the risk of COPD¹⁶.
香煙吸煙是慢性阻塞性肺病（COPD）的主要環境風險因素；然而，少於 50%的重度吸煙者會發展為 COPD ⁸ ，而且如下面所討論的，大約三分之一的 COPD 患者從未吸煙 ^9,10 。被動吸煙暴露也是 COPD 的風險因素 ¹¹ 。懷孕期間吸煙對胎兒構成風險，因為它會改變胎兒在子宮內的肺部生長和發展 ^3,12 。在低收入和中等收入國家（LMICs），非吸煙者的 COPD 可能佔高達 60-70%的病例 ¹⁰ 。木材、動物糞便、作物殘渣和煤（即生物質），通常在運作不良的爐具中燃燒，可能導致家庭空氣污染水平非常高 ¹³ ，並增加 COPD 的風險。非吸煙者的 COPD 在年輕女性中更為常見 ¹ 。症狀和肺活量測試的損害類似於吸煙引起的 COPD，但非吸煙者的肺氣腫較少，肺功能下降的幅度也較小。需要進行研究以確定這種類型 COPD 最合適的藥物治療 ¹⁰ 。職業暴露，包括有機和無機粉塵、化學劑和煙霧 ^14,15 ，以及空氣污染也增加 COPD 的風險 ¹⁶ 。

The time axis: lung function trajectories
時間軸：肺功能軌跡

At birth, the lungs are not fully developed. They grow and mature until about 20–25 years of age (earlier in females), when lung function reaches its peak¹⁷. This is followed by a relatively short plateau (which may vary from individual to individual) and a final phase of mild lung function decline due to physiological lung aging (Fig. 1). This normal lung function trajectory can be altered by processes occurring during gestation, birth, childhood, and adolescence that affect lung growth (hence, peak lung function) and/or processes shortening the plateau phase and/or accelerating the aging phase¹⁸ (Fig. 1). These processes include, among others, the following ones:
在出生時，肺部尚未完全發育。它們會持續生長和成熟，直到約 20 至 25 歲（女性較早），此時肺功能達到高峰 ¹⁷ 。隨後是相對較短的平穩期（可能因個體而異），以及由於生理性肺部老化導致的輕微肺功能下降的最終階段（圖 1）。這一正常的肺功能軌跡可能會受到妊娠、出生、童年和青春期期間發生的過程的影響，這些過程會影響肺部生長（因此，峰值肺功能）和/或縮短平穩期和/或加速老化階段 ¹⁸ （圖 1）。這些過程包括但不限於以下幾個方面：

• Childhood disadvantage factors, such as prematurity, low birth weight, maternal smoking during pregnancy, repeated respiratory infections and poor nutrition are key determinants of peak lung function attained in early adulthood^{19,20,21,22,23,24,25,26}. Reduced peak lung function in early adulthood increases the risk of COPD later in life^19,27,28. In fact, approximately 50% of patients develop COPD due to accelerated decline in FEV₁ over time while the other 50% develop it due to abnormal lung growth and development (with normal lung function decline over time)²⁹.
  童年不利因素，如早產、低出生體重、孕期母親吸煙、反覆呼吸道感染和營養不良，是決定早期成年時達到的肺功能峰值的關鍵因素 ^{19,20,21,22,23,24,25,26} 。早期成年時肺功能峰值降低會增加日後罹患慢性阻塞性肺病（COPD）的風險 ^19,27,28 。事實上，大約 50%的患者因 FEV 隨時間加速下降而發展為 COPD ₁ ，而另外 50%則因肺部生長和發展異常（隨時間正常肺功能下降）而發展為 COPD ²⁹ 。

• Poverty and low socioeconomic status increase the risk of COPD, likely because of exposure to household and outdoor air pollutants, crowding, poor nutrition, infections, or other factors related to low socioeconomic status³⁰.
  貧窮和低社會經濟地位增加了慢性阻塞性肺病（COPD）的風險，這可能是因為接觸到家庭和戶外空氣污染物、擁擠、營養不良、感染或其他與低社會經濟地位相關的因素 ³⁰ 。

• Severe respiratory infections in childhood have been associated with reduced lung function and increased respiratory symptoms in adulthood^31,32. In adults, chronic bronchial infection, particularly with Pseudomonas aeruginosa, is associated with accelerated FEV₁ decline³³. In many parts of the world, tuberculosis³⁴ and HIV infection³⁵ are also risk factors for COPD.
  兒童期的嚴重呼吸道感染與成年後肺功能下降和呼吸症狀增加有關 ^31,32 。在成年人中，慢性支氣管感染，特別是由綠膿桿菌引起的，與 FEV ₁ 下降加速 ³³ 有關。在世界許多地方，結核病 ³⁴ 和 HIV 感染 ³⁵ 也是 COPD 的風險因素。

For further explanations, see text. Reproduced with permission from reference ⁸⁹.
如需進一步說明，請參見文本。經參考文獻 ⁸⁹ 授權重製。

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As a result of all these factors, in the general population there is a range of lung function trajectories through the lifetime¹⁸ (Fig. 1). Trajectories below the normal range are associated with a higher prevalence and earlier incidence of multi-morbidity and premature death³⁶, whereas those above the normal range are associated with healthier aging, fewer cardiovascular and respiratory events, as well as with a survival benefit^37,38.
由於所有這些因素，普通人群中存在一系列的肺功能軌跡，貫穿整個生命週期 ¹⁸ （圖 1）。低於正常範圍的軌跡與多重疾病的較高流行率和較早的發病率以及過早死亡 ³⁶ 相關，而高於正常範圍的軌跡則與更健康的老化、較少的心血管和呼吸事件以及生存益處 ^37,38 相關。

