Alcohol as a risk factor for liver cirrhosis: A systematic review and meta‐analysis

Introduction and Aims. Alcohol is an established risk factor for liver cirrhosis. It remains unclear, however, whether this relationship follows a continuous dose–response pattern or has a threshold. Also, the influences of sex and end‐point (i.e. mortality vs. morbidity) on the association are not known. To address these questions and to provide a quantitative assessment of the association between alcohol intake and risk of liver cirrhosis, we conducted a systematic review and meta‐analysis of cohort and case–control studies. Design and Methods. Studies were identified by a literature search of Ovid MEDLINE, EMBASE, Web of Science, CINAHL, PsychINFO, ETOH and Google Scholar from January 1980 to January 2008 and by searching the references of retrieved articles. Studies were included if quantifiable information on risk and related confidence intervals with respect to at least three different levels of average alcohol intake were reported. Both categorical and continuous meta‐analytic techniques were used to model the dose–response relationship. Results. Seventeen studies met the inclusion criteria. We found some indications for threshold effects. Alcohol consumption had a significantly larger impact on mortality of liver cirrhosis compared with morbidity. Also, the same amount of average consumption was related to a higher risk of liver cirrhosis in women than in men. Discussion and Conclusions. Overall, end‐point was an important source of heterogeneity among study results. This result has important implications not only for studies in which the burden of disease attributable to alcohol consumption is estimated, but also for prevention. [Rehm J, Taylor B, Mohapatra S, Irving H, Baliunas D, Patra J, Roerecke M. Alcohol as a risk factor for liver cirrhosis: A systematic review and meta‐analysis. Drug Alcohol Rev 2010]     

Lower muscle tissue is associated with higher pulse wave velocity: A systematic review and meta‐analysis of observational study data

Muscle loss and arterial stiffness share common risk factors and are commonly seen in the elderly. We aimed to synthesise the existing literature on studies that have examined this association. We searched electronic databases for studies reporting correlations or associations between a measure of muscle tissue and a measure of arterial stiffness. Meta‐analysis was conducted using Fisher's Z‐transformed r‐correlation (r_Z) values. Pooled weighted r_Z and 95% confidence intervals were calculated in an inverse‐variance, random‐effects model. Heterogeneity was assessed by the inconsistency index (I²). Study quality was assessed on a checklist using items from validated quality appraisal guidelines. 1195 records identified, 21 satisfied our inclusion criteria totalling 8558 participants with mean age 52±4 years (range 23‐74). Most studies reported an inverse relationship between muscle tissue and arterial stiffness. Eight studies had data eligible for meta‐analysis. Muscle tissue was inversely associated with pulse wave velocity in healthy individuals [r_Z=?.15 (95% CI ?0.24, ?0.07); P=.0006; I²=85%; n=3577] and in any population [r_Z=?.18 (?0.26, ?0.10); P<.0001; I²=81%; n=3930]. In a leave‐one‐out sensitivity analysis, the results remained unchanged. Lower muscle tissue was associated with arterial stiffness. Studies were limited by cross‐sectional design. Cardiovascular risk monitoring may be strengthened by screening for low muscle mass and maintaining muscle mass may be a primary prevention strategy.     

Effectiveness and safety of direct oral anticoagulants in atrial fibrillation patients switched from vitamin K antagonists: A systematic review and meta‐analysis

A substantial proportion of atrial fibrillation patients initiating direct oral anticoagulants (DOAC) are vitamin K antagonists (VKA)‐experienced, for example switchers from VKA to DOAC. With this study, we aimed to summarize available evidence on the effectiveness and safety of DOAC vs VKA in real‐life VKA‐experienced atrial fibrillation patients. We searched EMBASE, MEDLINE and Cochrane Library systematically for English‐language studies indexed any time before October 2018. We included studies of VKA‐experienced atrial fibrillation patients initiating DOAC therapy, with continued VKA therapy as comparator. Outcomes included arterial thromboembolism and bleeding. When appropriate, meta‐analysis was performed by calculating pooled, weighted and adjusted hazard ratios (aHR) with 95% confidence intervals (CI). Eight cohort studies comparing VKA‐experienced DOAC (dabigatran or rivaroxaban) users with continued VKA users were included. When comparing DOAC to VKA, an increased risk of ischaemic stroke and myocardial infarction was found for dabigatran (pooled aHR of 1.61 [95% CI 1.19‐2.19, I² = 65%] and 1.29 [95% CI 1.10‐1.52, I² = 0%], respectively), but not for rivaroxaban. The use of dabigatran in VKA‐experienced users was associated with an increased risk of gastrointestinal bleeding (pooled aHR 1.63 [95% CI 1.36‐1.94, I² = 30%]), but a decreased risk of intracranial bleeding (pooled aHR 0.45 [95% CI 0.32‐0.64, I² = 0%]). In conclusion, the use of dabigatran in prior VKA users in clinical practice was associated with a slightly increased risk of arterial thromboembolism and gastrointestinal bleeding, but a decreased risk of intracranial bleeding. Importantly, observational studies of real‐life VKA‐experienced oral anticoagulant users may be confounded by the reason for switching.     

Association of endogenous DHEA/DHEAS with coronary heart disease: A systematic review and meta‐analysis

The clinical significance of dehydroepiandrosterone (DHEA) and its sulphate (DHEAS) in coronary heart disease (CHD) has not been thoroughly elucidated to date. We performed a meta‐analysis to clarify the correlations between endogenous DHEA(S) and CHD. We performed a literature search without language restriction up to August 10, 2017, and retrieved records from EMBase, PubMed, Web of Science, CNKI and WanFang databases to identify eligible cohort studies focused on the relation between DHEA(S) and CHD. A total of 26 studies were included in the systematic review and 14 case‐control studies were included in the meta‐analysis,which was performed using RevMan 5.1 and STATA 12. Subgroup analyses were used to discover possible sources of heterogeneity. Quality assessment was carried out using the Newcastle–Ottawa Scale. Odds ratios with 95% confidence intervals were calculated. Heterogeneity analyses were performed using meta‐regression and tests for publication bias were performed. The overall average DHEAS diffusivity of CHD cases was significantly lower than that of controls with a summarized standard (std) mean difference of ?0.23(95% CI, ?0.45 to ?0.01, P = .04). There was no association between DHEA concentration and CHD with a summarized mean difference of ?0.07 (95% CI, ?0.32 to 0.18, P = .59). No association was found between DHEAS concentration and arteriosclerosis patients with a summarized standard (std) mean difference of ?0.46(95% CI, ?0.96 to 0.04, P = .07). All of the results had a high degree of heterogeneity. The present study suggested that decreased DHEAS may be associated with coronary heart disease risk but not with arteriosclerosis. We did not find a significant association between DHEA and CHD risk.