ACLS-AHA-心肌梗塞使用嗎啡的效益與安全性Effect and Safety of Morphine Use in Acute Anterior ST‐Segment Elevation Myocardial Infarction

2026-05-14
Effect and Safety of Morphine Use in Acute Anterior ST‐Segment Elevation Myocardial Infarction- Originally Published 10 February 2018
STEMI=ST‐segment elevation myocardial infarction
NSTEMI=Non-ST‐segment elevation myocardial infarction
PCI=percutaneous coronary intervention
PPCI= primary PCI
MACE=major adverse cardiovascular event
重點
1. NSTEMI患者使用嗎啡會增加死亡和不良預後風險
2. STEMI患者做PPCI前使用嗎啡, 再灌注成功率降低, 心肌挽救指數低(具相關性. 但不能確定是否有因果性)
3. 在法國的兩個臨床研究中. 嗎啡並未增加院內併發症或一年內死亡率.



介紹
嗎啡目前被用於治療心肌梗塞引起的胸痛，並被推薦用於此用途，但由於缺乏支持性的臨床研究，其證據等級較低。
此外，美國心臟協會已將非ST段抬高型心肌梗塞（NSTEMI）患者使用嗎啡的建議等級從I級降至IIa級。這項調整是基於CRUSADE（快速風險分層不穩定型心絞痛患者能否透過早期實施美國心臟病學會/美國心臟協會指南來抑制不良預後）註冊研究的結果，該研究表明，在NSTEMI患者中，使用嗎啡會增加死亡和不良預後的風險。嗎啡也與ST段抬高型心肌梗塞（STEMI）患者行直接經皮冠狀動脈介入治療（PPCI）後再灌注成功率欠佳和心肌挽救指數低相關。
然而，在來自FAST-MI（法國急性ST段抬高型和非ST段抬高型心肌梗塞註冊研究）的兩個獨立隊列中，STEMI患者院前使用嗎啡並未增加院內併發症或1年死亡率。由於有這種爭議，需要進一步的研究。
本研究旨在探討嗎啡對接受 PPCI 治療的前壁 STEMI 患者族群臨床結局的影響。

Introduction
Morphine is currently used and recommended for the treatment of chest pain during myocardial infarction, but the level of evidence is low, attributed to the lack of supportive clinical studies.1, 2, 3, 4
Moreover, the American Heart Association has relegated morphine use in patients with non‐ST‐segment elevation myocardial infarction from a Class I to a Class IIa recommendation.3 This modification was driven by the results from the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines) registry showing that, in patients with non‐ST‐segment elevation myocardial infarction, morphine use increased the risk of death and adverse outcome.5 Morphine has also been associated with suboptimal reperfusion success and a low myocardial salvage index after primary percutaneous coronary intervention (PPCI) in patients presenting with ST‐segment elevation myocardial infarction (STEMI).6
Nevertheless, in 2 independent cohorts from the FAST‐MI (French Registry of Acute ST‐elevation and non‐ST‐elevation Myocardial Infarction) registry, prehospital morphine use in STEMI patients did not increase in‐hospital complications or 1‐year mortality.7 Because of this controversy, additional investigations are necessary.
The aim of this study was to explore the effect of morphine on clinical outcomes in a population of patients with anterior STEMI referred for PPCI.
結果
Results
The intent‐to‐treat CIRCUS population included 969 patients.8, 9 Two patients were not included in our analysis because of lack of information on morphine use. Morphine was used before PPCI in 554 (57.3%) patients. Baseline characteristics (Table 1) and periprocedural characteristics (Table 2) were well balanced between groups with and without morphine use. There was a nonsignificant trend toward younger age and a shorter total ischemic time in patients receiving morphine. There was also a trend toward more heart failure and cardiogenic shock in the morphine group: 13.1% versus 10.2% of patients admitted in Killip 2 or 3 and 1.4% versus 0% of patients admitted with cardiogenic in morphine and no‐morphine group, respectively (Table 2).
At 1 year, 236 (24.4%) patients had experienced at least 1 MACE. There was no significant difference in occurrence of MACE between groups: 145 (26.2%) and 91 (22.0%) patients in the groups with and without morphine, respectively (P=0.15; Table 3). Cumulative Kaplan–Meier estimates for the first occurrence of MACE (Figure 1) were not significantly different between groups (P=0.10).
In the Cox model, morphine use was not associated with the incidence of MACE (hazard ratio=1.25; 95% confidence interval [0.96; 1.62]; P=0.10), even after adjustment for age, ischemic time, infarct size (CPK peak), initial and final Thrombolysis in Myocardial Infarction flow, sex, smoking, hypertension, diabetes mellitus, previous myocardial infarction, and Killip class (hazard ratio=1.04; 95% confidence interval [0.75; 1.45]; P=0.82).
Incidence of individual MACE during 1 year was not significantly different between groups (Table 3; Figure 2).

There was no statistically significant difference on MACE occurrence (P=0.56) and on infarct size (P=0.61) between the 4 different treatment subgroups (Table 4). Interaction term, even after adjustment, was not significant and so for each clinical outcome individually (Table S1).