Because it is now recognized that COPD can originate from multiples causes (etiotypes), GOLD 2023 proposes a new taxonomic classification (Fig. 2) that reflects two recent proposals^39,40. This taxonomic classification does not yet have a direct clinical translation because scientific evidence on the natural history and/or best treatment of many of these etiotypes is still lacking (the vast majority of scientific evidence available relates to smoking-related COPD). However, it aims at raising awareness about these other, frequent, non-smoking related COPD and to stimulate research on the mechanisms, prevention, early diagnosis and management of these other etiotypes of COPD, which are highly prevalent around the globe¹⁰.
由於現在已認識到慢性阻塞性肺病（COPD）可以源自多種原因（病因類型），GOLD 2023 提出了新的分類法（圖 2），反映了兩個最近的提議 ^39,40 。這一分類法尚未有直接的臨床應用，因為對於許多這些病因類型的自然歷史和/或最佳治療的科學證據仍然不足（目前可用的絕大多數科學證據與吸煙相關的 COPD 有關）。然而，它旨在提高對這些其他常見的非吸煙相關 COPD 的認識，並促進對這些其他 COPD 病因類型的機制、預防、早期診斷和管理的研究，這些病因類型在全球範圍內高度流行 ¹⁰ 。

Reproduced with permission from www.goldcopd.org.
經過 www.goldcopd.org 的許可重製。

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A diagnosis of COPD should be considered in any patient who complains of dyspnoea, chronic cough or sputum production, a history of recurrent lower respiratory tract infections and/or a history of exposure to risk factors. However, forced spirometry showing the presence of a post-bronchodilator FEV₁/FVC < 0.7 is mandatory to establish the diagnosis of COPD. There is a debate on whether it would be better to use the lower limit of normal of the FEV₁/FVC ratio instead of a fixed value (<0.7). The full GOLD 2023 document (freely downloadable from www.goldcopd.org) discusses at length the pros and cons of both options. We invite the interested reader to read them there. In any case, it is of the outmost importance, thus, that all Primary Care Centres have access to standard spirometers. This should be considered a basic technological element included in the service portfolio of all public health centres. In addition, it is also essential to have professionals (physician, nurses, technicians) appropriately trained to perform valid spirometries. GOLD 2023 realizes, however, that this ideal scenario may not be feasible in LMIC^41,42, but considers that it is important to state clearly that the diagnosis of COPD requires a spirometric measurement and that, without it, this diagnosis cannot be confirmed. Given the very large underdiagnosis of COPD, GOLD 2023 advocates active case finding (i.e., performing spirometry in patients with symptoms and/or risk factors), but not screening spirometry¹. Small hand-held devices are useful to rule out COPD but not to confirm diagnosis.
應考慮對任何抱怨呼吸困難、慢性咳嗽或痰液產生、反覆下呼吸道感染病史和/或接觸風險因素病史的患者進行 COPD 診斷。然而，強制性肺活量測試顯示支氣管擴張劑後 FEV ₁ /FVC < 0.7 是確立 COPD 診斷的必要條件。關於是否應使用 FEV ₁ /FVC 比率的正常下限而不是固定值（<0.7）存在爭論。完整的 GOLD 2023 文件（可從 www.goldcopd.org 免費下載）詳細討論了這兩種選擇的利弊。我們邀請感興趣的讀者在那裡閱讀。無論如何，所有初級保健中心都必須能夠使用標準肺活量計，這是至關重要的。因此，這應被視為所有公共衛生中心服務組合中的基本技術元素。此外，還必須有適當訓練的專業人員（醫生、護士、技術人員）來進行有效的肺活量測試。 GOLD 2023 意識到，這種理想情況在低中收入國家（LMIC）可能不可行，但認為明確指出慢性阻塞性肺病（COPD）的診斷需要進行肺功能測試是重要的，沒有這項測試，無法確認此診斷。考慮到 COPD 的嚴重漏診，GOLD 2023 倡導積極尋找病例（即對有症狀和/或風險因素的患者進行肺功能測試），但不建議進行篩查性肺功能測試。小型手持設備對排除 COPD 有用，但無法確認診斷。

Another important consideration here is that non-fully reversible airflow obstruction is not specific for COPD and can occur in other respiratory diseases (e.g., asthma, bronchiectasis, post-tuberculosis, etc.). Thus, it is very important that the clinical context and risk factors (see above) must also be considered when establishing a diagnosis of COPD.
另一個重要的考量是，非完全可逆的氣流阻塞並不特定於慢性阻塞性肺病（COPD），也可能出現在其他呼吸系統疾病中（例如，哮喘、支氣管擴張症、肺結核後遺症等）。因此，在確立 COPD 的診斷時，臨床背景和風險因素（見上文）也必須考慮，這是非常重要的。

The FEV₁ values serve to determine the severity of airflow obstruction (GOLD grades 1,2,3, 4). The FEV1 thresholds for this severity gradation (mild (FEV1 ≥ 80% ref), moderate (FEV1 50-79% ref), severe (FEV1 30–49% ref) and very severe (FEV1 < 30% ref) have not changed from previous GOLD documents.
FEV ₁ 值用於確定氣流阻塞的嚴重程度（GOLD 分級 1、2、3、4）。這一嚴重程度分級的 FEV1 閾值（輕度（FEV1 ≥ 80% 參考）、中度（FEV1 50-79% 參考）、重度（FEV1 30–49% 參考）和非常重度（FEV1 < 30% 參考））與之前的 GOLD 文件沒有變化。

Finally, in asymptomatic individuals without any significant exposure to tobacco or other risk factors, screening spirometry is not indicated, but in those with symptoms and/or risk factors (e.g., >20 pack-years of smoking, recurrent chest infections, prematurity or other significant early life events), spirometry should be considered as a valid method for case finding¹.
最後，在沒有任何顯著接觸煙草或其他風險因素的無症狀個體中，不建議進行篩檢性肺活量測試，但對於有症狀和/或風險因素（例如，吸煙超過 20 包年、反覆胸部感染、早產或其他顯著的早期生活事件）的人，應考慮將肺活量測試作為有效的病例發現方法 ¹ 。

