朱燦麟運動創傷與慢性筋骨痛症網

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沒有發炎的慢性肌腱(筋膜組織)傷患

非類固醇消炎藥--幫你還是害你?

你還敷冰嗎?

泠水浴與恢復

唔敷冰,干卿何事?

「非科學化個人理解」的深層意義- 你還敷冰嗎? 續篇

足踝扭傷:不敷冰可怎樣?

給運動員的一點忠告

山徑石屎化

高山病

Straight to the point



好人難做!

慢性筋骨痛症是醫學問題,還是社會問題?


非類固醇消炎藥--幫你還是害你?

By Alain Chu 

處理急性軟組織損傷,除了常規的休息(Rest)、冰敷(Ice)、施壓(Compression)、抬高(Elevation)外,也常用非類固醇消炎藥(Non steroidal anti-inflammatory drugs, NSAIDs)來「消炎」,這些做法似乎已成常規定理。(冰敷的迷思在「冰敷熱熨,何者為適?」一章已討論過)使用NSAIDs的原意,就是及早抑制炎症,減輕痛楚及腫脹,使患者可提早作功能鍛鍊,從而防止肌力減弱及關節僵硬。

 過去對NSAIDs的研究,大多以痛楚及腫脹的消退、功能恢復的速度來作成效指標,甚少關注軟組織的生長速度及張力强度(Tensile strength)。但近代的研究發現,使用NSAIDs治療軟組織受傷勞損,往往弊多於利,為何如此?

 前列腺素(Prostaglandins) 是細胞分泌的化學物質,不同的前列腺素負責不同功能,包括:誘發炎症、產生痛楚、支援血小板的凝血功能及保護胃黏膜免受酸液損害。前列腺素是由花生四烯酸(Arachidonic Acid)衍化而成,這過程需要環氧化酶(Cyclo-oxygenase, COX)催化,NSAIDs的作用就是抑制COX的功能,從而阻止前列腺素的產生,即是所謂消炎,所以NSAIDs又稱COX抑制劑(COX Inhibitor)

 環氧化酶有兩種,分別是COX-1COX-2,兩者都能產生前列腺素,而COX-1主要產生保護胃黏膜的前列腺素,當使用NSAIDs抑制COX-1COX-2的功能時,同樣會抑制保護胃黏膜的前列腺素,是故不少人長期服食NSAIDs後患上胃潰瘍(Wolfe, et al., 1999),這就是要同時服食胃藥的原因。

 新一代的環氧化酶-2抑制劑(COX-2 inhibitor),只選擇性地抑制COX-2,所以不會影響胃黏膜,但同時又可抑制炎症,這好像是偉大的發明。

 然而,受傷後的炎症階段,其實是身體組織(包括肌肉、筋膜組織、骨骼)癒合過程的開始,是非常重要的環節。在這時期,巨噬細胞會除去壞死的損傷組織,生長因子會加速細胞再生,分泌膠原蛋白的纖維母細胞(Fibroblast)同趨活躍。

 那麽,過份壓抑炎症階段會否影響身體組織的修復?

 非類固醇消炎藥對肌腱及韌帶癒合的影響

 其實,不少學者認為,壓抑炎症反應即是阻礙軟組織的修復過程,甚至長遠影響軟組織的質量及強度(Cohen, et al., 2006; Dahners, et al., 1988; Elder, et al., 2001; Ferry, et al., 2007 ; Hertal, 1997; Magra, and Maffulli, 2006; McGriff-Lee, 2003)。在離體實驗中發現NSAIDs會抑制纖維母細胞及肌腱細胞的生長(Almekinders, et al. 1995; Tsai, et al., 2006),及阻礙肌腱細胞游移至受損部位進行修復(Tsai, et al., 2007)

 在動物實驗中又發現,把白鼠的肌腱切斷再接駁,然後餵以NSAIDs四星期,之後發現服食藥物組的肌腱張力强度只及對照組(無服食藥物組)20% (屈肌肌腱)30% (伸肌肌腱)(Kulick, 1986)

 而在三百六十四位足髁扭傷的澳洲軍人身上發現,服用NSAIDs的患者雖然比對照組痛楚較輕及能較快復操,但其足髁穩定性較差及活動幅度較窄(Slatyer, et al., 1997)。很明顯,這些就是關節韌帶癒合不理想的現象,不過Slatyer仍然建議在治療急性足髁扭傷時使用NSAIDs,似乎只著眼於藥物的止痛功效,卻輕視其對關節力學的長遠影響。

 此外,肌腱的新陳代謝過程及隨運動負荷而變粗壯的現象,都需要COX-1COX-2來控制(Trappe, et al., 2008),長期服食能抑制COXNSAIDs,肌腱及其他筋膜組織又怎會變强韌?怎能抵受運動時產生的負荷?

