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COPD. 2014 Jun;11(3):351-8. doi: 10.3109/15412555.2013.858315. Epub 2013 Dec 30.

Effect of high/low dose N-acetylcysteine on chronic obstructive pulmonary disease: a systematic review and meta-analysis.

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1
1Dongyang People's Hospital, Respiratory Medicine, Zhejiang, P.R. China.

Abstract

BACKGROUND:

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality and morbidity worldwide, characterised by persistent airflow limitation, mucus hypersecretion, oxidative stress and airway inflammation. N-acetylcysteine (NAC) have anti-oxidant and anti-inflammatory properties, which have been shown an uncertain benefit in COPD patients.

METHOD:

Systematic searches were conducted in Cochrane, Medline and Embase electronic databases. A meta-analysis was performed to evaluate the different effect between high and low-dose NAC treatment on COPD exacerbation.

RESULTS:

This review yielded 11 studies. The methodological quality of included studies were scored using the Jadad score, with a scale of 1 to 5 (score of 5 being the highest). Data showed high-dose NAC can reduce both the total number of exacerbations (RR = 0.59, 0.47 to 0.74, 95%CI, p < 0.001) and the proportion of patients with at least one exacerbation (RR = 0.76, 0.59 to 0.98, 95%CI, p = 0.03). In the low-dose group, subgroup with jadad ≤ 3 showed a significant decrease (RR = 0.69, 0.61 to 0.77, 95%CI, p < 0.001) in the proportion of patients with exacerbation, the other subgroup with Jadad score > 3 showed no significant decrease (RR = 0.98, 0.90 to 1.06, 95%CI, p = 0.59). And low-dose NAC showed no benefit in the total number of exacerbations (RR = 0.97, 0.68 to 1.37, 95%CI, p = 0.85). Neither high nor low-dose NAC treatment showed benefit in forced expiratory volume in one second(FEV1)(WMD = 1.08, -9.97 to 12.13, 95%CI, p = 0.85).

CONCLUSION:

Long-term high-dose NAC treatment may lead to a lower rate of exacerbations. But the effect of low-dose NAC treatment remains uncertain. Further researches are needed to confirm this outcome and to clarify its mechanisms.

KEYWORDS:

exacerbation; inflammation; lung function; oxidant stress

PMID:
24378052
DOI:
10.3109/15412555.2013.858315
[Indexed for MEDLINE]

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