GOLD 2023 also recognizes that some patients without airflow obstruction (i.e., FEV₁/FVC > 0.7) may present symptoms and/or other functional abnormalities (e.g., reduced carbon monoxide diffusing capacity or enhanced rate of FEV₁ decline) and/or structural lung abnormalities (e.g. emphysema on computed tomography (CT)) that may eventually progress (or not) to COPD (as defined by the presence of airflow obstruction); these patients are now termed pre-COPD¹. Likewise, GOLD 2023 recognizes that there are patients with preserved FEV₁/FVC ratio (so no evidence of airflow obstruction) with reduced FEV₁; these patients are named PRISm (Preserved Ratio with Impaired Spirometry) and, like pre-COPD patients, may progress (or not) over time to COPD¹. There is a lot to be learned about the mechanisms, natural history, and treatment of pre-COPD and PRISm patients, but the realization of their existence in real life open new opportunities for prevention, early diagnosis, and management¹.
GOLD 2023 也認識到一些沒有氣流阻塞的患者（即 FEV ₁ /FVC > 0.7）可能會出現症狀和/或其他功能異常（例如，碳一氧化碳擴散能力降低或 FEV ₁ 下降速率增強）和/或結構性肺部異常（例如，計算機斷層掃描（CT）上的肺氣腫），這些情況最終可能進展（或不進展）為 COPD（根據氣流阻塞的存在來定義）；這些患者現在被稱為前 COPD ¹ 。同樣，GOLD 2023 認識到有些患者的 FEV ₁ /FVC 比率保持正常（因此沒有氣流阻塞的證據），但 FEV ₁ 降低；這些患者被稱為 PRISm（保留比率但肺功能受損），並且與前 COPD 患者一樣，可能隨著時間的推移進展（或不進展）為 COPD ¹ 。關於前 COPD 和 PRISm 患者的機制、自然歷史和治療還有很多需要學習的地方，但他們在現實生活中的存在為預防、早期診斷和管理 ¹ 開辟了新的機會。

GOLD 2023 modifies the previous ABCD assessment tool⁴³ to a new one (ABE). This aims at recognizing the clinical impact of exacerbations, independently of the level of symptoms of the patient⁴⁴ (Fig. 3). The thresholds proposed for symptoms (X-axis: mMRC or CAT above or below 1 or 10, respectively) and history of exacerbations in the previous year (Y-axis: 0-1 moderate exacerbations vs. ≥2 moderate exacerbations or ≥1 exacerbation leading to hospital admission) are unchanged from previous GOLD documents. In this 2023 proposal, therefore, the A and B groups remain unchanged, but the former C and D groups are now merged into a single group termed “E” (for “Exacerbations”). This has implications for the initial pharmacological treatment recommendations, as discussed below.
GOLD 2023 將先前的 ABCD 評估工具 ⁴³ 修改為新的工具 (ABE)。這旨在獨立於患者的症狀水平，識別惡化的臨床影響 ⁴⁴ (圖 3)。對於症狀的閾值 (X 軸：mMRC 或 CAT 分別高於或低於 1 或 10) 和過去一年惡化的歷史 (Y 軸：0-1 次中度惡化 vs. ≥2 次中度惡化或 ≥1 次導致住院的惡化) 與先前的 GOLD 文件保持不變。因此，在這個 2023 年的提案中，A 和 B 組保持不變，但以前的 C 和 D 組現在合併為一個稱為 “E” (代表 “惡化”) 的單一組。這對於初始藥物治療建議有影響，詳情如下。

Exacerbation history refers to exacerbations suffered the previous year. *: single inhaler therapy may be more convenient and effective than multiple inhalers. mMRC: modified Medical Research Dyspnoea Questionnaire. CAT: COPD Assessment Test. LAMA: long-acting anti-muscarinic antagonist; LABA: long-acting β2 receptor agonist; ICS: inhaled corticosteroid; eos: eosinophils. Reproduced with permission from www.goldcopd.org.
惡化歷史指的是前一年所經歷的惡化情況。*: 單一吸入器療法可能比多個吸入器更方便和有效。mMRC：修訂版醫學研究呼吸困難問卷。CAT：慢性阻塞性肺病評估測試。LAMA：長效抗膽鹼拮抗劑；LABA：長效β2 受體激動劑；ICS：吸入性皮質類固醇；eos：嗜酸性粒細胞。經 www.goldcopd.org 授權重製。

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Choice and appropriate use of inhaler devices
吸入裝置的選擇與適當使用

Because inhaled therapy is the cornerstone of COPD treatment, the appropriate use of these devices (irrespective of the molecule(s) contained in them) is essential to optimize their therapeutic effect. This requires educating and training in the correct use of the device of both providers and patients: this is a key task of primary care professionals, preferably done in face-to-face consultations rather than by telemedicine. Regular assessment at follow-up is recommend to maintain their effective use regardless patients’ previous experience and time from first prescription. Patients’ and devices’ characteristics should be considered before making a decision about treatment. Box 1 summarizes the main principles that should be considered to guide the individualized selection of the appropriate device for a given patient¹. Besides, the following aspects need to be considered also:
因為吸入治療是慢性阻塞性肺病（COPD）治療的基石，因此適當使用這些裝置（無論其所含分子為何）對於優化其治療效果至關重要。這需要對提供者和患者進行正確使用裝置的教育和培訓：這是初級護理專業人員的一項關鍵任務，最好是在面對面的諮詢中進行，而不是通過遠程醫療。建議在隨訪中定期評估，以維持其有效使用，無論患者的先前經驗和首次處方的時間。患者和裝置的特徵應在做出治療決策之前考慮。框 1 總結了應考慮的主要原則，以指導為特定患者選擇適當裝置的個性化選擇 ¹ 。此外，還需要考慮以下方面：

• If a patient is currently taking inhaled therapy and able to use their current device correctly, new therapy is best prescribed in the same device¹. If a new device is required, either because the patient is not using their current device correctly or the drug is not available in the same device, an iterative process with the patient should be used to select a delivery system and ensure the patient can use it¹.
  如果患者目前正在接受吸入治療並能正確使用他們目前的裝置，則最好在相同的裝置中開立新療法 ¹ 。如果需要新的裝置，無論是因為患者未正確使用目前的裝置，還是因為該藥物在相同的裝置中不可用，都應與患者進行迭代過程，以選擇給藥系統並確保患者能夠使用它 ¹ 。

• Appropriate education must be provided by health care professionals, including physical, video- or be-based demonstration of the proper technique and live verification that the patient masters this technique. It is crucial to check regularly (ideally, at each visit) that patients continue to use their devices correctly. The lack of placebo devices within clinical areas is often a limitation and barrier to providing quality inhaler technique instruction to patients. Encouraging a patient to bring their own devices to the clinic is a useful alternative.
  適當的教育必須由醫療專業人員提供，包括實體、視頻或基於示範的正確技術，以及現場驗證患者掌握此技術。定期檢查（理想情況下，在每次就診時）患者是否繼續正確使用其設備至關重要。臨床領域缺乏安慰劑設備通常是提供高品質吸入器技術指導的限制和障礙。鼓勵患者攜帶自己的設備到診所是一個有用的替代方案。