 非類固醇消炎藥對肌肉癒合的影響

 雖然NSAIDs在肌肉受傷的初期,可能有助減少腫脹及痛楚,但研究發現服食NSAIDs後,在急性肌肉拉傷的部位發現不到巨噬細胞,只有少量肌肉可以再生(Greene, et al., 2002)。不要忘記,巨噬細胞除了負責清除壞死組織外,也會分泌生長因子、化學吸引物(Chemoattractants)及前列腺素幫助肌肉再生(Cantini, et al., 1994; Chazaud, et al., 2003; Lu, et al., 2011; Robertson, et al., 1993),沒有巨噬細胞,肌肉怎樣修復?

 不少學者都指出NSAIDs會阻礙身體清除壞死組織及減慢肌肉再生的速度(Almekinders, and Gilbert, 1986; Almekinder, et al., 1995; Best, and Hunter, 2000; Kellet, 1986; Mishra, et al., 1995; Peterson, et al., 2003; Weiler, 1992)

近代研究又發現COX-2 對肌肉創傷後的再生極其重要,使用NSAIDs (COX-2 抑制劑)便會阻礙肌肉再生(Bondesen, et al., 2004; Mendias, et al., 2004; Shen, et al., 2005)

 更諷刺的是,在嚴重急性肌肉拉傷後,安慰劑減輕痛楚的速度及程度明顯優於NSAIDs(Reynolds, et al., 1995)Reynolds認為NSAIDs的止痛作用,並不能抵銷因NSAIDs延遲肌肉復原所產生的疼痛。相反,安慰劑雖無治療作用,但卻容許肌肉自然癒合,「治療」效果更理想!

運動圈子中流行預防性地服食非類固醇消炎藥,以期減輕運動後肌肉痠痛及加速復原(Warden, 2009),但非類固醇消炎藥會抑制運動後的蛋白質合成(Trappe, et al., 2002),又怎會幫助運動後復原?

 非類固醇消炎藥對骨骼癒合的影響

 NSAIDs也常用於減輕骨折產生的痛楚,骨折的癒合與筋膜組織一樣,需要炎症期產生的生長因子介導(Simon, and OConnor, 2007)Dimmen發現非類固醇消炎藥會阻礙骨折癒合,尤其是疲勞性骨折 (Dimmen, et al., 2008)。阻礙骨折癒合的現象,在服用非類固醇消炎藥超過十五天後更為明顯(Simon, and OConnor, 2007)。類似的報告常見於有關文獻當中(Dahners, et al., 2004; Gerstenfeld, et al., 2007; Harder, and An, 2003; Simon, et al., 2002;)。不止皮質骨(硬骨)的修復受NSAIDs影嚮,軟骨的生長也會受阻,因為NSAIDs會抑制軟骨內蛋白聚糖的合成(McKenzie, et al., 1976; Palmoski, et al., 1980; Rashad, et al., 1989)

 

 

非類固醇消炎藥對抗氧化能力的影響

 NSAIDs除了會阻礙肌肉、筋膜組織、骨骼及軟骨的生長修復外,近年更發現NSAIDs會增加人體的氧化壓力(Oxidative Stress,自由基與抗氧化劑的比值),換句話說,就是削弱人體的抗氧化能力。 (自由基-Free Radicle是帶有不成對電子的氧分子,是細胞新陳代謝過程中必然產生的物質,自由基極之容易氧化脂肪酸,而細胞膜正是由脂肪酸組成,簡單點說就是破壞細胞) (McAnulty, et al., 2007)。部份退行性疾病如動脈粥樣硬化、帕金遜症、阿玆海默症(Alzheimer’s Disease)等都與氧化壓力增加有關。維他命C、維他命E、礦物質硒等都是中和自由基的物質,故又稱抗氧化劑。相反,NSAIDs則削弱人體的抗氧化能力,更有學者稱之為「抗抗氧化劑」。

