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Aims: The purpose of this research was to investigate the effectiveness of telemonitoring for chronic obstructive pulmonary disease.Methods: We searched MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials and CINAHL up to September 2018. We selected randomised controlled trials comparing telemonitoring and control groups for chronic obstructive pulmonary disease management. Two reviewers independently examined articles based on eligibility, extracted data and evaluated the risk of bias. The Cochrane tool was applied for assessing the risk of bias. The 95% confidence interval was calculated.Results: A total of 28 randomised controlled trials were included. Meta-analysis revealed that there were no variables showing a statistically significant difference between telemonitoring and control groups. Chronic obstructive pulmonary disease exacerbation rate (six studies) was not different between two groups (risk ratio 0.67, 95% confidence interval 0.31-1.42). Subgroup analysis showed that telemonitoring reduced exacerbation rates when the intervention continued for longer than six months or pulmonary function was monitored. No differences between groups were noticed for mortality (seven studies, risk ratio 0.89, 95% confidence interval 0.60-1.34). Similarly, no differences between groups were observed in the patient-reported outcomes (St George's Respiratory Questionnaire, Chronic Respiratory Disease Questionnaire-Dyspnea score) and for health service utilization (length of hospital stay, number of hospital admissions, number of emergency room visits).Conclusions: Telemonitoring for chronic obstructive pulmonary disease was unlikely to result in statistically significant improvements in health outcomes. However, our novel finding was that at least six months of intervention duration and monitoring of pulmonary function play roles in activating the effects of telemonitoring. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to carry out systematic review of the literature and meta-analysis to evaluate the diagnostic utility of cerebrospinal fluid (CSF) levels of the 42 amino acid form of amyloid-beta (Aβ1–42) as a biomarker for differentiating Alzheimer’s disease (AD) from non-AD dementia. Methods: Design. Systematic literature review was used to evaluate the effectiveness of the Aβ for the diagnosis of AD. The Scottish Intercollegiate Guidelines Network (SIGN) tool was used to evaluate independently the quality of the studies. Data sources. The literature review covered from January 1, 2004, to October 22, 2013, and searched eight domestic databases including Korea Med and international databases including Ovid-MEDLINE, EMBASE, and Cochrane Library. Data Extraction and Synthesis. Primary criteria for inclusion were valid studies on (i) patients with mild cognitive impairment with confirmed or suspected AD and non-AD dementia, and (ii) assessment of Aβ1–42 levels using appropriate comparative tests. Results: A total of 17 diagnostic evaluation studies were identified in which levels of CSF Aβ1–42 were assessed. Meta-analysis was performed on 11 robust studies that compared confirmed AD (n = 2211) with healthy individuals (n = 1030), 10 studies that compared AD with non-AD dementias (n = 627), and 5 studies that compared amnestic mild cognitive impairment (n = 1133) with non-amnestic type subjects (n = 1276). Overall, the CSF Aβ1–42 levels were reduced in AD compared to controls or non-AD dementia. The effectiveness of test was evaluated for diagnostic accuracy (pooled sensitivity, 0.80 (95% CI 0.78–0.82); pooled specificity, 0.76 (95% CI 0.74–0.78). Conclusions: Reduced CSF Aβ1–42 levels are of potential utility in the differential diagnosis of AD versus non-AD dementias and controls. Diagnostic accuracy was high in AD versus healthy controls. However, differential diagnosis for MCI or non-AD might be evaluated by other biomarkers. [ABSTRACT FROM AUTHOR]