Decrease in Mortality Rate of Chronic Obstructive Pulmonary Disease (COPD) with Statin Use: A Population-Based Analysis in Japan

Ishida, Wataru; Kajiwara, Takashi; Ishii, Mototsugu; Fujiwara, Fumikado; Taneichi, Haruhito; Takebe, Noriko; Takahashi, Kazuma; Kaneko, Yoshihito; Segawa, Ikuo; Inoue, Hiroshi; Satoh, Jo

doi:10.1620/tjem.212.265

Cited by 45 publications

(29 citation statements)

References 21 publications

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“…Before discussing these studies, it is necessary to briefly present five additional studies [32][33][34][35][36] that we excluded for various reasons from further analysis; some of them [32][33][34] have been included in similar reviews of the subject. Frost et al [32] conducted a matched-cohort study and a separate case-control study (including 397 influenza deaths), and found a significantly reduced risk of unspecified pneumonia/influenza death among moderate-dose statin users.…”

Section: Available Relevant Studiesmentioning

confidence: 99%

Statins for sepsis: a critical and updated review

Kopterides

Falagas

2009

Clinical Microbiology and Infection

103

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There is increasing discussion of a potential role for statins in the management of sepsis. A search of PubMed, Embase, Scopus and the Cochrane Library databases was performed by combining the terms 'statins', 'infection', 'sepsis', 'bacteraemia', 'pneumonia', and 'ICU infections'. A total of 22 studies were retrieved, which included 177,260 people and compared clinical outcomes between 51,193 statin users and 126,067 non-statin users. Nineteen were cohort studies (seven prospective and 12 retrospective), two were retrospective case-control studies, and one was a randomized controlled study. Nine studies examined the use of statins in sepsis, four in community-acquired pneumonia (CAP), three in bacteraemia, and three in post-operative patients. Mortality data were presented in 15 studies; in ten, mortality was lower among statin users (three of six sepsis studies, five of six CAP studies, and two of three bacteraemia studies). In four studies, there was no difference in mortality (two of six sepsis studies, one of six CAP studies, and one of three bacteraemia studies) and in one study there was increased mortality among septic intensive-care unit patients receiving statins. Five of the nine studies that examined the risk of developing sepsis/infection as a primary outcome (six of nine sepsis studies and all studies in the postoperative setting) found a decreased risk among statin users, whereas the remaining studies found no difference. Irrespective of their design (matched vs. non-matched), the majority of the studies suggested that statins have a beneficial effect on the outcome of infection; however, their observational design does not allow us to draw firm conclusions. The clinical benefit of statin therapy in sepsis remains to be determined by ongoing randomized controlled trials.

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Section: Available Relevant Studiesmentioning

confidence: 99%

Statins for sepsis: a critical and updated review

Kopterides

Falagas

2009

Clinical Microbiology and Infection

103

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“…Novel therapeutic strategies that have the potential to alter lung structure, therefore, are of interest as possible approaches to alter the long-term natural history of COPD. One type of therapy that is attracting interest for its potential in COPD is the use of statins, which have been associated with reduced acute events and mortality [3][4][5], as well as with reduced decline in lung function in retrospective database studies [6].…”

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confidence: 99%

Statins inhibit matrix metalloproteinase release from human lung fibroblasts

Kamio

Liu

Sugiura

et al. 2009

European Respiratory Journal

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Pleiotropic effects of statins have been reported to include inhibition of matrix metalloproteinase (MMP) release from macrophages and endothelial cells. We evaluated whether statins would inhibit MMP release from human lung fibroblasts, which play a major role in remodelling processes.Monolayer and three-dimensional (3D) collagen gel cultures of fibroblasts were used. Cytokines (tumour necrosis factor-a and interleukin-1a) were used to induce MMP release and mRNA expression. Collagen degradation induced by cytokines and neutrophil elastase (NE) was evaluated by quantifying hydroxyproline. Atorvastatin inhibited MMP-1 and -3 release and mRNA expression in both culture systems. Similar results were obtained with simvastatin and fluvastatin.In 3D cultures where cytokines also stimulated MMP-9 release, atorvastatin also inhibited MMP-9 release. In 3D cultures, cytokines together with NE induced collagen degradation, which was also inhibited by atorvastatin. The effect of atorvastatin was reversed by mevalonate and geranylgeranyl-pyrophosphate but not by farnesyl-pyrophosphate.The current data suggest that statins may modulate remodelling processes mediated by fibroblasts by inhibiting MMP release.

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“…[22][23][24][25][26][27][28][29][30][31][32][33][34] Part of their apparent benefit may lie in the fact that clearance of apoptotic cells (efferocytosis) is defective in patients with COPD and statins (lovastatin) enhance efferocytosis. 22,23 Furthermore, statins address other aspects of both the local and systemic inflammation responses in patients with COPD.…”

Section: Chronic Obstructive Pulmonary Diseasementioning

confidence: 99%