There was no significant difference in rates of all‐cause death at 1 year between groups (32 [5.3%] and 22 [5.8%] deaths in the groups with and without morphine, respectively; P=0.89).
The unadjusted Kaplan–Meier hazard curve for 1‐year all‐cause mortality is presented in Figure 3. No significant difference was observed between the groups with and without morphine (P=0.77).
CPK peak blood concentrations after PPCI were comparable in both groups (4023±118 and 3903±149 IU/L in the groups with and without morphine, respectively; P=0.52; Figure 4).
Rates of adverse left ventricular remodeling were also similar in both groups (205 [37.0%] and 134 [32.4%] patients with adverse remodeling in the groups with and without morphine, respectively; P=0.21).

討論
在一項針對大量急性前壁STEMI患者的研究中，有一半患者在接受PPCI治療前使用了嗎啡，但嗎啡對包括心血管死亡、心臟衰竭、心因性休克、復發性心肌梗塞、不穩定型心絞痛和中風在內的MACE複合主要終點沒有顯著影響。
鮮有其他研究評估急性冠狀動脈綜合症（ACS）患者在接受嗎啡治療以緩解胸痛後的臨床結局。 ¹⁶與我們的研究結果一致，兩項回顧性研究得出結論，嗎啡/靜脈注射麻醉劑不會對ACS患者的預後產生不良影響。其中一項納入1758例患者（765例ST段抬高型心肌梗塞[STEMI]和993例非ST段抬高型心肌梗塞[NSTEMI]）的研究顯示，使用靜脈注射麻醉劑並未增加30天死亡率。 ¹⁷第二項研究分析了兩組STEMI患者（分別來自FAST-MI 2010註冊研究的2438例和FAST-MI 2005註冊研究的1726例）⁷，結果顯示院前使用嗎啡與院內併發症和1年死亡率的增加無關。
相反，一項基於CRUSADE註冊研究的美國回顧性研究⁵（納入57039例非ST段抬高型急性冠狀動脈綜合症患者）報告稱，嗎啡治療會增加死亡率，並質疑其在這些患者中的安全性。由於在人群、研究日期和設計方面的差異，很難將CRUSADE研究與我們的研究進行比較。 CRUSADE研究回顧性地納入了非ST段抬高型急性冠狀動脈綜合症患者，這與ST段抬高型心肌梗塞患者不同。研究於2002年至2003年間開展，當時口服抗血小板藥物僅限於氯吡格雷，而氯吡格雷與嗎啡的藥理交互作用比替格瑞洛和普拉格雷等近期核准的藥物更為顯著^18,19。
因此，目前似乎沒有太多證據顯示嗎啡在 STEMI 患者中會產生不良後果，而對於 NSTEMI 患者，可能需要格外謹慎。
在本研究中，嗎啡的使用似乎與任何顯著的心臟保護作用無關。關於鴉片類藥物的心肌保護作用，過去報告並不一致。一些研究表明，嗎啡在冠狀動脈繞道手術等外科手術中具有心臟保護作用，但這些研究的樣本量較小，且評估的是間接結果。 ^20,21 在接受急診經皮冠狀動脈介入治療（PPCI）的ST段抬高型心肌梗塞（STEMI ）患者中，嗎啡除了具有遠距缺血預適應的基礎作用外，還顯示出心臟保護作用，²²但在接受度期²³
在缺血再灌注損傷的實驗模型中，嗎啡透過μ和κ心肌阿片受體抑製粒線體通透性轉換孔24的開放性^25,26，誘導顯著的心臟保護作用²⁷ 。嗎啡還能活化再灌注損傷的挽救激酶路徑²⁴。在動物研究中，這些機制與再灌注前或再灌注後立即靜脈或鞘內注射嗎啡可減少梗塞面積相關^28,29,30。然而，由於疾病的複雜性和相關合併症，從動物模型到人類的轉化並非易事，而且我們的數據並未顯示嗎啡對缺血再灌注損傷具有任何心臟保護作用。在不久的將來，兩項尚未發表的研究（臨床試驗 NCT01186445 和 NCT01738100）可能會進一步揭示 ACS 期間冠狀動脈內嗎啡的心臟保護作用。
近年來，人們越來越關注嗎啡在急性冠狀動脈綜合症（ACS）患者鎮痛的應用。嗎啡會抑制胃腸道吸收³⁵並誘發嘔吐¹⁶，從而延遲並減弱口服抗血小板藥物在ACS患者^31,32,33和健康人群^18,19,34中的釋放高峰和療效。然而，目前尚無證據顯示這些影響具有臨床意義。在本研究中，雖然嗎啡與ST段抬高型心肌梗塞（STEMI）患者的任何不良預後無關，但嗎啡治療組患者發生主要不良心血管事件（MACE）的趨勢略有增加，但差異無統計學意義。特別是，在經皮冠狀動脈介入治療（PPCI）前使用嗎啡似乎會增加復發性心肌梗塞和心臟衰竭的發生率，儘管這些結果未達到統計學意義（P值分別為0.08和0.28；表 3）。
無論在急性冠狀動脈綜合症（ACS）中使用嗎啡可能對預後產生何種影響，緩解疼痛對於減輕患者不適和避免誘發心律不整的焦慮至關重要。在本研究中，42.7% 的患者未接受任何鎮痛治療，這意味著疼痛可能未被充分控制。這種情況是不可接受的，緩解疼痛應是所有醫療照護的首要任務。由於缺乏符合倫理的安慰劑對照隨機研究，因此難以就嗎啡在此適應症中的安全性得出明確結論。目前尚無嗎啡在此適應症中的替代鎮痛藥物，唯一正在評估的新方法是等摩爾氧氣/氧化亞氮混合物（MEOPA）聯合對乙醯氨基酚，該方案正在正在進行的 SCADOLII（急性冠脈綜合徵鎮痛中 MEOPA + 對乙醯氨基酚與嗎啡治療的比較）試驗中進行研究。正如最近一項綜述所總結的那樣，在缺乏明確不良反應證據的情況下，應在 STEMI 中使用嗎啡，無需限制。

