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Prevalence of hepatitis C virus genotypes in Italy.

Hepatitis C viruses (HCV) present in 110 Italian patients were characterized by genotype-specific PCRs. Among the 65 cases of community-acquired hepatitis, HCV genotype II was dominant (60%), followed by genotypes IV (15%), III (11%), and I (3%). Among the 45 hemophilia-associated cases, the distribution of the four HCV genotypes was markedly different: genotype I was the most prevalent (61%), followed by genotypes II (25%), III (4%), and IV (2%). Double infections were observed in eight patients. Two HCV remained unclassified. For the 45 community-acquired cases from which a liver biopsy was available, genotype II was associated with more severe liver damage than the other types.

Adolescent↗

Deletion polymorphisms in the angiotensin converting enzyme gene are associated with pulmonary hypertension evoked by exercise challenge in patients with chronic obstructive pulmonary disease.

Angiotensin converting enzyme (ACE) plays an important role in the pathogenesis of pulmonary hypertension. In this study we determined whether the deletion (D)/insertion (I) polymorphism in the ACE gene may be associated with pulmonary hypertension evoked by exercise challenge in patients with chronic obstructive pulmonary disease (COPD). ACE genotypes were determined in 19 patients with COPD. All patients underwent right heart catheterization followed by a constant-load exercise test while breathing room air or oxygen. Subgroups were created of seven patients with the II genotype, six with the ID genotype, and six with the DD genotype who were well-matched with respect to age, blood gas data at rest or after exercise, baseline lung function, results of incremental exercise testing, and hemodynamic data at rest. The mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (Rpv) at rest in the three subgrpoups did not differ significantly during breathing of either room air or oxygen. However, the Ppa after exercise challenge in patients with the DD genotype (55.7 +/- 4.9 mm Hg [mean +/- SD]) was significantly higher than in patients with the II genotype (42.6 +/- 7.1 mm Hg, p = 0.008). The Rpv after exercise in patients with the DD genotype was also significantly higher than in patients with the ID and II genotypes. During breathing of oxygen to diminish acute hypoxic pulmonary vasoconstriction, the Ppa in patients with the DD genotype (52.3 +/- 3.1 mm Hg) was higher than in patients with the ID genotype (40.5 +/- 5.9 mm Hg, p = 0.0049) or the II genotype (37.7 +/- 5.9 mm Hg, p = 0.0027). In addition, the Rpv in patients with the DD genotype was higher than in patients with the ID and II genotypes. These results suggest that D-I polymorphism in the ACE gene may be associated with pulmonary hypertension evoked by exercise challenge in patients with COPD. However, the number of patients in this study was very small for a genetic association study, and our results should be examined in larger studies.

Aged↗

The DD genotype of angiotensin converting enzyme polymorphism is a risk factor for coronary artery disease and coronary stent restenosis in Japanese patients.

Stent implantation has decreased the incidence of restenosis after coronary intervention, but has not eliminated it. The contribution of the angiotensin-converting enzyme (ACE) genotype to the development of coronary artery disease and restenosis after coronary stenting was investigated in 67 Japanese patients in whom 103 lesions in which stents had been successfully implanted were assessed by quantitative coronary angiography, before, immediately after coronary stenting, and during follow-up. The distribution of the patients with the DD, ID, and II genotypes was 13%, 54%, and 33%, respectively. The prevalence of multivessel disease in the DD genotype was significantly higher (DD genotype: 78%; ID genotype: 58%; II genotype: 27%, chi2=8.13, p=0.016) and the late loss in the DD genotype (1.43+/-0.96 mm) was significantly greater (ID genotype: 0.78+/-0.98 mm and II genotype: 0.79+/-0.88 mm, p<0.05 vs DD genotype). However, there was no significant difference in the restenosis rate among the 3 genotypes. The present study in Japanese patients indicates that the DD genotype is associated with more extensive coronary artery disease and progression of the inward remodeling within the stented lesion, which is primarily caused by neointimal hyperplasia.

Aged↗

Efficacy of interferons in treating children with chronic hepatitis C.

