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      The role of inflammation and potential use of sex steroids in intracranial aneurysms and subarachnoid hemorrhage

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          Abstract

          Background:

          Aneurysmal subarachnoid hemorrhage (aSAH) continues to be a devastating neurological condition with a high risk of associated morbidity and mortality. Inflammation has been shown to increase the risk of complications associated with aSAH such as vasospasm and brain injury in animal models and humans. The goal of this review is to discuss the inflammatory mechanisms of aneurysm formation, rupture and vasospasm and explore the role of sex hormones in the inflammatory response to aSAH.

          Methods:

          A literature review was performed using PubMed using the following search terms: “intracranial aneurysm,” “cerebral aneurysm,” “dihydroepiandrosterone sulfate” “estrogen,” “hormone replacement therapy,” “inflammation,” “oral contraceptive,” “progesterone,” “sex steroids,” “sex hormones” “subarachnoid hemorrhage,” “testosterone.” Only studies published in English language were included in the review.

          Results:

          Studies have shown that administration of sex hormones such as progesterone and estrogen at early stages in the inflammatory cascade can lower the risk and magnitude of subsequent complications. The exact mechanism by which these hormones act on the brain, as well as their role in the inflammatory cascade is not fully understood. Moreover, conflicting results have been published on the effect of hormone replacement therapy in humans. This review will scrutinize the variations in these studies to provide a more detailed understanding of sex hormones as potential therapeutic agents for intracranial aneurysms and aSAH.

          Conclusion:

          Inflammation may play a role in the pathogenesis of intracranial aneurysm formation and subarachnoid hemorrhage, and administration of sex hormones as anti-inflammatory agents has been associated with improved functional outcome in experimental models. Further studies are needed to determine the therapeutic role of these hormones in the intracranial aneurysms and aSAH.

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          Most cited references147

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          Mitogen-activated protein kinases in innate immunity.

          J. Simon C. Arthur, Steven C Ley (2013)
          Following pathogen infection or tissue damage, the stimulation of pattern recognition receptors on the cell surface and in the cytoplasm of innate immune cells activates members of each of the major mitogen-activated protein kinase (MAPK) subfamilies--the extracellular signal-regulated kinase (ERK), p38 and Jun N-terminal kinase (JNK) subfamilies. In conjunction with the activation of nuclear factor-κB and interferon-regulatory factor transcription factors, MAPK activation induces the expression of multiple genes that together regulate the inflammatory response. In this Review, we discuss our current knowledge about the regulation and the function of MAPKs in innate immunity, as well as the importance of negative feedback loops in limiting MAPK activity to prevent host tissue damage. We also examine how pathogens have evolved complex mechanisms to manipulate MAPK activation to increase their virulence. Finally, we consider the potential of the pharmacological targeting of MAPK pathways to treat autoimmune and inflammatory diseases.
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            Delayed neurological deterioration after subarachnoid haemorrhage.

            R. Loch Macdonald (2014)
            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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              Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies.

              Derrick Bennett, Jan van Lanschot, Carlene M M Lawes … (2005)
              After a 1996 review from our group on risk factors for subarachnoid hemorrhage (SAH), much new information has become available. This article provides an updated overview of risk factors for SAH. An overview of all longitudinal and case-control studies of risk factors for SAH published in English from 1966 through March 2005. We calculated pooled relative risks (RRs) for longitudinal studies and odds ratios (ORs) for case-control studies, both with corresponding 95% CIs. We included 14 longitudinal (5 new) and 23 (12 new) case-control studies. Overall, the studies included 3936 patients with SAH (892 cases in 14 longitudinal studies and 3044 cases in 23 case-control studies) for analysis. Statistically significant risk factors in longitudinal and case-control studies were current smoking (RR, 2.2 [1.3 to 3.6]; OR, 3.1 [2.7 to 3.5]), hypertension (RR, 2.5 [2.0 to 3.1]; OR, 2.6 [2.0 to 3.1]), and excessive alcohol intake (RR, 2.1 [1.5 to 2.8]; OR, 1.5 [1.3 to 1.8]). Nonwhite ethnicity was a less robust risk factor (RR, 1.8 [0.8 to 4.2]; OR, 3.4 [1.0 to 11.9]). Oral contraceptives did not affect the risk (RR, 5.4 [0.7 to 43.5]; OR, 0.8 [0.5 to 1.3]). Risk reductions were found for hormone replacement therapy (RR, 0.6 [0.2 to 1.5]; OR, 0.6 [0.4 to 0.8]), hypercholesterolemia (RR, 0.8 [0.6 to 1.2]; OR, 0.6 [0.4 to 0.9]), and diabetes (RR, 0.3 [0 to 2.2]; OR, 0.7 [0.5 to 0.8]). Data were inconsistent for lean body mass index (RR, 0.3 [0.2 to 0.4]; OR, 1.4 [1.0 to 2.0]) and rigorous exercise (RR, 0.5 [0.3 to 1.0]; OR, 1.2 [1.0 to 1.6]). In the studies included in the review, no other risk factors were available for the meta-analysis. Smoking, hypertension, and excessive alcohol remain the most important risk factors for SAH. The seemingly protective effects of white ethnicity compared to nonwhite ethnicity, hormone replacement therapy, hypercholesterolemia, and diabetes in the etiology of SAH are uncertain.
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                Author and article information

                Contributors
                Jack W. Barrow
                Nefize Turan
                Pasang Wangmo
                Anil K. Roy
                Gustavo Pradilla
                Journal
                Journal ID (nlm-ta): Surg Neurol Int
                Journal ID (iso-abbrev): Surg Neurol Int
                Journal ID (publisher-id): SNI
                Title: Surgical Neurology International
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2229-5097
                ISSN (Electronic): 2152-7806
                Publication date Collection: 2018
                Publication date (Electronic): 26 July 2018
                Volume: 9
                Electronic Location Identifier: 150
                Affiliations
                [1 ]Cerebrovascular Research Laboratory, Department of Neurosurgery, Emory University School of Medicine, Atlanta, Georgia, USA
                [2 ]Mercer University School of Medicine, Savannah, Georgia, USA
                Author notes
                [* ]Corresponding author
                Article
                Publisher ID: SNI-9-150
                DOI: 10.4103/sni.sni_88_18
                PMC ID: 6080146
                PubMed ID: 30105144
                SO-VID: 7eebd3b1-ff3c-453d-8f60-ad11c2fc5439
                Copyright © Copyright: © 2018 Surgical Neurology International
                License:

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                Date received : 20 March 2018
                Date accepted : 15 May 2018
                Categories
                Subject: Inflammation: Review Article

                ScienceOpen disciplines: Surgery
                Keywords: estrogen,inflammation,intracranial aneurysms,progesterone,sex hormones,subarachnoid hemorrhage
                Data availability:
                ScienceOpen disciplines: Surgery
                Keywords: estrogen, inflammation, intracranial aneurysms, progesterone, sex hormones, subarachnoid hemorrhage

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