Initial pharmacological treatment
初始藥物治療

As shown in Fig. 3, the recommended initial treatment of patients in Group A has not changed (a bronchodilator). In contrast, for patients in Group B, a dual long-acting bronchodilator combination (β2 adrenergic (LABA) + anti-muscarinic (LAMA) bronchodilators) is now recommended since dual therapy is more effective than monotherapy with similar side-effects^45,46,47. The same initial treatment (LAMA + LABA) is also recommended for patients in group E, except for those individuals with blood eosinophils ≥ 300 cells/µL, in whom starting with triple therapy (LABA + LAMA + ICS) can be considered. The use of LABA + ICS in COPD is no longer encouraged¹. If there is an indication for an ICS, then LABA + LAMA + ICS has been shown to be superior to LABA + ICS and is therefore the preferred choice^48,49. If patients with COPD have concomitant asthma, they should be treated as if they have asthma⁵⁰.
如圖 3 所示，A 組患者的建議初始治療未發生變化（支氣管擴張劑）。相反，對於 B 組患者，現在建議使用雙重長效支氣管擴張劑組合（β2 腎上腺素能（LABA）+ 抗副交感神經（LAMA）支氣管擴張劑），因為雙重療法比單一療法更有效且副作用相似 ^45,46,47 。對於 E 組患者，也建議相同的初始治療（LAMA + LABA），但對於血嗜酸性粒細胞數量≥300 細胞/µL 的個體，可以考慮從三重療法（LABA + LAMA + ICS）開始。在 COPD 中不再鼓勵使用 LABA + ICS ¹ 。如果有使用 ICS 的指徵，則 LABA + LAMA + ICS 已被證明優於 LABA + ICS，因此是首選 ^48,49 。如果 COPD 患者同時患有哮喘，則應按哮喘進行治療 ⁵⁰ 。

Follow-up pharmacological treatment
後續藥物治療

Following initiation of treatment, patients should be reassessed, and treatment should be adjusted if needed. GOLD 2023 continues to recommend that follow-up treatment be based on two key treatable traits^51,52: dyspnoea and exacerbations (Fig. 4).
在治療開始後，應對患者進行重新評估，如有需要應調整治療。GOLD 2023 繼續建議後續治療應基於兩個關鍵可治療特徵 ^51,52 ：呼吸困難和加重發作（圖 4）。

*: single inhaler therapy may be more convenient and effective than multiple inhalers; **: Consider de-escalation of ICS if pneumonia or other considerable side-effects. In case of blood eos ≥300 cells/μl de-escalation is more likely to be associated with the development of exacerbations. Exacerbation history refers to exacerbations suffered the previous year. mMRC: modified Medical Research Dyspnea Questionnaire. CAT: COPD Assessment Test. LAMA: long-acting anti-muscarinic antagonist; LABA: long-acting β2 receptor agonist; ICS: inhaled corticosteroid; eos: eosinophils. Reproduced with permission from www.goldcopd.org.
*: 單一吸入器療法可能比多個吸入器更方便和有效；**: 如果有肺炎或其他顯著副作用，考慮減少吸入性類固醇（ICS）的劑量。在血液嗜酸性細胞數≥300 cells/μl 的情況下，減少劑量更可能與加重發作的發展相關。加重病史指的是前一年經歷的加重發作。mMRC: 修訂版醫學研究呼吸困難問卷。CAT: 慢性阻塞性肺病評估測試。LAMA: 長效抗膽鹼劑；LABA: 長效β2 受體激動劑；ICS: 吸入性類固醇；嗜酸性細胞: 嗜酸性白血球。經 www.goldcopd.org 授權重製。

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For patients with persistent dyspnoea on bronchodilator monotherapy (left column), it is critical to check inhaler technique; if good technique is assured, then a step up to LABA + LAMA is recommended if the patient was started on mono-bronchodilator treatment. If this does not improve symptoms clinicians should consider switching inhaler device or molecules, as well as investigating and treating other causes of dyspnoea and consider referral for pulmonary rehabilitation¹.
對於在支氣管擴張劑單藥治療下持續出現呼吸困難的患者（左欄），檢查吸入器的使用技術至關重要；如果確保技術良好，則建議在患者開始單一支氣管擴張劑治療後，升級至長效β2-腎上腺素能激動劑（LABA）+ 長效抗膽鹼劑（LAMA）。如果這樣做仍未改善症狀，臨床醫生應考慮更換吸入裝置或藥物，並調查和治療其他呼吸困難的原因，並考慮轉診進行肺部康復 ¹ 。

For patients continuing to have exacerbations (with or without persistent dyspnoea) on bronchodilator monotherapy (right column), escalation to LABA + LAMA is recommended, except for patients with blood eosinophils ≥ 300 cells/µL who may be escalated to LABA + LAMA + ICS. For patients with persistent exacerbations on LABA + LAMA, escalation to LABA + LAMA + ICS is recommended if they have blood eosinophils ≥ 100 cells/µL. This is important since two recent large randomized clinical trials have shown that tiple therapy in patients with frequent exacerbations reduce all-cause mortality^53,54. For patients continuing to exacerbate despite therapy with LABA + LAMA + ICS or those who have an eosinophil count of < 100 cells/µL, the addition of roflumilast (particularly in patients with chronic bronchitis and an FEV₁ < 50% predicted)^55,56,57 or a macrolide (particularly in patients who are not current smokers) may be considered^58,59.
對於在支氣管擴張劑單藥治療（右欄）下仍持續出現惡化（有或沒有持續性呼吸困難）的患者，建議升級至 LABA + LAMA，除了血液嗜酸性粒細胞數 ≥ 300 cells/µL 的患者可升級至 LABA + LAMA + ICS。對於在 LABA + LAMA 下持續惡化的患者，如果他們的血液嗜酸性粒細胞數 ≥ 100 cells/µL，建議升級至 LABA + LAMA + ICS。這一點很重要，因為最近兩項大型隨機臨床試驗顯示，對於頻繁惡化的患者，三重療法可降低全因死亡率 ^53,54 。對於在 LABA + LAMA + ICS 治療下仍持續惡化的患者或嗜酸性粒細胞數 < 100 cells/µL 的患者，可以考慮添加 roflumilast（特別是對於慢性支氣管炎且 FEV ₁ < 50%預測的患者） ^55,56,57 或大環內酯（特別是對於非吸煙者） ^58,59 。