Discussion
In a large cohort of patients with acute anterior STEMI, morphine was used in half of patients before PPCI and had no significant effect on the composite primary outcome including cardiovascular death, heart failure, cardiogenic shock, recurrent myocardial infarction, unstable angina, and stroke.
Few other studies have evaluated the clinical outcomes of patients who received morphine to alleviate chest pain during an ACS.16 In line with our results, 2 retrospective studies concluded that morphine/intravenous narcotics did not adversely affect the outcomes in patients with ACS. In 1 study including 1758 patients (765 STEMI and 993 non‐ST‐segment elevation myocardial infarction), the rate of 30‐day death was not increased with the use of intravenous narcotics.17 In the second study, the analysis of 2 cohorts of STEMI patients (2438 patients from the FAST‐MI 2010 registry and 1726 from the FAST‐MI 2005)7 suggested that prehospital morphine use was not associated with increased in‐hospital complications and 1‐year mortality.
On the contrary, an American retrospective study based on the CRUSADE registry,5 which included 57 039 patients who presented with non‐ST‐segment elevation ACS, reported an increase in mortality and challenged the safety of morphine use in these patients. It is difficult to compare the CRUSADE study with ours because of differences in population, study dates, and design. The CRUSADE study retrospectively enrolled non‐ST‐segment elevation ACS patients, who are different from STEMI patients. It was conducted between 2002 and 2003, at a time when oral antiplatelet agent use was limited to clopidogrel, which has more pharmacological interactions with morphine than more recently approved agents such as ticagrelor and prasugrel.18, 19
Thus, it seems that there is currently limited evidence for adverse outcomes associated with morphine use in STEMI patients, whereas additional caution may be necessary in NSTEMI patients.
In our study, morphine use did not appear to be associated with any significant cardioprotective effect. Myocardial protection with opioid use has been inconsistently reported. Several studies suggest a cardioprotective effect especially with morphine in the surgical context of coronary artery bypass graft, but these studies were conducted in small surgical patient populations and assessed indirect outcomes.20, 21 In STEMI patients undergoing PPCI, a cardioprotective effect could be demonstrated for morphine in addition to the basal effect of remote ischemic conditioning,22 but no additional myocardial protection was observed with fentanyl in patients undergoing elective PPCI.23
In experimental models of ischemia reperfusion injury, morphine inhibits the mitochondrial permeability transition pore24 opening through μ and κ myocardial opioid receptors,25, 26 and induced a significant cardioprotective effect.27 Morphine also stimulates the reperfusion injury salvage kinase pathway.24 In animal studies, these mechanisms have been associated with a reduction of infarct size following intravenous or intrathecal morphine use before or immediately after reperfusion.28, 29, 30 However, the translation from animal models to humans is not straightforward owing to disease complexity and associated comorbidities, and our data do not suggest any cardioprotective effect of morphine on ischemia‐reperfusion injury. In the near future, 2 noncurrently published studies (Clinical Trials NCT01186445 and NCT01738100) may provide additional understanding of the cardioprotective effects of intracoronary morphine during ACS.
In recent years, there has been a growing concern about the use of morphine for pain relief in patients with ACS. Morphine delays and attenuates the release peak and efficacy of oral antiplatelet agents in ACS31, 32, 33 and healthy18, 19, 34 patients, by inhibiting gastrointestinal absorption35 and inducing to vomiting.16 However, there is no evidence for the clinical relevance of these effects. In our study, although morphine was not associated with any adverse outcome in STEMI patients, there was a nonsignificant trend toward an increase in individual MACE in patients treated with morphine. In particular, recurrent myocardial infarction and heart failure seemed to be more frequent when morphine was used before PPCI, although these results did not reach statistical significance (P=0.08 and 0.28, respectively; Table 3).
Regardless of the potential outcome modifications associated with morphine use during ACS, pain release is essential to decrease patients' discomfort and to avoid proarrhythmic anxiety. In our study, 42.7% patients did not receive any analgesia, meaning that pain was probably undertreated. This is not acceptable, and pain release should be a priority of any medical care. Without ethical possibility of a placebo‐controlled, randomized study, it is difficult to conclude definitively about morphine safety in this indication. There is no analgesic alternatives to morphine in this indication, and the only new approach currently evaluated is equimolar oxygen/nitrous oxide mixture (MEOPA) associated with paracetamol, under investigation in the ongoing SCADOLII (Comparison of MEOPA + Paracetamol Versus Morphine Treatment in Acute Coronary Syndrome Analgesia) trial. In the absence of clear evidence of adverse effects, morphine should be used without restraint in STEMI as was concluded in a recent review.16

愛滋病傳染性-偵測不到病毒幾乎不會傳染

2026-05-13 下午14:20 

連續六個月HIV病毒量200以下. 幾乎不會傳染. 

且. HIV非常脆弱. 離開人體3分鐘會死亡. 乾掉的血液或體液通常不具備傳染性. 

