DD Genotype Of ACE Gene Research Articles

Association of RAAS gene polymorphisms with susceptibility to essential hypertension in military secret service personnel

Objective: To analyze the relationship between renin-angiotensin-aldosterone system (RAAS) gene polymorphisms and susceptibility to essential hypertension (EH) in military secret service personnel. Methods: In October 2019, military secret service personnel (162 people) who were recuperating in a sanatorium from January to December 2017 were selected as the research subjects, all of whom were Han and male. The patients (79 people) who were diagnosed with EH according to the diagnostic criteria of hypertension in the "Chinese Guidelines for the Prevention and Treatment of Hypertension" (2016 Revised Edition) were the case group, and the people with normal blood pressure (83 people) were the control group. Occupational epidemiological investigation was conducted, 5 ml of fasting cubital venous blood was collected, genomic DNA was extracted by phenol-chloroform method, and RAAS gene polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism method. The distribution differences of genotype and allele frequency between groups were compared, and the relationship between genotype, allele frequency and EH was analyzed. Results: The average age of military secret service personnel was (38.2±5.3) years old, and there was no statistical significance in the average age and the age distribution over 40 years old of the case group and the control group (P>0.05) . There were significant differences in the distribution of AGT gene M235T locus, ACE gene I/D polymorphism genotype and allele between the case group and the control group (P<0.05) . The TT genotype with AGT gene M235T locus (OR=3.28, 95%CI: 1.21-8.91) and DD genotype with ACE gene (OR=2.86, 95%CI: 1.17-7.00) were risk factors for EH in military secret service personnel. Conclusion: The TT genotype of AGT gene M235T and the DD genotype of ACE gene may be the susceptibility genotypes of military secret service personnel for EH.

ACE ID gene polymorphism contributes to chronic kidney disease progression but not NOS3 gene among Type 2 diabetes with nephropathy patients

AimDiabetic nephropathy (DN) is one of the major life-threatening complications of diabetes and it leads to end-stage renal disease. Altered angiotension converting enzyme and nitric oxide synthase are probably the cause of initiation and the progression of diabetic nephropathy. The present study aims to investigate the effect of ACE ID and NOS3 VNTR gene polymorphisms on the progression of chronic kidney disease among diabetic nephropathy. Methods253 DN patients and 104 controls were genotyped for ACE ID and NOS3 VNTR polymorphisms by following PCR-RFLP method. The diabetic nephropathy cases were divided into two groups based on CKD stages: 138 DN cases were at early stage (CKD1 to CKD3) and 115 DN cases were at advanced stage (CKD4 and CKD5). Association χ2 and univariate analysis were performed. ResultsA significant difference was found in genotype frequencies of ACE ID and NOS3 VNTR polymorphisms between the DN patients and the controls. On univariate analysis, the DD genotype of ACE gene was found to have a significant association with the advancement of CKD in DN (OR=0.37; 95 % CI=0.14–0.94; p=0.033). ConclusionsThe results suggest the association of ACE ID and NOS3 VNTR polymorphism with diabetic nephropathy in South Indian population. Furthermore, the present study evidences the association between DD genotype of ACE gene and advancement of CKD progression in DN.

Gene polymorphisms and risk of preeclampsia in Egyptian women

Aim: The aim of this study was to evaluate the possible association between ACE I/D, AT1 receptor 1166 A:C, AT2receptor-1332 A:G, and MMP-9-1562 C:T polymorphisms and risk of preeclampsia in Egyptian women.Materials and Methods: This case-control study included 108 pregnant women was allocated into two groups, 54pre-eclamptic women group and control group which included 54 normotensive pregnant women. Genotyping of AT1 1166A:C and AT2 −1332 A: G were performed by duplex polymerase chain reaction-restriction fragment length polymorphismPCR-RFLP. Genotyping of I/D polymorphism of ACE was carried out by PCR and genotyping of MMP-9 −1562C/T wasperformed by tetra-primer amplification refractory mutation system T- ARMS–PCR.Results: The DD genotype of ACE gene was significantly associated with increased risk of preeclampsia[OR (95% CI) = 2.47 (0.72–8.5), p = 0.02] and the D allele was significantly associated with an increased risk ofpreeclampsia [OR (95% CI) = 1.95 (1.08–3.54), p = 0.02]. The AT2 GG genotype frequency was significantly higher inpreeclampsia [OR (95% CI) = 3.24 (1.25–8.41), p = 0.002] and the G allele [OR (95% CI) = 2.41 (1.39–4.18), p = 0.002]. However, the AT1 CC and MMP9 TT genotypes frequency were insignificantly associated with preeclampsia.Conclusion: ACE gene I/D and -1332A/G of AT2 receptor polymorphisms, but not AT1 receptor gene A1166C andMMP-9 (-1562 C/T) polymorphisms, could be related to the risk of preeclampsia in Egyptian women.