Patients whose pharmacological treatment has been modified should be closely monitored. ICS de-escalation or withdrawal can be considered if pneumonia or other considerable side effects occur, although if the blood eosinophil count is ≥300 cells/μl, ICS de-escalation is more likely to be associated with the development of exacerbations.
應密切監測藥物治療已被修改的患者。如果出現肺炎或其他顯著副作用，可以考慮減少或停止吸入性類固醇（ICS），儘管如果血液嗜酸性粒細胞計數≥300 細胞/μl，則 ICS 減少更可能與惡化的發展相關。

Finally, if a patient with COPD and no features of asthma has already been treated—for whatever reason—with LABA + ICS and is well controlled in terms of symptoms and exacerbations, then LABA + ICS could be continued. However, if they remain dyspnoeic switching to LABA + LAMA should be considered, and if they have further exacerbations, treatment should be escalated to LABA + LAMA + ICS.
最後，如果一位患有慢性阻塞性肺病（COPD）且沒有哮喘特徵的患者已經接受過治療——無論出於何種原因——使用長效β2 激動劑（LABA）+ 吸入性類固醇（ICS），並且在症狀和惡化方面控制良好，那麼可以繼續使用 LABA + ICS。然而，如果他們仍然感到呼吸困難，則應考慮轉換為 LABA + 長效抗膽鹼劑（LAMA），如果他們有進一步的惡化，則應將治療升級為 LABA + LAMA + ICS。

Non-pharmacological treatment is a key part of the adequate management of COPD and should always be considered in combination with the pharmacologic treatment discussed above. It includes one or more of the following¹:
非藥物治療是慢性阻塞性肺病（COPD）適當管理的關鍵部分，應始終與上述藥物治療結合考慮。它包括以下一項或多項 ¹ :

• Education and supported self-management. All patients should receive basic information about COPD and its treatment (respiratory medications and inhalation devices) and advice about when to seek help. Primary care is the right place to educate COPD patients and health-care professionals should be given the right tools to do that. However, education by itself does not often change behaviour. Education needs to be delivered in the context of a supportive behaviour change intervention that is personalized to the individual and their sociodemographic/cultural context.
  教育和支持自我管理。所有患者應該獲得有關慢性阻塞性肺病（COPD）及其治療（呼吸藥物和吸入裝置）的基本信息，以及何時尋求幫助的建議。初級護理是教育 COPD 患者的合適場所，醫療專業人員應該獲得適當的工具來實現這一點。然而，僅僅進行教育通常不會改變行為。教育需要在支持性行為改變干預的背景下進行，並根據個人及其社會人口/文化背景進行個性化。

• Smoking cessation. All patients who continue to smoke should be offered help and treatment to quit. Brief intervention in primary care is effective and pharmacologic treatment should be offered if possible⁶⁰. Likewise, strategies for reducing exposure to indoor air pollution need to be considered too.
  戒菸。所有持續吸煙的患者應該獲得幫助和治療以戒菸。初級保健中的簡短介入是有效的，並且應該在可能的情況下提供藥物治療 ⁶⁰ 。同樣，減少室內空氣污染暴露的策略也需要考慮。

• Vaccination. Depending on local guidelines, patients should be offered vaccination against influenza, pneumococcus, COVlD-19, pertussis, and herpes zoster.
  疫苗接種。根據當地指導方針，應為患者提供流感、肺炎球菌、COVID-19、百日咳和帶狀皰疹的疫苗接種。

• Physical activity. All COPD patients should be encouraged to keep active. Technology-based interventions have the potential to provide convenient and accessible means to enhance exercise self-efficacy, and to educate and motivate patients to make healthy lifestyle changes⁶¹.
  身體活動。所有 COPD 患者應被鼓勵保持活躍。基於技術的干預措施有潛力提供方便且可及的方式來增強運動自我效能，並教育和激勵患者進行健康的生活方式改變 ⁶¹ 。

• Nutritional and Psychosocial assessment and support are important aspects to consider and treat if needed. Up to 50% of people with COPD weigh less than 90% of ideal body weight⁶². Dietary advice and oral supplementation have been reported to improve body weight, quality of life, respiratory muscle strength and 6-minute walk distance in patients with COPD¹. Psychosocial consideration and support is also important in the management of these patients¹.
  營養和心理社會評估及支持是需要考慮和治療的重要方面。如果需要，最多有 50%的慢性阻塞性肺病（COPD）患者的體重低於理想體重的 90% ⁶² 。有報導指出，飲食建議和口服補充劑能改善 COPD 患者的體重、生活質量、呼吸肌肉力量和 6 分鐘步行距離 ¹ 。在這些患者的管理中，心理社會考量和支持也非常重要 ¹ 。

• Pulmonary Rehabilitation (PR). PR, including community and home-based, is beneficial¹. Accordingly, patients with high symptom burden and risk of exacerbations (GOLD groups B and E) should be recommended to take part in a formal PR program designed and delivered in a structured manner, considering the individual’s COPD characteristics and comorbidities^63,64,65,66. In some settings, this may be combined with rehabilitation for cardiovascular patients.
  肺部復健 (PR)。PR，包括社區和居家型，對患者有益 ¹ 。因此，症狀負擔高且有惡化風險的患者 (GOLD B 和 E 組) 應被建議參加一個正式的 PR 計劃，該計劃應以結構化的方式設計和提供，考慮個體的 COPD 特徵和合併症 ^63,64,65,66 。在某些環境中，這可能與心血管患者的復健相結合。

• Oxygen therapy and ventilatory support. The criteria for prescribing long term oxygen therapy and ventilator support remain unchanged and are described in detail in the GOLD 2023 report¹.
  氧氣治療和通氣支持。長期氧氣治療和通氣支持的處方標準保持不變，並在 GOLD 2023 報告中詳細描述 ¹ 。