B型肝炎病毒傳染性是HIV的50-100倍

C型肝炎病毒傳染性是HIV的10倍

醫療人員工作中. 接觸到含有HIV的體液血液. 發生感染機率約 0.3% (千分之三). 目前台灣尚無醫療人員在工作中被傳染HIV的案例. 

建議若發生針扎, 立即做病毒篩檢. 之後後六周. 三個月/ 六個月. 各檢驗血清追蹤一次. 

理論上. HIV最容易傳染的階段是在個案尚未做病毒篩檢. 或沒有治療的HIV感染者. 所以在民眾感染HIV後. 自己不知道自己已經被感染. 當然也無法讓醫護人員提前預防. 因此臨床工作中. 對所有病患都當成HIV感染者對待. 是最安全的方式. 而對待HIV感染者. 一般基礎防護就足夠. 

台灣有170-300萬名B肝感染者. 40-60萬個C肝感染者. 

2017年台灣曾有一波A型肝炎大流行.  

HIV感染者若未經過治療. 罹患肺結核風險是一般人的 10-100倍

下圖來自 疾管署U=U科學實證懶人包

針扎傳染HIV機率 0.23%

(疾病管制署致醫界通函第558號)「U=U (愛滋病毒量測不到＝傳不出去)」，正確認知消除愛滋污名與歧視，實踐愛滋健康與平權2025-01-08 
全國醫界朋友，您好：
依聯合國愛滋規劃署(UNAIDS)指引及現有最佳可得之科學及醫學證據顯示，感染者穩定接受抗病毒藥物治療，並維持體內愛滋病毒量有效抑制達測不到(<200 copies/ml)，就不會透過性行為傳染愛滋病毒給他人，也就是國際共識「Undetectable = Untransmittable」(簡稱U=U)，愛滋病毒量測不到就傳不出去。我國存活感染者96%已服藥治療、95%接受治療者病毒量成功抑制，疾病管制署(下稱疾管署)也在本(114)年1月7日透過記者會與台灣愛滋病學會洪健清理事長一同呼籲，愛滋病毒雖透過血液或體液傳染，但病毒量的高低才是傳染力的關鍵。台灣目前愛滋感染第一線治療處方單錠複方藥物，只要一天一顆，感染者便能控制病毒量，鼓勵感染者持續穩定治療並維持體內愛滋病毒量低於200 copies/ml，也就是醫學上定義為測不到病毒(undetectable)。

近10年來，隨著醫療進步與愛滋治療藥物研發進展，透過高效能抗愛滋病毒藥物治療，感染者遵醫囑持續穩定服藥，有效控制體內愛滋病毒量，不但促進感染者自身健康與生活品質，讓愛滋病毒感染成為可控制的慢性病。自2018年UNAIDS發表「U=U國際愛滋治療共識」以來，已經受到全球超過105個國家、1千多個政府機構和組織的支持與響應，「U=U」是當前重要的愛滋防治策略之一，主要奠基於4項發表於國際知名醫學期刊的關鍵醫學實證研究結果，均證實當感染者體內病毒量被藥物穩定有效控制時，無透過性行為傳染給伴侶的案例，並可大幅減少其他途徑的傳染風險(如：母子垂直傳染等)，達到治療即預防(Treatment as Prevention)的效益，詳見附件U=U科學實證懶人包。

目前我國存活感染者超過9成(96%*95%=91%)已穩定服藥達病毒量測不到狀態。依據台灣愛滋病學會及台灣愛滋病護理學會「2024年醫事人員愛滋認知度調查」，於全台23家醫院共回收5,114份有效問卷，其中87%醫事人員表示在了解U=U後會提升其治療/服務感染者的意願，顯示醫事人員正確認知U=U，可以降低其心理壓力，有助於營造友善醫病關係。相對於2023年的「愛滋防治政策」調查結果，顯示只有49%社會大眾了解U=U，顯見醫事人員是可以擔任領頭羊，引領台灣社會朝向友善與健康平權的方向發展。

疾管署呼籲，擴大推廣愛滋防治新觀念「U=U」，提升醫事人員及社會大眾對於愛滋防治的正確認知，有助於消除疾病污名與歧視，營造友善環境，也將促進感染者願意接受篩檢或治療、及早就醫，降低社區傳播風險，提升愛滋防治成效。

感謝您與我們共同維護全民的健康安全。

台灣健保總額9772.2億元

我一直停留在台灣健保總額六千億的記憶. 今天看新聞才發現總額一直上升. 

衛生福利部全民健康保險會第3次會議公布健保明（116）年度預算推估，收入依照115年度一般保險費率5.17%、補充保險費率2.11%推估，保險收入是8955億元，保險成本主要按照115年度總額9883.35億元，116年度總額暫用5.5%推估，所以保險成本是9772.2億元。

野外與登山醫學- 受傷之後需要冰敷嗎?

2026-05-08
發炎反應有助於肌肉再生復原, 冰敷可能會延遲肌肉恢復, 冰敷會阻礙巨噬細胞的出現. 減少局部發炎反應, 冰敷會延遲再生肌肉細胞的出現. 也會減少再生肌肉細胞的大小 (注意. 肌腱或韌帶受傷後的恢復過程或影響因素可能與肌肉受損不同)

冰敷的時間, 數分鐘至20分鐘, 有些文獻建議須根據受傷部位大小給予不同時間, 例如手指頭冰敷幾分鐘, 大腿冰敷 10-20 分鐘等等. 但醫界對於冰敷時間並無一致共識. 