DD genotype of the I/D Angiotensin-Converting Enzyme Gene Polymorphism is a higher Risk for Atopic Asthma

Background: Atopic asthma begins with exposure to allergens causing airway hyperresponsiveness and chronic inflammation. Angiotensin II involved in the pathogenesis of atopic asthma by causing airway hyperresponsiveness. Angiotensin II levels are influenced by the levels of ACE and ACE levels are influenced by I / D ACE gene polymorphisms. Study about the role of I/D ACE gene polymorphism in the incidence and severity of asthma in several countries and etnic showed inconsistency result. Study in Indonesian subjects had never been reported. Method: This Case-control study aimed to evaluate influence of I/D ACE gene polymorphism in incidence and severity of atopic asthma. Eighty subjects aged 15-50 years including Forty non–asthmatic and Forty atopic asthmatic patients were included in this study.. Result: DD genotype with atopic asthma (85.7%) was higher than non atopic asthma (14,3%). Non-DD genotype (ID,II) with atopic asthma (46.6%) was lower than atopic asthma (53.4%). DD genotype of the ACE gene had risk 6.8 times to become atopic asthma than non-DD genotype (OR=6.8,p=0.05). DD genotype of ACE gene was not a risk factor for severe obstruction (OR=0.50, p=0.48) and uncontrolled atopic asthma compared to non-DD genotype (OR = 1.8,p=0.49) Conclusions: This study concluded that DD genotype of ACE gene was a risk factor for the incidence of atopic asthma but not a risk factor for severe obstruction and uncontrolled atopic asthma.

Does angiotensin-converting enzyme-1 (ACE-1) gene polymorphism lead to chronic kidney disease among hypertensive patients?

Background: Hypertension is one of the important contributing factors linked with both causation and development of kidney disease. It is a multifactorial, polygenic, and complex disorder due to interaction of several risk genes with environmental factors. The present study was aimed to explore genetic polymorphism in ACE-1 gene as a risk factor for CKD among hypertensive patients. Methods: Three hundred patients were enrolled in the study. Ninety were hypertensive patients with CKD taken as cases, whereas 210 hypertensive patients without CKD were taken as controls. Demographic data including age, sex, Body mass index (BMI), and other risk factors were also recorded. DNA was extracted from blood by salting out method. Genotyping of ACE gene was done by PCR technique. All the statistical analysis was done by using Epi Info and SPSS version 16 software (SPSS Inc., Chicago, IL). Results: Mean age was higher in the control group (p < 0.05). Variables among two groups were compared out of which age, BMI, hemoglobin (Hb) was found to be statistically significant whereas other variables like systolic blood pressure, triglyceride and low-density lipoprotein were not. Blood urea and serum creatinine levels were statistically significant in the two genotypes (p < 0.05). Total and HDL cholesterol were statistically significant for DD genotype of ACE gene (OR = 1.42, 95% CI = 0.72–2.81). Similarly, the risk for CKD among hypertensive patients was also associated with D allele of ACE gene (OR = 1.25, 95% CI = 0.86–1.79). Conclusion: It is concluded that ACE-DD genotype may be a risk factor for the causation and development of chronic kidney failure among hypertensive patients.