UNLABELLED: Twenty-two children with chronic hepatitis serologically positive for hepatitis C virus (HCV) were treated with interferon-alpha (IFN-alpha). Liver biopsy showed chronic active hepatitis in 13 and chronic persistent hepatitis in 9 patients. A sustained clearance of HCV was observed in 8/22 children 12 months after the administration of IFN-alpha for 26 weeks, associated with normalization of HCV core antibody. Of these eight patients six had HCV genotype III and two HCV genotype II or IV. Hepatitis relapsed in seven other patients after completion of IFN-alpha with an increase in HCV core antibody titre, five with HCV genotype II, and two with HCV genotype III or IV. A second course of IFN-alpha suppressed the reactivation of HCV in all seven patients. Three of seven responders who relapsed after the first course remained negative for HCV RNA 12 months after their second course of IFN-alpha. However, the remaining four patients with HCV genotype II again relapsed after completing their second course of IFN-alpha. Seven children with the HCV genotype II resistant to IFN, including 8 weeks of IFN-beta administration, and showed no significant reduction in HCV core antibody titre. CONCLUSION: The genotype of HCV (III) and a reduction in the core antibody titre appear to be useful parameters for predicting the response to IFN-alpha therapy.

Adolescent↗

Endothelial cell damage and angiotensin-converting enzyme insertion/deletion genotype in elderly hypertensive patients.

OBJECTIVES: The purpose of this study was to investigate the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) genotype and endothelial cell dysfunction or hypercoagulable state in elderly hypertensive patients. BACKGROUND: Angiotensin-converting enzyme (ACE) insertion/ deletion (I/D) polymorphism was recently reported to be associated with various cardiovascular diseases. However, the precise mechanism of this association remains unknown, and some confounding factors might also affect the association. Endothelial cell dysfunction and coagulation activation play important roles in both the atherosclerotic process and the onset of cardiovascular events. METHODS: We identified the ACE I/D genotype and measured the plasma levels of markers of endothelial cell damage (von Willebrand factor [vWF] and thrombomodulin) and of coagulation activation (prothrombin fragment F1 + 2 [F1 + 2]) in 318 asymptomatic elderly patients with hypertension, aged 59-93 years. RESULTS: The vWF level was significantly higher in those with the DD genotype (n = 54) than in those with the II genotype (n = 131, p < 0.0001) or with the ID genotype (n = 133, p < 0.0001). The TM levels were also higher in patients with the ID genotype (p < 0.005) and the DD genotype (p < 0.01) than in those with the II genotype. There were no differences in F1 + 2 level among the groups. Positive correlations of systolic blood pressure with levels of both vWF and thrombomodulin were found predominantly in patients with the II genotype (both p < 0.001), but no correlation was noted in those with the DD genotype. CONCLUSIONS: Considering the increased plasma levels of both endothelial cell-derived markers in the hypertensive patients with ACE DD genotype, we speculate that the ACE D allele is a risk factor for the development of hypertensive cardiovascular disease associated with endothelial cell damage.

Aged↗

[Do left ventricular mass, diameters and long-axis systolic function differ according to angiotensin converting enzyme genotypes?].

OBJECTIVE: Angiotensin converting enzyme (ACE) is a key enzyme in angiotensin II production which causes myocardial hypertrophy and hyperplasia. In this study we aimed to investigate the relation between ACE I/D gene polymorphism and left ventricular mass (LVM), dimensions and systolic functions calculated by mitral annular motion (MAM) in young healthy male subjects. METHODS: Complete echocardiographic examination was performed in 49 male healthy subjects (mean age 22.9+/-2.1 years) consisting of 18 ACE DD, 18 ACE DI and 13 ACE II genotypes. We calculated LVM and mass index (LVMI) by M-Mode echocardiography. The systolic MAM was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and the MAM-ejection fraction (EF) was calculated from above four sites. Ejection fraction was also calculated by Simpson's method. RESULTS: There was no significant difference among the three genotypes according to age, body mass index, systolic and diastolic blood pressure and heart rate. Interventricular septum (IVS) and left ventricular posterior wall (LVPW) diastolic thickness, LVM and LVMI were found significantly different among 3 ACE genotypes. Those measurements were higher in DD genotype in comparison to the DI and II genotypes. There was no significant difference among the three genotypes according to EF-MAM and EF by Simpson's method. CONCLUSION: In young healthy male subjects having ACE DD genotype, even though LVM and LVMI were within normal limits, their measurements were found to be higher than in subjects with ACE DI and II genotypes respectively. There was no difference among the three genotypes according to left ventricular systolic functions.