• Surgical and endoscopic lung volume reduction. In selected patients with symptomatic heterogeneous or homogenous emphysema and significant hyperinflation refractory to optimized medical care, surgical or bronchoscopic modes of lung volume reduction may be indicated. The complete GOLD report provides specific recommendations for different procedures ¹. Likewise, younger COPD patients with severe COPD should be considered for lung transplant¹.
  外科及內視鏡肺容積減少。在選定的有症狀的異質或同質肺氣腫患者中，若存在對優化醫療護理無法改善的顯著過度膨脹，則可能需要進行外科或支氣管鏡肺容積減少。完整的 GOLD 報告提供了針對不同程序的具體建議 ¹ 。同樣，年輕的重度 COPD 患者應考慮進行肺移植 ¹ 。

• End of Life and Palliative Care. All patients with advanced COPD should be considered for end of life and palliative care support to optimize symptom control and allow patients and their families to make informed choices about future management¹.
  末期生命與緩和醫療。所有晚期 COPD 患者應考慮接受末期生命與緩和醫療支持，以優化症狀控制，並使患者及其家屬能夠對未來的管理做出知情選擇 ¹ 。

New definition  新定義

The previous GOLD definition of ECOPD was non-specific (“acute worsening of respiratory symptoms that results in additional therapy”) and its severity was determined post facto (mild, moderate or severe) based on the use of healthcare resources⁶⁷. This is useless to guide treatment at the point of care.
之前的 GOLD 定義的 ECOPD 是非特異性的（“呼吸症狀急性惡化，導致額外治療”），其嚴重程度是根據醫療資源的使用事後確定的（輕度、中度或重度） ⁶⁷ 。這對於在護理現場指導治療是無用的。

To address these limitations, GOLD 2023 now proposes a more specific definition: “ECOPD is an event characterized by increased dyspnoea and/or cough and sputum that worsens in <14 days which may be accompanied by tachypnoea and/or tachycardia and is often associated with increased local and systemic inflammation caused by infection, pollution, or other insults to the airways”⁶⁸. Providing a time frame (<14 days) facilitates the differentiation of an exacerbation of COPD from disease worsening. As discussed below, a number of biomarkers can help determining the severity of the ECOPD (hence, to guide treatment) at the point of care. Primary care is the most important setting for the detection and early recognition of signs and symptoms suggestive of an exacerbation of COPD.
為了解決這些限制，GOLD 2023 現在提出了一個更具體的定義：“ECOPD 是一種事件，其特徵是呼吸困難和/或咳嗽及痰液在 <14 天內加重，可能伴隨有呼吸急促和/或心跳過速，並且通常與由感染、污染或其他對氣道的損害引起的局部和全身性炎症增加有關” ⁶⁸ 。提供一個時間框架（<14 天）有助於區分 COPD 的惡化與疾病的加重。如下面所討論的，許多生物標記可以幫助在護理點確定 ECOPD 的嚴重程度（因此，指導治療）。初級護理是檢測和早期識別提示 COPD 惡化的徵兆和症狀的最重要環境。

Differential Diagnosis  鑑別診斷

Patients with COPD are at increased risk of other acute events, particularly decompensated heart failure, pneumonia and/or pulmonary embolism that may mimic or aggravate an ECOPD (Fig. 5)⁶⁹. Thus, careful differential diagnosis is essential since these other conditions also deserve treatment if present (Fig. 5).
慢性阻塞性肺病（COPD）患者面臨其他急性事件的風險增加，特別是失代償性心臟衰竭、肺炎和/或肺栓塞，這些情況可能模仿或加重急性加重型 COPD（ECOPD）（圖 5） ⁶⁹ 。因此，仔細的鑑別診斷至關重要，因為如果存在這些其他情況，也應該進行治療（圖 5）。

Definition of abbreviations: VAS: visual analog scale; RR: respiratory rate; HR: heart rate; CRP: C-reactive protein. SaO₂: arterial oxygen saturation; PaO₂: arterial partial pressure of oxygen; ABG: arterial blood gases; ABG should show new onset/worsening hypercapnia or acidosis since a few patients may have chronic hypercapnia. Adapted from ref. ⁶⁸. Reproduced with permission from www.goldcopd.org.
縮寫定義：VAS：視覺類比量表；RR：呼吸頻率；HR：心率；CRP：C-反應蛋白。SaO ₂ ：動脈氧飽和度；PaO ₂ ：動脈氧分壓；ABG：動脈血氣；ABG 應顯示新發作/惡化的高碳酸血症或酸中毒，因為一些患者可能有慢性高碳酸血症。改編自參考文獻 ⁶⁸ 。經 www.goldcopd.org 授權重製。

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Assessment of ECOPD severity
慢性阻塞性肺病急性加重嚴重程度評估

GOLD 2023 suggests using several, easy to obtain clinical variables to define the severity of ECOPD (mild, moderate or severe) at the point of care (Fig. 5)⁶⁸. In a primary care setting, severity can be determined by determining dyspnoea intensity (using a VAS 0 to 10 dyspnoea scale, with zero being not short of breath at all and 10 the worst shortness of breath you have ever experienced), respiratory rate, heart rate and oxygen saturation level; where available, measuring blood C-reactive protein (CRP) levels is recommended (Fig. 5). To move from a mild to a moderate level, three of the variables need to exceed the proposed thresholds (Fig. 5). To determine the need for ventilatory support (usually in the emergency room or hospital setting) arterial blood gases should be measured.
GOLD 2023 建議使用幾個易於獲得的臨床變數來定義 ECOPD 的嚴重程度（輕度、中度或重度）在護理點（圖 5） ⁶⁸ 。在初級護理環境中，可以通過確定呼吸困難的強度（使用 0 到 10 的 VAS 呼吸困難量表，0 表示完全不呼吸困難，10 表示您曾經經歷過的最嚴重的呼吸困難）、呼吸頻率、心率和氧飽和度來確定嚴重程度；如有可能，建議測量血液中的 C-反應蛋白（CRP）水平（圖 5）。要從輕度轉變為中度，三個變數需要超過建議的閾值（圖 5）。要確定是否需要通氣支持（通常在急診室或醫院環境中），應測量動脈血氣。