  

參考資料1. : Does Ice Help in the Healing Process?By Corrina Aitken, January 9th, 2024
在過度腫脹可能危及康復的情況下，例如嚴重的關節扭傷或伴隨明顯水腫的情況，冰敷仍然是可行的選擇。此時，治療目標從完全消除腫脹轉變為限制腫脹程度。如果肌肉撕裂導致的水腫較輕，那麼冰敷在早期損傷管理的有效性就值得商榷了。
However, there’s a crucial caveat – in cases where excessive swelling poses a threat to recovery, such as severe joint sprains or situations with significant oedema, ice may still be a viable option. The goal shifts from preventing all swelling to limiting its extent. In instances where muscle tears result in less oedema, the efficacy of ice in early injury management becomes questionable.


參考資料2. : THE EFFICACY OF ICING FOR INJURIES AND RECOVERY - A CLINICAL COMMENTARY-June 14, 2024 CDT
1940年代. 冰敷普遍被用於截肢手術患者. 目的是保存斷肢. 減輕疼痛. 減少感染率. 降低手術過程的併發症及死亡率. 但後來被用於各種外傷治療.

加布·米爾金醫師在1978年提出 RICE療法, 但隨著更多醫學研究出現. 在 2013 年另一個醫師加里·雷恩爾的著作"冰敷,虛幻的治療", 加布醫師在這本著作的前言, 撤回了他自己 43年前提出的 RICE 建議。

他承認：「後續研究表明，冰敷會延緩恢復。輕微的活動有助於組織更快癒合，而冷敷會抑制啟動並加速恢復的免疫反應。冰敷確實有助於緩解疼痛，但運動員通常更希望盡快重返賽場。因此，如今RICE療法並非急性運動損傷的首選治療方法。

Dr. Gabe Mirkin came out in 2013 in the forward to the 2nd edition of the groundbreaking book “Iced! The Illusionary Treatment Option” by Gary Reinl and withdrew his original statement.
Subsequent research shows that ice can delay recovery. Mild movement helps tissue to heal faster, and the application of cold suppresses the immune responses that start and hasten recovery. Icing does help suppress pain, but athletes are usually far more interested in returning as quickly as possible to the playing field. So, today, RICE is not the preferred treatment for an acute athletic injury”


下面簡述不同醫學研究的結果(有些研究納入的樣本不多. 因此結果的信度效度需存疑)
2014年一項針對11名男性的研究表明，冰敷並未改善癒合效果，反而延緩了離心運動引起的肌肉損傷後的恢復，導致肌肉血紅蛋白濃度較對照組出現反彈。
Van den Bekerom 等人在研究冰敷治療踝關節扭傷時，並未發現任何證據或正面效果，並得出結論，冰敷對損傷並無顯著療效。
Khoshnevis等人發現，冷療會造成深層血流減少，可能導致組織壞死。
2008 年和 2011 年的 4 項動物研究表明，過度冰敷或局部冷卻會對軟組織造成嚴重損傷
2010 年的一項研究表明，冰敷的療效不如物理治療。
2004 年的一項研究得出結論，幾乎沒有證據表明冰敷對癒合結果有任何作用。
Yackzan等人的一項研究發現，在訓練後48-72小時內進行冰敷治療後，肌肉酸痛加劇，活動範圍減小

參考資料3: 維基百科-RICE

2019年，布萊斯·杜波依斯（Blaise Dubois）提出了「PEACE & LOVE」這個助記詞。 PEACE代表保護（Protection）、抬高（Elevation）、避免使用抗發炎藥物（Avoid Anti-Inflammatories）、加壓（Compression）和教育（Education）。 LOVE代表負荷（Load）、樂觀（Optimism）、血管化（Valistization）和運動（Exercise）。它首先指導軟組織損傷的初始治療，其次指導後續治療。^[ 10 ]然而，一些指南仍然支持使用非類固醇抗發炎藥（NSAIDs）。^[ 23 ]一些指引也建議使用熱療來治療急性軟組織損傷。

Keratosis Pilaris 毛孔角化症 uptodate

2026-05-07 剛剛一個小朋友來打疫苗. 小腿上有一些明顯突起的毛孔. 應該是毛孔角化症 Keratosis Pilaris(KP). 上網搜尋一下.

UPTODATE: Keratosis pilaris

總結與建議

●臨床表現－毛周角化症（KP）是一種常見的毛囊角化異常疾病。它通常在兒童期或青春期出現，表現為棘狀角化性丘疹（圖1C），主要涉及上肢和大腿近端伸側（圖1A）。臉部、軀幹、臀部和四肢遠端也可能受影響。已有文獻描述了伴隨明顯背景紅斑的變異型（圖6A-B）。毛週角化症常與異位性皮膚炎和尋常型魚鱗病有關。 （請參閱上文「臨床表現」、「臨床變異型」及「相關疾病」部分。）

●診斷－毛周角化症的診斷主要依據臨床表現。眉毛受累、明顯的發炎以及伴隨脫髮的萎縮性瘢痕提示萎縮性毛周角化症（圖9A-C）。 （請參閱上文「診斷」與「鑑別診斷」以及 「萎縮性毛周角化症」。）

●治療－毛周角化症通常會隨著年齡增長而自行改善，無需治療。然而，對於毛周角化症廣泛且有外觀困擾的患者，使用潤膚劑和局部角質溶解劑可以緩解症狀。如果潤膚劑和角質溶解劑治療無效，則可使用局部維他命A酸類藥物（例如，0.05%維A酸乳膏、 0.1%阿達帕林乳膏或0.05%他扎羅汀乳膏）作為二線治療方案。 