Pharmacogenetic efficacy of perindopril in children and adolescents with type 1 diabetes mellitus in prediction of diabetic nephropathy

DD genotype of ACE gene is a predisposing factor for chronic kidney disease terminating nephrotic syndrome in children with type 1 diabetes mellitus, while ACE gene II genotype upon diabetic nephropathy appears to be a protective one. The work was initiated to assess efficacy of perindopril in normoalbuminuric patients with type 1 diabetes mellitus by ACE genotype in the primary intervention of diabetic nephropathy. 22 normoalbuminuric patients with type 1 diabetes mellitus aged from 12 to 70 with diabetic nephropathy duration of 10 and more years were examined to be divided into two groups by ACE polymorphism including eleven-by-eleven carriers of II genotype and DD genotype, respectively. Perindopril in low doses is recommended to treat normoalbuminuric children and adolescents for optimization of intervention and therapy of diabetic nephropathy. GULNARA RAKHIMOVA 1,2 , AKIDA SADYKOVA 1,NASIBA ALIMOVA 1

DD genotype of ace gene I/D polymorphism is associated in a turkish study population with osteoarthritis

This study was conducted in Turkish osteoarthritis patients to determine the frequency of I/D polymorphism genotypes of angiotensin converting enzyme gene, and to examine the role of this polymorphism in osteoarthritis development. Genomic DNA obtained from 200 persons (135 patients with osteoarthritis and 65 healthy controls) was used in the study. DNA was multiplied by polymerase chain reaction using I and D allele-specific primers. Polymerase chain reaction products were assessed with CCD camera by being exposed to 2% agarose gel electrophoresis. There was statistically significant difference between the groups with respect to genotype distribution (P < 0.001). The D allele frequency was indicated as 69% and I allele was as 31% in the patients, whereas it was 55-45% in the control group. Consequently, in this study, we may assert that ACE gene I/D polymorphism DD genotype determination is significant criteria for identifying patients who are likely to develop osteoarthritis in east population of Turkey.

INFLUENCE OF LONG-TERM PHARMACOGENETICALLY DETERMINED TREATMENT ON ENDOTHELIUM FUNCTION AND INTIMA-MEDIA THICKNESS (IMT) IN DEPENDENCE ON FIVE GENES POLYMORPHISM: PP.6.246

Objective: To evaluate endothelium function (EF) and IMT in hypertensive patients (EAH) under treatment during 12 months depending on I/D polymorphism (ACE gene), À1166Ñ (AGTR1 gene), T894G (eNOS gene), Pro12Ala (PPAR-γ2), Arg389Gly (ADRβ1 gene). Design/Methods: 249 patients (EAH I – 26.5%; EAH 22 – 45.8%; EAH 222 – 27.7%; women – 48.2%, men – 51.8%, mean age 50.5 ± 10.4 yrs) underwent combination therapy (hydrochlorothiazide (HCTZ)+angiotensin II receptor blocker (ARB), HCTZ + β1-blockers (BB), HCTZ + ACE inhibitors (ACEI), calcium antagonists (CA) + ARB, CA + BB, CA + ACEI). EF evaluated by Flow Mediated brachial artery Dilation (FMD). Efficacy criteria – FMD > 10.0%, IMT < .9 mm (ESC/ESH 2007). Results: Number of patients with target IMT (<.9 mm) and FMD (>10.0%) increased by 15.9% and 29.3%, p < .001. HCTZ + ARB increased percentage by 13.3% and 23.3%, p < .001: reliable in ACE gene' II-genotype (ð < .002), AGTR1 gene' A-allele (.001 > ð < .05), eNOS gene' G-allele carriers (.006 > ð < .023), PPARγ2 gene' Pro-allele (.005 > ð < .028) and ADRβ1 gene' Arg-allele (.003 > ð < .028). HCTZ + BB caused 8.8% IMT increase (p = .007): reliable in ID-genotype of ACE gene and TG-genotype of eNOS gene (p = .045), without significant changes of FMD. Target IMT and FMD patients increase under HCTZ + ACEI by 18.0% and 36.0%, p < .001: reliable in ACE gene' ID-genotype (ð < .001), eNOS gene' G-allele (.001 > ð < .046), PPARγ2 gene' Pro-allele and ADRβ1 gene' Arg-allele (.001 > ð < .014). 13.3% and 33.3% increase under CAs + ARB, ð < .001, certainly in DD-genotype of ACE gene. CA + BB – increase by 20.0% (p = .011) and 53.3% (p < .001): reliable in DD-genotype of ACE gene (p < .011), independent on AGTR1 gene' genotypes (p < .024), TG-genotype of eNOS gene, ProPro-genotypes of PPARγ2 gene and Gly-allele of ADRβ1 gene (p < .001). CA + ACEI caused increase by 25.9% and 33.3%, ð < .001, certainly in ACE gene' DD-genotype (ð < .001), A-allele of AGTR1 gene, G-allele of eNOS gene, Pro-allele of PPARγ2 gene and Arg-allele carriers of ADRβ1 gene (.001 > ð < .023). Conclusions: Reliable advantage in endothelial function improvement observed in all combinations of CA (better CAs + ACEI), rather than with HCTZ (p < .05) in D-allele carriers of ACE gene. CA + ARB and CA + ACEI are more preferable than HCTZ + BB (p < .05) in D-allele of ACE gene.