 非類固醇消炎藥的取捨

 處理急性軟組織受傷,要考慮的是在短暫快速舒緩痛楚,與長期身體組織修復理想之間取得平衡,沒有炎症,軟組織不會理想地癒合 (Stovitz, and Johnson, 2003)。若患者因服藥後疼痛減輕而誤以為復原,但其實軟組織韌度根本未足以抵受活動的要求,再次受傷的機會便大增(Orchard, and Best, 2002)。可惜當患者在受傷後,往往要求立即止痛,嚷着翌日便要繼續運動、工作,所以消炎止痛藥就是最「見效」的「治療」方法,醫者、患者雙方都皆大歡喜。即時止痛消炎才是大眾的期望,誰理會將來的後果。

 究竟處方NSAIDs治療軟組織創傷的做法是基於其醫療價值,還是商業利益?若不標榜NSAIDs的消炎止痛功能,只强調其對肌肉、筋膜組織、骨骼癒合的抑制作用,是否也可稱為「非類固醇抗修復藥」(Non-steroidal anti-healing drugs, NSAHDs)?只求短暫止痛卻無視深遠害處又是否合理的療法?

 上述研究結果並非國家機密,讀者可隨時在互聯網上查閱,但這些資訊卻永遠不會在電視廣告播出,更絕少有醫者向患者說明。我們日常接收的廣告資訊,大都是精心部署的行銷策略,當中的知識真假夾雜,目的就是所謂開拓市場,提升銷量。

 除了急性軟組織創傷,在慢性筋骨痛症的治療上,使用NSAIDs也十分普遍,基本上已成常規。所持的理據,就是認為這些慢性痛症是發炎引起,只要將炎症消除,便能治好痛症,使用NSAIDs,不單免卻類固醇的副作用,又能達到消炎的目的。這理論似乎言之成理,不少教科書也如是說,但這論據其實存在謬誤。

 以一般認為的退化性關節炎為例,使用NSAIDs治療差不多已成常規定理。患者當中不乏長者,可是長者的肌肉生長及再生能力已經較弱(McGeachie, and Ground, 1995)NSAIDs又會阻礙肌肉的生長(Mackey, et al., 2007),長期服用NSAIDs只會損害肌肉的功能,那麼肌肉又如何能控制關節?更何況這些所謂退化性關節炎,疼痛其實大部份源自關節鄰近的慢性筋膜病變(Fasciosis)或瘢痕攣縮(Adhesion)而非發炎,使用NSAIDs的理據何在?更諷刺的是,有研究發現服食NSAIDs六個月後,反而會加速膝及髖關節的軟骨磨蝕程度(Reijman, et al., 2005)

 當眾醫者都鸚鵡學舌般嚷着「實証醫學」(Evidence Based Medicine)之時,豈不知原來並沒有堅實的理據支持使用NSAIDs治療慢性筋骨痛症,但又為何成為常規療法?實在諷刺!不過在一個講傳統、論輩份的專業王國,對一些根深蒂固的慨念,無論研究結果怎樣否定,醫者也會依然顧我,除非有份量的權威肯出來指正,眾人才會唯唯諾諾的付和,但所謂專家權威又豈會輕易推翻自己以往的主張?

 使用類固醇及非類固醇消炎藥治療軟組織炎症,其實是源自四十年前治療風濕性關節炎的經驗(Leadbetter, 1995)。然而風濕性關節炎與因創傷勞損引起疼痛的病理相異,治療目的也不同。炎症是風濕性關節炎的主要徵狀,主因是免疫系統的異常反應,在未有更佳治療方法時,用上述藥物消炎也許是權宜之計。但對軟組織創傷,炎症是修復過程的首要步驟,軟組織的修復才是重點,把兩者混為一談,用同樣的思路方法治療,實在說不過去。

 不過,非類固醇消炎藥對治療慢性筋骨痛症並非一無是處,對那些不問因由,盲塞愚昧,只求即時止痛又迷信藥物的患者,是最合適的療法。

多年來,本人苦口婆心勸喻別人謓用非類固醇消炎止痛藥,更不應敷冰。可惜換來的卻是冷嘲熱諷,更被自以為是的醫者評擊為非科學化個人理解、對病人患者不公!只是本人覺得,罔顧事實,不去尋真,又是否專業之道?證據確鑿,公諸於世,還惹來諸般質疑。不明不信,大可繼續服藥消炎、冰敷鎮痛,悉隨專便。

 

http://stoneathleticmedicine.com/2013/11/why-ice-and-anti-inflammatory-medication-is-not-the-answer/

http://physicaltherapyweb.com/paradigm-shifts-use-ice-nsaids-post-acute-soft-tissue-injuries-part-1-2/

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2770552/

http://www.electrotherapy.org/assets/Downloads/nsaid%20delay%20healing.pdf

http://www.sciencedirect.com/science/article/pii/S1877065710000576

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