SUMMARY AND RECOMMENDATIONS
●Clinical presentation – 

Keratosis pilaris (KP) is a common disorder of follicular keratinization. It typically appears during childhood or adolescence with spiny, keratotic papules (picture 1C) predominantly involving the extensor aspects of proximal arms and thighs (picture 1A). The face, trunk, buttocks, and distal extremities may also be affected. Variants with prominent background erythema have been described (picture 6A-B). KP is often associated with atopic dermatitis and ichthyosis vulgaris.
●Diagnosis – 

The diagnosis of KP is clinical, based on clinical features. Involvement of the eyebrows, marked inflammation, and atrophic scarring with alopecia suggest the diagnosis of keratosis pilaris atrophicans (picture 9A-C).
●Management – 

KP typically improves with age without treatment. However, for patients with widespread KP who have cosmetic concerns, treatment with emollients and topical keratolytics can provide symptomatic relief. Topical retinoids (eg, tretinoin 0.05% cream, adapalene 0.1% cream, or tazarotene 0.05% cream) are a second-line therapy for KP that fails to respond to emollients and keratolytics.

介紹

毛周角化症（KP）是一種常見的毛囊角化異常疾病，其特徵是出現角化性毛囊丘疹，伴隨程度不一的毛囊周圍紅斑。皮損主要涉及上臂近端、大腿和臉頰的伸側（圖1A-C）。毛週角化症常與異位性皮膚炎及尋常型魚鱗病並存[ 1,2 ]。

INTRODUCTION
Keratosis pilaris (KP) is a common disorder of follicular keratinization characterized by keratotic follicular papules with variable perifollicular erythema. Lesions involve predominantly the extensor aspects of proximal arms, thighs, and cheeks (picture 1A-C). KP is often seen in association with atopic dermatitis and ichthyosis vulgaris [1,2].

流行病學

KP通常發生於兒童或青少年，無性別差異。所有種族群體均可見KP，據估計，兒童族群的盛行率為2%至12%

EPIDEMIOLOGY
Onset of KP typically occurs in children or adolescents without sex predilection. It is seen in all ethnic groups, with an estimated prevalence of 2 to 12 percent in pediatric populations

病因和發病機制

毛周角化症 (KP) 的病因尚未完全明確，但與絲聚蛋白基因突變有關 [ 6,7 ]。它被認為是一種遺傳性角化障礙，導致毛囊口形成角質栓。其遺傳模式尚未確定，但在許多情況下符合體染色體顯性遺傳模式，且具有不完全外顯率。研究發現，全身型 KP 患者存在 18p 染色體缺失 [ 8,9 ]。有少數報告稱，尼洛替尼（一種核准用於治療伊馬替尼抗藥性慢性骨髓性白血病的第二代酪胺酸激酶抑制劑）可誘發 KP

ETIOLOGY AND PATHOGENESIS
The cause of KP is not fully understood, but it has been associated with filaggrin mutations [6,7]. It is thought to be a genetic disorder of keratinization that results in the formation of horny plugs in the hair follicle orifices. The mode of inheritance has not been determined, although in many cases it fits into an autosomal dominant pattern with incomplete penetrance. Patients with a generalized form of KP have been found to have a chromosome 18p deletion [8,9]. There are a few reports of KP induced by nilotinib, a second-generation tyrosine kinase inhibitor approved for the treatment of imatinib-resistant chronic myeloid leukemia

病理

角化過度形成的角質栓，可能包含一根或多根扭曲的毛髮，填充並擴張毛囊漏斗部，並突出於皮膚表面（圖2）。真皮上層可能出現輕度血管周圍淋巴球浸潤

PATHOLOGY
An orthokeratotic keratin plug, which may contain one or more twisted hairs, fills and dilates the infundibulum of the hair follicle and protrudes above the skin surface (picture 2). There may be a mild perivascular lymphocytic infiltrate in the upper dermis [14].

臨床表現

典型表現 － 毛周角化症通常在兒童期或青春期發病，但也可能發生於嬰兒（圖3）[ 15 ]。其主要表現為棘狀角化性丘疹，多見於上臂和大腿近端伸側（圖1B和圖1C）。臉部、軀幹、臀部和四肢遠端也可能受影響（圖1A-D）。丘疹可成簇或散在分佈，常伴隨輕度毛囊周圍紅斑。

CLINICAL MANIFESTATIONS
Typical findings — KP typically manifests during childhood or adolescence but may also occur in infants (picture 3) [15]. It presents with spiny keratotic papules predominantly involving the extensor aspects of the proximal arms and thighs (picture 1B and picture 1C). The face, trunk, buttocks, and distal extremities may also be affected (picture 1A-D). The papules may be grouped or scattered, and there is often an associated mild perifollicular erythema.

毛周角化症通常無症狀，可能在身體檢查時偶然發現。部分患者會感覺皮膚粗糙，外觀不佳。由於毛週角化症常與其他皮膚疾病有關，例如異位性皮膚炎或尋常型魚鱗病，因此這些疾病也可能出現在患者的皮膚上。

冬季病情加重較為常見，可能是由於皮膚乾燥或厚衣物摩擦所致[ 16 ]。也有報告指出妊娠期病情會加重（圖4）[ 17 ]。毛周角化症通常會隨著年齡增長而改善，但也可能持續到成年[ 16 ]。

KP is usually asymptomatic and may be an incidental finding during physical examination. Some patients report a rough texture and an unsightly appearance of their skin. Since KP is associated with other skin conditions, such as atopic dermatitis or ichthyosis vulgaris, these conditions may also be seen on the patient's skin.