ACE (I/D) AND ENOS (T894G) GENES’ POLYMORPHISMS INFLUENCE NEW CARDIOVASCULAR (CV) EVENTS: PHARMACOGENOMIC UPDATE ON THERAPY: PP.21.328

Objective: To determine the association between ACE (I/D) and eNOS (T894G) genes polymorphisms and new CV events in hypertensive patients with coronary artery disease (CAD) and acute coronary syndrome (ACS) in response to pharmacogenetically determined treatment. Design/Methods: 249 mild-severe hypertensive patients (126 female, 123 male, age 50.5 ± 10.4), 70 – CAD (27 – ACS, 43 – stable angina (SA) participated in prospective pharmacogenetic study based on individual genotype-dependent BP reduction, according to ESH/ESC (2007). Genotyping of ACE and eNOS genes – PCR test. CV risk – by SCORE and Framingham scales. Results: Age, gender, risk area of living, systolic BP, dyslipidemia, heart rate, left ventricular hypertrophy, residual ischemia, smoking, diabetes mellitus, WBC, claudicating, fibrinogen and electrical myocardial instability were independent risk factors for CV events. Baseline fatal and non-fatal CV risks for the next 10-years (SCORE and Framingham10) and 4-years (Framingham4) were significantly higher in D-homozygous patients than in I-allele carriers of ACE gene: 10.54 ± 3.70% (p < .05), 32.59 ± 5.67% (p = .048) and 17.99 ± 3.29% (p = .01), DD, ID and II, accordingly. Differences in CV risks were generally independent on eNOS (T894) gene polymorphism (p > .05), but associated with CAD (not ACS) in TT-genotype carriers: 14.76 ± 6.15% (p < .05), 33.76 ± 6.54% (p < .05) and 13.47 ± 4.35 (p = .05). The median reduction of CV risk in response to 12 months therapy (SCORE/Framingham10/Framingham4) was reliable in all genotypes carriers of ACE gene: II- (−55.1/−29.0/−47.3%, p < .05), ID- (−47.7/−31.4/−31.3%, p < .05), DD- (−50.2/−24.0/−47.9%, p < .02), with some deviation according to eNOS gene: fatal CV risk decreased significantly in all genotypes (in GG −62.0, TG −45.8, TT −41.8%, p < .02), non-fatal Framingham10 in TG-carriers (−20.7%, p < .05), Framingham4 – in G-allele carriers (−42.8/ −38.3%, p < .05). Conclusions: DD-genotype of ACE gene has direct association with increased CV risks in hypertensive patients. eNOS (T894G) gene didn't influence CV risks, but TT-genotype is associated with CAD and new CV events in hypertensive patients. Pharmacogenetically modified treatment caused reliable reduction of patients with fatal CV risk (SCORE > 5.0%) by 42.8% and non-fatal (Framingham10/4 >20.0/15.0%) by 31.3% and 30.3%, accordingly (p < .001).

P50 Association of DD genotype of ACE gene with lupus nephritis in South Indian Tamil patients with SLE

P50 Association of DD genotype of ACE gene with lupus nephritis in South Indian Tamil patients with SLE