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      Effects of clazosentan, cilostazol, and statins on aneurysmal subarachnoid hemorrhage : A protocol for systematic review and meta-analysis

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          Abstract

          Background

          : Aneurysmal subarachnoid hemorrhage (aSAH) is a disease caused by the infiltration of blood into the subarachnoid space due to the rupture of an intracranial aneurysm. It is a serious cerebrovascular disease, with a mortality rate of about 40% worldwide, which seriously threatens human life and health. Many drugs are used to treat aSAH and its complications, and some have been tested in systematic reviews and have shown good effects. But which drug has the best effect remains unclear. This network meta-analysis (NMA) aims to assess the effectiveness and feasibility of clazosentan, cilostazol, and statins in patients with aSAH.

          Methods

          : We will search for EMBASE.com, PubMed, the Cochrane Library, and Web of Science from inception to December 2019. Randomized controlled trials (RCTs) reporting efficacy and safety of clazosentan, cilostazol, and statins compared with the control, or compared with each other for the treatment of aSAH will be included. Two independent reviewers will assess the risk of bias of the included RCTs with the Cochrane “Risk of bias” tool. The pairwise meta-analysis will be performed with the random-effects model. The NMA will be performed in a Bayesian hierarchical framework using Markov Chain Monte Carlo method in WinBUGS 1.4.3. Egger test and funnel plot will be used to assess the publication bias. We will evaluate the quality of evidence for each outcome according to the GRADE approach.

          Results

          : The results of this NMA will be submitted to a peer-reviewed journal for publication.

          Conclusion

          : This study will summarize up-to-date evidence to compare the efficacy and safety of clazosentan, cilostazol, and statins on aSAH.

          PROSPERO registration number: CRD42019147523.

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          Most cited references27

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          Delayed neurological deterioration after subarachnoid haemorrhage.

          Subarachnoid haemorrhage (SAH) causes early brain injury (EBI) that is mediated by effects of transient cerebral ischaemia during bleeding plus effects of the subarachnoid blood. Secondary effects of SAH include increased intracranial pressure, destruction of brain tissue by intracerebral haemorrhage, brain shift, and herniation, all of which contribute to pathology. Many patients survive these phenomena, but deteriorate days later from delayed cerebral ischaemia (DCI), which causes poor outcome or death in up to 30% of patients with SAH. DCI is thought to be caused by the combined effects of angiographic vasospasm, arteriolar constriction and thrombosis, cortical spreading ischaemia, and processes triggered by EBI. Treatment for DCI includes prophylactic administration of nimodipine, and current neurointensive care. Prompt recognition of DCI and immediate treatment by means of induced hypertension and balloon or pharmacological angioplasty are considered important by many physicians, although the evidence to support such approaches is limited. This Review summarizes the pathophysiology of DCI after SAH and discusses established treatments for this condition. Novel strategies--including drugs such as statins, sodium nitrite, albumin, dantrolene, cilostazol, and intracranial delivery of nimodipine or magnesium--are also discussed.
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            Demystifying trial networks and network meta-analysis.

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              • Article: not found

              The methodological and reporting quality of systematic reviews from China and the USA are similar.

              To compare the methodological and reporting quality of systematic reviews by authors from China and those from the United States (USA).
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                April 2020
                24 April 2020
                : 99
                : 17
                : e19902
                Affiliations
                [a ]Department of Neurological Rehabilitation, Rehabilitation Center Hospital of Gansu Province
                [b ]The Third Ward of Cardiovascular Clinical Medical Center, Affiliated Hospital of Gansu University of Chinese Medicine
                [c ]Pathogens Biology Institute, School of Basic Medical Sciences of Lanzhou University
                [d ] The Second Clinical Medical College of Lanzhou University
                [e ]Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou
                [f ]Basic Medical School, Guilin Medical University, Guilin
                [g ]Gansu Provincial Hospital, Lanzhou, China.
                Author notes
                []Correspondence: Min Wei, Affiliated Hospital of Gansu University of Chinese Medicine, No. 732 Jiayuguan West Road, Chengguan District, Lanzhou City, Gansu Province, China (e-mail: 3441828719@ 123456qq.com ).
                Article
                MD-D-20-01035 19902
                10.1097/MD.0000000000019902
                7440251
                32332668
                640f9713-19ef-44a2-89af-7c64d74730d4
                Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                : 06 March 2020
                : 13 March 2020
                Categories
                5300
                Research Article
                Study Protocol Systematic Review
                Custom metadata
                TRUE

                aneurysmal subarachnoid hemorrhage,cilostazol,clazosentan,network meta-analysis,statins

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