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      Association between polymorphisms of DNA repair genes and intracranial aneurysms: A systematic review and meta‑analysis

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          Abstract

          Intracranial aneurysms (IAs) are present in ~2% of the general population, and genetic factors cannot be excluded for the risk of their development. The gene factors that result in the changes in the vascular extracellular matrix (ECM) may also be a key reason for IAs being hereditary. The VCAN gene [also known as chondroitin sulfate proteoglycan 2 ( CSPG2)] plays various roles in maintaining ECM functions. The present systematic review and meta-analysis aimed to investigate all eligible articles involving IAs on the association with germ line SNPs of DNA repair genes (up to January, 2024). The total number of patients was 2,308 [987 cases (poor outcomes) and 1,321 controls (good outcomes)]. The results revealed that rs2287926 G/G genotype and G allele and rs251124 T/T genotype and minor allele T increased the risk of developing IAs. However, further studies are required to examine these gene polymorphisms as screening markers for IAs.

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          Stroke Risk Factors, Genetics, and Prevention.

          Amelia K. Boehme, Charles Esenwa, Mitchell S. V. Elkind (2017)
          Stroke is a heterogeneous syndrome, and determining risk factors and treatment depends on the specific pathogenesis of stroke. Risk factors for stroke can be categorized as modifiable and nonmodifiable. Age, sex, and race/ethnicity are nonmodifiable risk factors for both ischemic and hemorrhagic stroke, while hypertension, smoking, diet, and physical inactivity are among some of the more commonly reported modifiable risk factors. More recently described risk factors and triggers of stroke include inflammatory disorders, infection, pollution, and cardiac atrial disorders independent of atrial fibrillation. Single-gene disorders may cause rare, hereditary disorders for which stroke is a primary manifestation. Recent research also suggests that common and rare genetic polymorphisms can influence risk of more common causes of stroke, due to both other risk factors and specific stroke mechanisms, such as atrial fibrillation. Genetic factors, particularly those with environmental interactions, may be more modifiable than previously recognized. Stroke prevention has generally focused on modifiable risk factors. Lifestyle and behavioral modification, such as dietary changes or smoking cessation, not only reduces stroke risk, but also reduces the risk of other cardiovascular diseases. Other prevention strategies include identifying and treating medical conditions, such as hypertension and diabetes, that increase stroke risk. Recent research into risk factors and genetics of stroke has not only identified those at risk for stroke but also identified ways to target at-risk populations for stroke prevention.
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            Subarachnoid haemorrhage.

            Jan van Gijn, Richard Kerr, Gabriel J. E. Rinkel (2007)
            Subarachnoid haemorrhage accounts for only 5% of strokes, but occurs at a fairly young age. Sudden headache is the cardinal feature, but patients might not report the mode of onset. CT brain scanning is normal in most patients with sudden headache, but to exclude subarachnoid haemorrhage or other serious disorders, a carefully planned lumbar puncture is also needed. Aneurysms are the cause of subarachnoid haemorrhage in 85% of cases. The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital. Rebleeding is the most imminent danger; a first aim is therefore occlusion of the aneurysm. Endovascular obliteration by means of platinum spirals (coiling) is the preferred mode of treatment, but some patients require a direct neurosurgical approach (clipping). Another complication is delayed cerebral ischaemia; the risk is reduced with oral nimodipine and probably by maintaining circulatory volume. Hydrocephalus might cause gradual obtundation in the first few hours or days; it can be treated by lumbar puncture or ventricular drainage, dependent on the site of obstruction.
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              Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies.

              Valery L Feigin, Gabriel J E Rinkel, 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

                Journal
                Journal ID (nlm-ta): Med Int (Lond)
                Journal ID (iso-abbrev): Med Int (Lond)
                Journal ID (publisher-id): MI
                Title: Medicine International
                Publisher: D.A. Spandidos
                ISSN (Print): 2754-3242
                ISSN (Electronic): 2754-1304
                Publication date Collection: Nov-Dec 2024
                Publication date (Electronic): 24 July 2024
                Publication date PMC-release: 24 July 2024
                Volume: 4
                Issue: 6
                Electronic Location Identifier: 59
                Affiliations
                [1 ]Department of Neurosurgery, General University Hospital of Larissa, 41221 Larissa, Greece
                [2 ]Department of Pathophysiology, National and Kapodistrian University of Athens, 11527 Athens, Greece
                [3 ]Department of Pediatrics, General Hospital of Zakynthos ‘Agios Dionysios’, 29100 Zakynthos, Greece
                [4 ]Department of Biochemistry, Sismanogleio Hospital, 15126 Athens, Greece
                Author notes
                Correspondence to: Dr George Fotakopoulos, Department of Neurosurgery, General University Hospital of Larissa, Mezourlo 1, 41221 Larissa, Greece gfotakopyahoo.gr zhanggangnjmu@ 123456126.com
                Article
                Publisher ID: MI-4-6-00183
                DOI: 10.3892/mi.2024.183
                PMC ID: 11289859
                PubMed ID: 39092011
                SO-VID: 75346254-6fde-42e2-be19-d82a256bbc01
                Copyright © Copyright: © 2024 Montasr et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.

                History
                Date received : 13 March 2024
                Date accepted : 17 July 2024
                Funding
                Funding: No funding was received.
                Categories
                Subject: Articles

                Keywords: intracranial aneurysms,aneurysms,gene associations,single nucleotide polymorphisms,chondroitin sulfate proteoglycan 2 gene
                Data availability:
                Keywords: intracranial aneurysms, aneurysms, gene associations, single nucleotide polymorphisms, chondroitin sulfate proteoglycan 2 gene

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