COPD病情的惡化與痰液中新菌種的出現有關


  8月15日《New England Journal of Medicine》雜誌報導一項具前瞻性研究的結果顯示,新菌種的出現可能是慢性阻塞性肺病(COPD)惡化的原因。
  
  紐約水牛城的大學的Timothy Murphy醫師提及,多年以來,人們一直假設細菌在COPD惡化中扮演的角色,但數十年來的研究結果,並未發現在平穩期和加劇期細菌的存在有何差別。利用分子分型的新技術可以更加準確的檢測呼吸道中細菌菌群的轉變,且已證實此假設是正確的。
  
  在超過56個月的研究中,有1,975名患者接受了西部榮民業務紐約醫療系統(Veterans Affairs Western New York Hospital System)的檢查,每個月收集81名患者的痰液標本,以及其中374名COPD惡化的患者。經分子分型發現,COPD惡化情形為原來的兩倍是因為新菌種的出現。有33%COPD惡化病患的臨床訪視分離出痰液中有新菌種,但也有15.4%COPD惡化病患則無新菌種被分離出。(P<0.001;相對危險度,2.15;95%可信區間,1.83-2.53)。有3種主要的病原體與COPD的惡化有關,這三種新的菌株為,Hemophilus influenzae、Moraxella catarrhalis和 Streptococcus pneumoniae。
  
  Dr. Murphy指出,目前的發現並未證實新菌種導致COPD的惡化。然而,這些結果提供細菌導致明顯COPD惡化的部分證據。這個新資訊在發展新方法來治療與預防惡化將充當一重要的指導者,且應發展新疫苗來預防此新菌種的感染。
  
  加拿大Manitoba,Winnipeg呼吸道疾病醫院的醫師,Nick R. Anthonsen博士指出,這些發現不可能改變治療方法,因為普遍治療COPD惡化的方法是利用抗體。假設這些新病原體為同屬的新菌種,具有避開宿主防禦的能力,而感染呼吸道並導致發炎。如果不是細菌感染導致的COPD惡化,則這些結果將很難被解釋。
  

COPD Flare-ups Linked to New B

By Laurie Barclay醫師
Medscape Medical News

Aug. 15, 2002 — New bacterial strains may be the culprit in flare-ups of chronic obstructive pulmonary disease (COPD), according to results of a prospective study published in the August 15 issue of the New England Journal of Medicine.

"For years, people have hypothesized that bacteria played a role in COPD exacerbations, but studies performed decades ago found no difference in bacterial presence during stable periods and flare-ups," senior author Timothy Murphy, MD, from the University at Buffalo in New York, says in a news release. "Using the new technology of molecular typing, where you can look at turnover of bacteria in the respiratory tract in a more accurate way, we have shown that that hypothesis is correct."

Over 56 months and 1,975 clinic visits at the Veterans Affairs Western New York Hospital System, sputum samples were collected from 81 patients monthly and during 374 COPD exacerbations. Molecular typing revealed that exacerbations were twice as likely in conjunction with the appearance of a new bacterial strain. Exacerbations occurred in 33% of clinic visits in which a new strain was isolated but in only 15.4% of visits in which no new strain was isolated (P<.001; relative risk, 2.15; 95% confidence interval, 1.83-2.53). The three major pathogens linked to exacerbations were new strains of Hemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae.

"Our findings don't prove that a new strain causes an exacerbation," Murphy says. "However, the results contribute to the growing body of evidence that bacteria cause a significant portion of exacerbations. This new information will act as an important guide in developing novel ways to treat and prevent exacerbations [and] should lead to the development of vaccines to prevent colonization by the offending strains."

In an accompanying editorial, Nick R. Anthonsen, MD, PhD, from Respiratory Hospital in Winnipeg, Manitoba, Canada, notes that these findings are unlikely to change clinical practice, because it is common practice to treat COPD flares empirically with antibiotics.

The authors "hypothesize that new pathogens, including new strains of the same organism, are capable of evading host defenses, infecting the airways, and causing inflammation," Anthonsen writes. "It is difficult to interpret these results as indicating anything other than a role of bacterial infections in exacerbations."

N Engl J Med. 2002;347(7):465-471, 526-527

Reviewed by Gary D. Vogin, MD

    
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