Background and Purpose— There is no consensus on the comparative efficacy and safety of carotid artery stenting (CAS) versus carotid endarterectomy (CEA) in patients with asymptomatic carotid artery stenosis. To evaluate CAS versus CEA in asymptomatic patients, we conducted a systematic review and meta-analysis of randomized controlled trials. Methods— We systematically searched EMBASE, PubMed, MEDLINE, and the Cochrane Library for randomized controlled trials comparing CAS to CEA in asymptomatic patients using a pre-specified protocol. Two independent reviewers identified randomized controlled trials meeting our inclusion/exclusion criteria, extracted relevant data, and assessed quality using the Cochrane risk of bias tool. Random effects models with inverse-variance weighting were used to estimate pooled risk ratios (RRs) comparing the incidences of periprocedural and long-term outcomes between CAS and CEA. Results— We identified 11 reports of 5 randomized controlled trials for inclusion (n=3019) asymptomatic patients. The pooled incidences of any periprocedural stroke (RR, 1.84; 95% confidence interval [CI], 0.99–3.40), periprocedural nondisabling stroke (RR, 1.95; 95% CI, 0.98–3.89), and any periprocedural stroke or death (RR, 1.72; 95% CI, 0.95–3.11) trended toward an increased risk after CAS. We could not rule out clinically significant differences between treatments for long-term stroke (RR, 1.24; 95% CI, 0.76–2.03) and the composite outcome of periprocedural stroke, death or myocardial infarction, or long-term ipsilateral stroke (RR, 0.92; 95% CI, 0.70–1.21). Conclusions— Although uncertainty surrounds the long-term outcomes of CAS versus CEA, the potential for increased risks of periprocedural stroke and periprocedural stroke or death with CAS suggests that CEA is the preferred option for the management of asymptomatic carotid stenosis.
Residential combustion of solid fuel is a major source of air pollution. In regions where space heating and cooking occur at the same time and using the same stoves and fuels, evaluating air-pollution patterns for household-energy-use scenarios with and without heating is essential to energy intervention design and estimation of its population health impacts as well as the development of residential emission inventories and air-quality models. We measured continuous and 48 h integrated indoor PM2.5 concentrations over 221 and 203 household-days and outdoor PM2.5 concentrations on a subset of those days (in summer and winter, respectively) in 204 households in the eastern Tibetan Plateau that burned biomass in traditional stoves and open fires. Using continuous indoor PM2.5 concentrations, we estimated mean daily hours of combustion activity, which increased from 5.4 h per day (95% CI: 5.0, 5.8) in summer to 8.9 h per day (95% CI: 8.1, 9.7) in winter, and effective air-exchange rates, which decreased from 18 ± 9 h(-1) in summer to 15 ± 7 h(-1) in winter. Indoor geometric-mean 48 h PM2.5 concentrations were over two times higher in winter (252 μg/m(3); 95% CI: 215, 295) than in summer (101 μg/m(3); 95%: 91, 112), whereas outdoor PM2.5 levels had little seasonal variability.
Objectives Pyruvate kinase deficiency (PK deficiency) is a rare disorder caused by compound heterozygosity or homozygosity for > 300 mutations in the PKLR gene. To understand PK deficiency prevalence, we conducted a systematic literature review. Methods We queried Embase and Medline for peer‐reviewed references reporting PK deficiency prevalence/incidence, PKLR mutant allele frequency (MAF) among the general population, or crude results from which these metrics could be derived. Results Of 1390 references screened, 1296 were excluded after title/abstract review; 60 were excluded after full‐text review. Four of the remaining 34 studies were considered high‐quality for estimating PK deficiency prevalence. Two high‐quality studies identified cases from source populations of known sizes, producing estimates of diagnosed PK deficiency prevalence of 3.2 and 8.5 per million. Another high‐quality study derived an estimate of diagnosed PK deficiency prevalence of 6.5 per million by screening jaundiced newborns. The final high‐quality study estimated total diagnosed and undiagnosed PK deficiency prevalence to be 51 per million through extrapolation from observed MAFs. Conclusions We conclude that prevalence of clinically diagnosed PK deficiency is likely between 3.2 and 8.5 per million in Western populations, while the prevalence of diagnosed and undiagnosed PK deficiency could possibly be as high as 51 per million.
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