Management of ECOPD  慢性阻塞性肺病急性加重的管理

Treatment setting  治療環境

Depending on the episode severity, as well as that of the underlying COPD and comorbidities, an ECOPD can be managed in either the outpatient or inpatient setting. The following are indications for hospitalization: (1) severe symptoms such as sudden worsening of resting dyspnoea, high respiratory rate, oxygen saturation ≤92%, confusion, drowsiness; (2) acute respiratory failure; (3) onset of new physical signs (e.g., cyanosis, peripheral oedema); (4) failure to respond to initial medical management; (5) presence of serious comorbidities (e.g., heart failure, newly occurring arrhythmias, etc.); and, (6) insufficient home support¹.
根據發作的嚴重程度，以及潛在的慢性阻塞性肺病（COPD）和合併症的情況，急性加重的 COPD（ECOPD）可以在門診或住院環境中進行管理。以下是住院的指徵：（1）嚴重症狀，如靜息呼吸困難突然加重、呼吸頻率高、氧飽和度≤92%、意識混亂、嗜睡；（2）急性呼吸衰竭；（3）出現新的身體徵象（例如，發紺、周邊水腫）；（4）對初始醫療管理無反應；（5）存在嚴重合併症（例如，心力衰竭、新發性心律不整等）；以及（6）家庭支持不足 ¹ 。

Pharmacological treatment
藥物治療

• Bronchodilators. Short-acting inhaled β2-agonists (SABA), with or without short-acting anticholinergics (SAMA), are the initial bronchodilators for acute treatment of ECOPD, administered using a metered-dose inhaler (MDI, with a spacer device if necessary, or nebulization¹. If a nebulizer is chosen, air-driven is preferable to oxygen-driven nebulization to avoid the potential risk of increasing PaCO₂⁷⁰. Intravenous methylxanthines (theophylline or aminophylline) are not recommended due to lack of efficacy and significant side effects^71,72.
  支氣管擴張劑。短效吸入型β2-激動劑（SABA），可與或不與短效抗膽鹼劑（SAMA）合併使用，是急性治療慢性阻塞性肺病（ECOPD）的初始支氣管擴張劑，通過定量吸入器（MDI，必要時可使用間隔裝置，或霧化 ¹ ）給藥。如果選擇霧化，建議使用空氣驅動的霧化器，而非氧氣驅動的霧化，以避免增加動脈二氧化碳分壓（PaCO） ₂ ⁷⁰ 的潛在風險。由於缺乏療效和顯著的副作用，不建議使用靜脈甲基黃嘌呤（茶鹼或氨茶鹼） ^71,72 。

• Glucocorticoids. Systemic glucocorticoids in COPD exacerbations improve lung function, oxygenation, risk of early relapse, and reduce treatment failures and length of hospitalization^73,74,75. A dose of 40 mg prednisone-equivalent per day for 5 days is recommended⁷⁶. Longer courses increase risk of pneumonia and mortality⁷⁷. Therapy with oral prednisolone is equally effective as intravenous administration⁷⁸.
  糖皮質激素。在慢性阻塞性肺病（COPD）惡化中，系統性糖皮質激素可改善肺功能、氧合、早期復發風險，並減少治療失敗和住院時間 ^73,74,75 。建議每日使用相當於 40 毫克的潑尼松，持續 5 天 ⁷⁶ 。較長的療程會增加肺炎和死亡率的風險 ⁷⁷ 。口服潑尼松龍的療效與靜脈給藥同樣有效 ⁷⁸ 。

• Antibiotics. Antibiotics should be given to patients with ECOPD who have increased sputum volume and sputum purulence and most of those require mechanical ventilation (invasive or non-invasive)⁷⁹. CRP-guided prescribing of antibiotics for ECOPD in primary care clinics resulted in a reduced proportion antibiotic use with no evidence of harm⁸⁰. The recommended length of antibiotic therapy is 5-7 days⁸¹. The choice of the antibiotic should be based on the local bacterial resistance pattern.
  抗生素。對於有增加痰量和痰膿性分泌物的慢性阻塞性肺病（ECOPD）患者，應給予抗生素，大多數患者需要機械通氣（侵入性或非侵入性） ⁷⁹ 。在初級保健診所中，根據 C 反應蛋白（CRP）指導的抗生素處方對於 ECOPD 導致抗生素使用比例降低，且沒有證據顯示有害 ⁸⁰ 。建議的抗生素治療長度為 5-7 天 ⁸¹ 。抗生素的選擇應基於當地的細菌耐藥模式。

Non-pharmacologic treatment
非藥物治療

• Oxygen therapy. Supplemental oxygen for hypoxemia should be titrated to a target saturation of 88-92%⁸². Venturi masks offer more accurate and controlled delivery of inspired oxygen than do nasal prongs¹.
  氧氣治療。對於低氧血症的補充氧氣應調整至目標飽和度 88-92% ⁸² 。文丘里面罩提供比鼻導管更準確和可控的吸入氧氣供應 ¹ 。

• Non-invasive ventilatory support (NIV). NIV is indicated in patients with respiratory acidosis since it improves gas exchange and decreases respiratory rate, work of breathing, the severity of breathlessness, intubation rates, and mortality^83,84.
  非侵入性通氣支持（NIV）。NIV 適用於有呼吸性酸中毒的患者，因為它改善氣體交換，降低呼吸頻率、呼吸工作量、呼吸困難的嚴重程度、插管率和死亡率 ^83,84 。

It is important that patients are reviewed clinically, and treatment adjusted if needed, after the exacerbation episode.
在惡化發作後，對患者進行臨床評估並在必要時調整治療是很重要的。

COPD almost invariably coexists with other chronic diseases (multimorbidity) that affect the patient’s clinical condition⁸⁵. In general, the presence of comorbidities should not alter COPD treatment and comorbidities should be treated per usual standards regardless of the presence of COPD¹. The most common comorbidities include:
COPD 幾乎總是與其他慢性疾病（多重疾病共存）共存，這會影響患者的臨床狀況 ⁸⁵ 。一般來說，合併症的存在不應改變 COPD 的治療，合併症應根據常規標準進行治療，無論是否存在 COPD ¹ 。最常見的合併症包括：