Exacerbation during the winter months is common, likely due to xerosis or friction from thick clothing [16]. Worsening during pregnancy has also been reported (picture 4) [17]. KP usually improves with age but may persist into adult life [16].

臨床變異型 － 在某些患者中，毛囊周圍紅斑可能很明顯，尤其是在臉頰、前額和頸部（圖 5和圖 6A）。這種類型的毛周角化症稱為「毛週紅角化症」[ 18 ]。

「臉部和頸部毛囊紅斑黑變病」是另一種KP變異型，主要見於青少年和青年。其臨床表現為太陽穴和臉頰出現紅斑、色素沉澱和毛囊性丘疹，並可延伸至耳前區和頸側（圖6B）[ 19,20 ]。與單純性KP類似，毛囊性角化性丘疹常出現於手臂伸側。

Clinical variants — In some patients, perifollicular erythema may be prominent, particularly on the cheeks, forehead, and neck (picture 5 and picture 6A). This form of KP is called "keratosis pilaris rubra" [18].

"Erythromelanosis follicularis faciei et colli" is another variant of KP, primarily seen in adolescents and young adults. It presents with erythema, hyperpigmentation, and follicular papules involving the temples and cheeks, with extension to the preauricular areas and sides of the neck (picture 6B) [19,20]. Follicular keratotic papules, similar to simple KP, are often found on the extensor aspects of the arms.
相關疾病 － 毛周角化症常見於尋常型魚鱗病和異位性皮膚炎患者[ 21 ]。也有報告指出與第1型糖尿病[ 22 ]和肥胖[ 23,24 ]有關。
Associated conditions — KP is commonly seen in patients with ichthyosis vulgaris and atopic dermatitis [21]. It is also reported in association with type 1 diabetes mellitus [22] and obesity [23,24].

診斷

毛周角化症的診斷主要依據臨床表現，即在近端手臂和大腿伸側發現棘狀角化性丘疹，伴隨不同程度的紅斑（圖1A-C）。若涉及眉毛、發炎明顯、出現萎縮性疤痕且伴隨掉髮，則提示萎縮性毛周角化症的診斷。

通常無需進行活檢；如果進行活檢，則會顯示毛囊漏斗部擴張和角化過度形成的角蛋白栓。 

DIAGNOSIS
The diagnosis of KP is clinical, based upon the finding of spiny keratotic papules with variable erythema involving the extensor aspects of proximal arms and thighs (picture 1A-C). Involvement of the eyebrows, marked inflammation, and atrophic scarring with alopecia suggest the diagnosis of KP atrophicans.
Biopsy is usually not necessary; if performed, it reveals a dilated follicular infundibulum and an orthokeratotic keratin plug.

治療

隨著年齡增長，毛周角化症（KP）可能會自行改善，許多情況下無需治療。然而，對於存在大面積毛周角化症和/或嚴重紅斑，且有美容顧慮的患者，他們可能會要求治療以減輕皮膚粗糙和紅斑。改善通常是暫時的；對治療有效的患者應接受指導，以繼續治療並維持緩解。

所有患有毛周角化症的患者都可以透過採取皮膚護理措施來防止皮膚過度乾燥，包括使用溫和的肥皂或無皂清潔劑，以及避免熱水浴或淋浴。

●潤膚劑和角質溶解劑－潤膚劑和外用角質溶解劑是治療毛周角化症的第一線療法。含有乳酸、水楊酸或外用尿素的製劑有助於軟化和撫平角化丘疹，但不能減輕或緩解相關的紅斑[ 1,29 ]。在一項納入30例毛周角化症患者的研究中，將含有20%尿素的保濕霜塗抹於患處四周，可有效改善皮膚質地和外觀[ 30 ]。

●外用維他命A酸類藥物－對於使用潤膚劑和角質溶解劑無效的患者，可使用外用維他命A酸類藥物（例如，0.05%維他命A酸乳膏、 0.1%阿達帕林乳膏或0.05%他扎羅汀乳膏）。外用維他命A酸類藥物每日一次，療程為8至12週。在一項小型隨機試驗中，0.05%他扎羅汀乳膏在減輕上臂後側超過20個角化過度性丘疹患者的瘙癢、粗糙和發紅方面比安慰劑更有效[ 31 ]。在一項小型開放性研究中，0.01%他扎羅汀乳劑在4至8週內減輕或消除了角化過度性丘疹病變[ 32 ]。

●局部皮質類固醇－若發炎明顯，可短期使用低至中等效力的局部皮質類固醇（表1中的第4至6組）與其他局部用藥合併使用[ 33 ]。局部皮質類固醇每日塗抹於患處1至2次，療程1至2週。

●其他療法－其他療法包括全身性維他命A酸類藥物、雷射療法[ 34 ]或其他剝脫性手術。有些患者嘗試了雷射（例如，脈衝染料雷射、長脈衝755 nm翠綠寶石雷射、810 nm長脈衝二極體雷射、長脈衝1064 nm釹摻雜釔鋁石榴石[Nd:YAG]雷射）聯合微晶磨皮術，結果顯示毛囊紅斑和皮膚粗糙度暫時減輕[ 35-38 ]。