Adult↗

Effects of angiotensin-converting enzyme gene polymorphism on the left-ventricular function and mass in patients with acromegaly.

In this study we have investigated the contribution of the ACE genotype to the development of left-ventricular hypertrophy (LVH) and systolic and diastolic dysfunctions in acromegalic patients. The study group consisted of 30 acromegalic patients (21 women and 9 men, age: 37.9 +/- 10.8 years, disease duration: 9.0 +/- 6.9 years). The distribution of the DD, ID and II genotypes was 40.0 (n = 12), 46.6 (n = 14) and 13.3% (n = 4), respectively, being similar to frequencies observed in a healthy population. Plasma ACE levels were 55.0 +/- 12.0 (45-84), 28.7 +/- 15.7 (8-58) and 24.5 +/- 12.0 (16-33) U/I in patients with the DD, ID and II genotype, respectively. The mean serum ACE activity in the DD genotype was significantly higher than in the heterozygous group (p < 0.0001). Serum ACE activity showed a significant negative association with the mean growth hormone level (r = -0.52, p = 0.007). The LV early diastolic flow velocity/LV presystolic flow velocity (E/A) ratios were 1.2 +/- 0.4 for the DD genotype, 1.3 +/- 0.3 for the ID genotype and 0.7 +/- 0.1 for the II genotype. The E/A ratio was considerably lower in acromegalic patients with the II genotype compared to the other genotypes (p = 0.03). The LV mass index (LVMI) values were 131.5 +/- 4.2 g/m2 for the DD genotype, 141.7 +/- 50.3 g/m2 for the ID genotype and 159.6 +/- 48.2 g/m2 for the II genotype. However, there was no significant difference in LVMI among allelic groups. All other indices of systolic and diastolic function were not statistically different in the acromegalic patients. The present data fail to support a role of ACE gene polymorphism in determining LVH in acromegalic patients. However, the I allele may prove as a useful marker predicting the development of diastolic dysfunction in acromegalic patients.

Acromegaly↗

Prevalence, genotypes, and an isolate (HC-C2) of hepatitis C virus in Chinese patients with liver disease.

China has not been extensively investigated for the prevalence of hepatitis C virus (HCV) infection among people with or without liver disease. We analyzed serum from 2,177 liver disease patients from 7 cities in different areas of China. Of 435 acute hepatitis patients, only 11% were positive for HCV RNA, while hepatitis B surface antigen (HBsAg) was detected in 33%. Of 1,668 patients with chronic liver disease, 14% and 74% were positive for HCV RNA and HBsAg, respectively. Nearly 80% of non-B chronic liver disease were negative for HCV RNA. The frequency of HCV RNA in chronic liver disease was significantly higher in Hami (32%) and Shenyang (30%) than in other cities (6-12%). The HCV genotype distribution varied by region. Genotype III was detected in 46-70% of HCV infections in Hami, Shenyang, and Lanzhou, while more than 90% of patients from southern cities (Nanjing, Nanning, and Chengdu) had genotype II. No evidence for genotype I or IV infections was found. A full-length HCV genome sequence (HC-C2) derived from a Beijing patient with genotype II was closely related to previous isolates from Japanese and Taiwanese patients. These results suggest that HCV prevalence and genotype distribution vary from region to region in China, and that the HCV now predominant in China may have evolved epidemiologically with infections in Japan and Taiwan. The study identified a high frequency of non-B, non-C chronic liver disease in China, suggesting possibly a new agent or infections with extreme variants of HCV.

Base Sequence↗

Association of angiotensin I-converting enzyme gene polymorphism with myocardial ischemia and patency of infarct-related artery in patients with acute myocardial infarction.

