دورية أكاديمية
أعرض في EDS

Effects of angiotensin converting enzyme gene polymorphism on hypertension in Africa: A meta-analysis and systematic review.

التفاصيل البيبلوغرافية
العنوان: Effects of angiotensin converting enzyme gene polymorphism on hypertension in Africa: A meta-analysis and systematic review.
المؤلفون: Mengesha HG; Department of Pharmacy, College of Medicine and Health Sciences, Adigrat University, Adigrat, Ethiopia., Petrucka P; University of Saskatchewan, College of Nursing, Saskatoon, SK, Canada, Adjunct Nelson Mandela African Institute of Science and Technology, Arusha, Tanzania., Spence C; Univeristy of Saskatchewan, International Research Specialist, International Office, Saskatoon, SK, Canada., Tafesse TB; School of Pharmacy, College of Health and Medical Sciences, Haramaya Univeristy, Harar, Ethiopia.
المصدر: PloS one [PLoS One] 2019 Feb 14; Vol. 14 (2), pp. e0211054. Date of Electronic Publication: 2019 Feb 14 (Print Publication: 2019).
نوع المنشور: Journal Article; Meta-Analysis; Systematic Review
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Models, Genetic* , Polymorphism, Genetic*, Hypertension/*genetics , Peptidyl-Dipeptidase A/*genetics, Africa South of the Sahara/epidemiology ; Africa, Northern/epidemiology ; Female ; Humans ; Hypertension/epidemiology ; Male
مستخلص: Background: Hypertension is dramatically increasing in Africa with evidence of increased severity and resistance to treatment. Although angiotensin converting enzyme gene polymorphism is associated with higher prevalence of hypertension, the evidence is inconclusive on its influence on the emerging pattern in Africa. This meta-analysis is conducted to pool the available evidence to inform future research and interventions.
Methods: Articles published through May 2018 were systematically searched in PubMed, Scopus and EMBASE databases. Studies were assessed for inclusion by two independent researchers. Six models were used to assess the effect of angiotensin converting enzyme deletion-insertion gene polymorphism. Heterogeneity and publication bias were tested and sensitivity analysis was carried out. Odds ratio and 95% confidence intervals were measured for pooled effect. Both random effect and fixed effect models were used, whilst the frequency of DD, II and DI genotypes were computed and compared.
Result: Patients with D allele were 1.49 times more likely to develop essential hypertension compared with patients who carry the I allele (OR:1.49; CI:1.07, 2.07). Similarly, patients who had homozygous co-dominance genotype DD (i.e., DD vs II) were at a 2.17 times higher risk of essential hypertension compared to the co-dominant genotype II (OR:2.17, CI:1.79, 3.18), dominant model (I.e., DD+ID vs II) (OR:1.48; CI:1.03, 2.12), and recessive model (OR:1.64; CI:1.03, 2.61). On subgroup analysis, participants from Sub-Saharan Africa were more genetically susceptible to hypertension compared to their North Africa counterparts. There was no publication bias found, but there was high to moderate heterogeneity.
Conclusion: ACE I/D polymorphism is associated with essential hypertension in Africa in the allele contrast model, as well as the dominant, recessive and homozygous codominance model. On subgroup analysis, ACE I/D was associated with essential hypertension in patients from Sub-Saharan Africa but not in North Africa. A future large scale study, which includes different ethnic groups, is recommended.
Competing Interests: The authors have declared that no competing interests exist.
References: J Hum Hypertens. 2003 Apr;17(4):277-85. (PMID: 12714973)
Intern Med J. 2012 Apr;42(4):439-44. (PMID: 21883781)
Am J Hum Genet. 2013 Sep 5;93(3):545-54. (PMID: 23972371)
Clin Lab. 2013;59(1-2):85-92. (PMID: 23505911)
J Hypertens. 2007 Mar;25(3):565-70. (PMID: 17278972)
Lancet. 2005 Jan 15-21;365(9455):217-23. (PMID: 15652604)
Circulation. 2005 Dec 6;112(23):3562-8. (PMID: 16330697)
Am J Hypertens. 1997 May;10(5 Pt 1):558-61. (PMID: 9160768)
J Hypertens. 1997 Dec;15(12 Pt 2):1579-92. (PMID: 9488209)
Nature. 2007 Jun 7;447(7145):661-78. (PMID: 17554300)
Hum Hered. 2004;57(1):28-38. (PMID: 15133310)
Tunis Med. 2010 Jan;88(1):38-41. (PMID: 20415212)
Bratisl Lek Listy. 2012;113(1):14-8. (PMID: 22380495)
Int J Occup Environ Health. 2014 Jul-Sep;20(3):194-206. (PMID: 25000107)
Circulation. 2005 Jun 28;111(25):3374-83. (PMID: 15967849)
Int J Hypertens. 2015;2015:979631. (PMID: 26351579)
Lancet. 2002 Dec 14;360(9349):1903-13. (PMID: 12493255)
Hypertension. 2006 May;47(5):948-54. (PMID: 16567584)
Adv Biomed Res. 2014 May 28;3:118. (PMID: 24949289)
J Clin Hypertens (Greenwich). 2018 Mar;20(3):485-495. (PMID: 29520984)
BMC Med. 2013 May 30;11:141. (PMID: 23721258)
Nat Genet. 2011 Jun;43(6):531-8. (PMID: 21572416)
Ann Intern Med. 2004 Oct 19;141(8):614-27. (PMID: 15492341)
Hypertension. 2013 Nov;62(5):853-9. (PMID: 24001895)
J Am Soc Hypertens. 2014 Apr;8(4):232-8. (PMID: 24524886)
Nature. 2011 Sep 11;478(7367):103-9. (PMID: 21909115)
BMC Bioinformatics. 2017 Dec 16;18(1):563. (PMID: 29246109)
المشرفين على المادة: EC 3.4.15.1 (Peptidyl-Dipeptidase A)
تواريخ الأحداث: Date Created: 20190215 Date Completed: 20191029 Latest Revision: 20231005
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC6375551
DOI: 10.1371/journal.pone.0211054
PMID: 30763326
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0211054