TREATMENT
KP may improve spontaneously with age and, in many cases, does not require treatment. However, patients with widespread KP and/or intense erythema who have cosmetic concerns may request treatment to reduce skin roughness and erythema. Improvement is usually temporary; responsive patients should be educated to continue therapy to maintain remission.
All patients with KP may benefit from skin care measures to prevent excessive skin dryness, including using mild soaps or soap-free cleansers and avoiding hot baths or showers.
Emollients and keratolytics – Emollients and topical keratolytics are the first-line therapy for KP. Preparations containing lactic acid, salicylic acid, or topical urea are helpful in softening and flattening the keratotic papules, but do not reduce or relieve the associated erythema [1,29]. In a series of 30 patients with KP, a moisturizer cream containing 20% urea applied to the involved skin for four weeks was effective in improving the skin texture and appearance [30].
●Topical retinoids – Topical retinoids (eg, tretinoin 0.05% cream, adapalene 0.1% cream, or tazarotene 0.05% cream) may be used for patients who fail to respond to emollients and keratolytics. Topical retinoids are applied once a day for 8 to 12 weeks. In a small, randomized trial, tazarotene 0.05% cream was more effective than placebo in reducing itching, roughness, and redness in patients with more than 20 hyperkeratotic papules on the posterior upper arms [31]. In a small, open study, tazarotene 0.01% emulsion reduced or resolved KP lesions in four to eight weeks [32].
●Topical corticosteroids – Short courses of low- to medium-potency topical corticosteroids (groups 4 to 6 (table 1)) may be used in conjunction with other topical agents if there is prominent inflammation [33]. Topical corticosteroids are applied to the involved areas once or twice daily for one to two weeks.
●Other therapies – Other therapies include systemic retinoids, laser therapy [34], or other ablative procedures. Combination treatments with lasers (eg, pulsed dye laser, long-pulsed 755 nm alexandrite laser, 810 nm long-pulsed diode laser, long-pulsed 1064 nm neodymium-doped yttrium aluminum garnet [Nd:YAG] laser) and microdermabrasion have been tried in a few patients with temporary reduction of perifollicular erythema and skin roughness

還蠻多醫師都有寫此病的中文衛教文章. 下面全文轉貼
毛孔角化症(keratosis pilaris) 北市聯醫 皮膚科 許智恭醫師
炎熱的夏季來臨，大家紛紛換穿短袖的衣服，涼爽透氣的短褲。此時有 相當可觀的人卻長期受到一種常見的皮膚問題困擾，雖然不常造成搔癢疼痛的不適症狀，可是因為呈現不怎麼整潔雅觀的樣貌，想努力洗刷這些不太美觀的皮膚疹子 卻總是令人失望。這種發生在側臉部與頸部、手臂外側、腿部外側，呈現許多密集的毛孔突起粗糙小顆粒，顏色有灰、黑、紅等不同色澤的病變，有些人俗稱雞皮疙 瘩，正式的醫學名稱是「毛孔角化症」keratosis pilaris。

　　「毛孔角化症」是種常見的皮膚問題，無論在皮膚診療室或是日常生活中都很容易看到這類情形，特別是年輕人。研究統計顯示約有半數的人在十歲以前開始發 生，到了十幾歲的青年期有高達50%~80%的人表現出毛孔角化症的病徵，男女比例相當，有家族遺傳史的佔30%~50%左右，隨著年紀增長，大概有ㄧ半 的人會逐漸好轉，可是角化症存在的時間長達20年以上。如果病情加劇或是因出汗或摩擦刺激而產生紅腫發癢的情形，仍需要接受治療。冬季常見深色突起的毛孔 顆粒更加明顯，夏季雖然角化有緩和傾向，但是紅癢的症狀反而增多，同時因為穿著短袖衣服容易看到變化部位，尋求治療的意願反而提高。
　　大部分的患者身體健康，有少部分人併有魚鱗癬、乾皮症等角質異常病症，其他有異位性皮膚炎、過敏性鼻炎、氣喘的異位性體質，惟可能只是共存的病症，無 直接因果關聯。毛孔角化症好發於臉頰側面、手臂外側、大腿前外側，嚴重的在頸部、背上、臀部、小腿都可看見。外觀上在毛孔開口處可見黑而硬的角化顆粒，凸 出於皮表面，周圍有時可見輕微的發紅現象，尤其是在臉頰側面，特稱「紅色毛孔角化症」。檢查阻塞的毛孔內偶而可見黑色的細毛陷在裡面。這種變化與青春痘的 粉刺有些相似但是原因與特徵均不同，可請教醫師分辨出來。
　　治療上要強調刻意強力清潔或用刷子、粗布摩擦表面會導致發炎紅腫，進而演變成發炎後色素沉積，但卻是ㄧ般人最常想到的作法，應記取前人的失敗經驗，避 免ㄧ再重複犯錯。外用角質軟化劑、外用A酸(retinoid)藥膏、發炎抑制劑、果酸煥膚治療、脈衝式染料雷射(PDL)、釹雅克雷射(Nd:YAG laser)眾多藥品與醫療科技選擇須在專業皮膚科醫師的協助下才能得到理想的療效，這正是美容醫學有所發揮，達成提升生活品質，促進身心健康印象的目 標。