• Cardiovascular diseases, including hypertension, ischemic heart disease, congestive heart failure, arrythmias, and peripheral vascular disease.
  心血管疾病，包括高血壓、缺血性心臟病、充血性心臟衰竭、心律不整和周邊血管疾病。

• Lung cancer. Primary care professionals should always keep in mind that former or current smokers with COPD, particularly those with emphysema, are at higher risk of lung cancer. Given that lung cancer screening with low-dose CT is now recommended in many countries because it reduces all-cause mortality in older current or former smokers in the general population (https://view-health-screening-recommendations.service.gov.uk/lung-cancer/) it may seem advisable to consider early lung cancer detection by CT-scan in COPD patients seen in primary care.
  肺癌。初級保健專業人員應始終記住，患有慢性阻塞性肺病（COPD）的前吸煙者或現任吸煙者，特別是那些患有肺氣腫的人，肺癌風險較高。考慮到許多國家現在建議使用低劑量 CT 進行肺癌篩查，因為這可以降低一般人群中年長的現任或前吸煙者的全因死亡率（https://view-health-screening-recommendations.service.gov.uk/lung-cancer/），因此在初級保健中考慮對 COPD 患者進行 CT 掃描以早期檢測肺癌似乎是明智的。

• Bronchiectasis. A chest CT scan is recommended if bronchiectasis is suspected.
  支氣管擴張症。如果懷疑有支氣管擴張症，建議進行胸部 CT 掃描。

• Sleep apnoea occurs in about 14% of COPD patients and worsens their prognosis.
  睡眠呼吸暫停症在約 14%的慢性阻塞性肺病患者中發生，並惡化他們的預後。

• Osteoporosis. Osteoporosis is often under-diagnosed and associated with poor health status and prognosis. Recurrent use of systemic corticosteroids increases the risk of osteoporosis and should be avoided if possible.
  骨質疏鬆症。骨質疏鬆症常常被低估診斷，並與健康狀況不佳和預後不良相關。反覆使用全身性皮質類固醇會增加骨質疏鬆症的風險，應盡可能避免。

• Diabetes and metabolic syndrome. Both are frequent in COPD and affect their prognosis.
  糖尿病和代謝症候群。兩者在慢性阻塞性肺病中都很常見，並影響其預後。

• Gastroesophageal reflux. It is an independent risk factor for exacerbations and is associated with worse health status.
  胃食道逆流。它是加重的獨立風險因素，並與較差的健康狀態相關。

• Anaemia and polycythaemia can occur in patients with COPD and impact their health status and prognosis.
  貧血和紅血球增多症可以出現在慢性阻塞性肺病（COPD）患者中，並影響他們的健康狀況和預後。

• Mental health. Anxiety and depression are important and underdiagnosed comorbidities in COPD.
  心理健康。焦慮和抑鬱是慢性阻塞性肺病（COPD）中重要且未被充分診斷的共病。

COPD patients are not at increased risk of infection with SARS-CoV-2 but, if they get infected, then they do have a higher risk of hospitalization, ICU admission, and mortality⁸⁶. Thus, COPD patients should follow strictly preventive measures, including social distancing and washing hands, wearing a facial mask, should receive COVID-19 vaccination in line with national guidelines and should keep taking their oral and inhaled respiratory medications for COPD ¹. Patients should stay in contact with their friends and families by telecommunication and continue to keep active.
COPD 患者並不會增加感染 SARS-CoV-2 的風險，但如果他們感染，則確實有更高的住院、重症監護室入院和死亡風險 ⁸⁶ 。因此，COPD 患者應嚴格遵循預防措施，包括社交距離和洗手、佩戴口罩，應根據國家指導方針接種 COVID-19 疫苗，並應繼續服用他們的口服和吸入性呼吸藥物以治療 COPD ¹ 。患者應通過電信與朋友和家人保持聯繫，並繼續保持活躍。

COPD is a common, preventable, and treatable disease, but extensive under-diagnosis and misdiagnosis leads to patients receiving no treatment or incorrect treatment¹. The realization that environmental factors other than tobacco smoking can contribute to COPD, that it can start early in life and affect young individuals, and that there are precursor conditions (“Pre-COPD”, “PRISm”), opens new windows of opportunity for its prevention, early diagnosis, and prompt and appropriate therapeutic intervention^40,87. Importantly, several pharmacological (triple therapy) and non-pharmacological therapies (smoking cessation, long-term oxygen therapy, non-invasive positive pressure ventilation and lung volume reduction surgery) have now been shown to reduce mortality of COPD patients¹ but, in order to implement them, COPD must be first diagnosed. Thus, any strategy aimed at addressing and improving the huge underdiagnosis of COPD in the community should be reinforced. This is particularly relevant in a Primary Care setting. Further, because spirometry may not only diagnose respiratory diseases, but it can also identify a group of young adults (20-25 years of age) at risk of other cardiovascular and metabolic comorbidities and premature mortality³⁶, it has been proposed as a global marker of health⁸⁸. Box 2 summarizes the main recommendations for the pharmacologic treatment of COPD in Primary Care.
慢性阻塞性肺病（COPD）是一種常見的、可預防和可治療的疾病，但廣泛的漏診和誤診導致患者未接受治療或接受不正確的治療 ¹ 。意識到除了吸煙以外的環境因素也可能導致 COPD，該病可能在生命早期開始並影響年輕人，以及存在前驅狀況（“前 COPD”，“PRISm”），為其預防、早期診斷和及時適當的治療干預開啟了新的機會 ^40,87 。重要的是，幾種藥物治療（三重療法）和非藥物療法（戒煙、長期氧療、非侵入性正壓通氣和肺容積減少手術）現在已被證明能降低 COPD 患者的死亡率 ¹ ，但為了實施這些治療，必須首先診斷 COPD。因此，任何旨在解決和改善社區中 COPD 巨大漏診的策略都應得到加強。這在初級保健環境中特別相關。 此外，因為肺活量測試不僅可以診斷呼吸系統疾病，還可以識別一群有其他心血管和代謝共病及早死風險的年輕成年人（20-25 歲） ³⁶ ，因此它被提議作為健康的全球指標 ⁸⁸ 。框 2 總結了初級護理中慢性阻塞性肺病（COPD）藥物治療的主要建議。

Reporting summary

Further information on research design is available in the Nature Research Reporting Summary linked to this article.