OBJECTIVES: We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction. BACKGROUND: The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has been implicated in predisposition to myocardial infarction and ventricular remodeling. METHODS: I/D genotyping, predischarge adenosine-thallium-201 perfusion tomography and radionuclide angiography were performed in 113 patients (72 men, 41 women) with a diagnosis of acute myocardial infarction. A subgroup of 96 patients also underwent coronary angiography. RESULTS: Genotypes DD, ID and II were present in 27, 56 and 30 patients, respectively. There was no significant difference in the baseline characteristics of patients, total creatine kinase, peak MB fraction, Killip class, mean ejection fraction or the number of diseased vessels in patients with the DD, ID or II genotype. However, the size of the total and the reversible perfusion defects was greater in those with DD than in those with ID or II genotype (total defect size [mean +/- SD] 33.7 +/- 22.5%, 29.5 +/- 19.2% and 22.2 +/- 16.0%, respectively [p = 0.022]; reversible defect size 18.0 +/- 16.0%, 12.1 +/- 11.6% and 8.2 +/- 7.8%, respectively [p = 0.006]). Occlusion of the infarct-related artery was also more common in patients with DD genotype (odds ratio 3.9, 95% confidence interval 1.4 to 11.0). Multivariate analysis showed that the I/D genotype was an independent predictor of perfusion defect size and patency of the infarct-related artery (p = 0.001). CONCLUSIONS: DD genotype was associated with a larger ischemic defect and occlusion of the infarct-related artery. Patients with DD genotype, having a larger ischemic defect, are expected to be at a greater risk for subsequent cardiovascular events.

Adenosine↗

Predictive factors for efficacy of interferon therapy in chronic hepatitis type C.

BACKGROUND/AIMS: It has recently become possible to quantify HCV-RNA in serum and to analyze the HCV-RNA genotype. In this study, we investigated the relationship among the response to interferon therapy, the HCV-RNA concentration, genotype and histological findings of the liver. PATIENTS AND METHODS: Sixty-three patients with chronic hepatitis type C received interferon alfa therapy for 24 weeks. The HCV-RNA concentration in serum was measured semiquantitatively with reverse transcript semi-nested polymerase chain reaction and classified as negative to +3. HCV-RNA genotype was analyzed using a mixture of four type specific primers. RESULTS: HCV-RNA concentration was significantly higher in patients with genotype II and CAH2B than genotype III, CPH and CAH2A (p < 0.05). At 24 weeks after the end of interferon therapy, HCV-RNA in serum disappeared in 24 of 63 patients (38%). Strong resistance to the therapy was noted in patients with both genotype II and a high concentration of HCV-RNA in serum (the efficacy was only 7%). Therapy efficacy decreased with the severity of liver histological findings, reaching only 20% in those with CAH2B. CONCLUSION: Both the concentration and genotype of HCV-RNA seem to be important factors in determining the efficacy of interferon therapy.

Adult↗

Differences in the genetic background of latent autoimmune diabetes in adults (LADA) and type 1 diabetes mellitus.

OBJECTIVES: According to the recent classification of diabetes mellitus the Latent Autoimmune Diabetes in Adults (LADA) belongs to the group of type 1 autoimmune diabetes, as a slowly progressive form. Our aim was to determine (i) the prevalence of HLA-DRB1 and DQB1 genotypes, and (ii) to determine the tumor necrosis factor (TNF) alpha promoter polymorphism at position -308 (the G-->A substitution, designated the TNF2 allele) in patients with type 1 diabetes and with LADA compared with the healthy population. METHODS: The major histocompatibility complex (MHC) II genotypes and the TNF alpha promoter polymorphism were determined by PCR method. We examined 69 type 1 diabetic and 42 LADA patients. As control samples of 336 cadaver kidney donors and 138 volunteers were used. RESULTS: Both type 1 diabetes mellitus and LADA were positively associated with the DRB1*04-DQB1*0302 (DR4/DQ8) haplotype (P=0.00001, and P=0.0005, respectively), and negatively associated with the DRB1*11-DQB1*0301 (DR11/DQ7) haplotype (P=0.00006, and P=0.007, respectively) compared with control population. There were differences between the two disease entities in the frequency of the DRB1*03-DQB1*02 (DR3/DQ2) haplotype (P=0.00008 vs. P=0.177) compared with control group. The presence of the TNF2 allele was significantly lower in LADA than type I diabetes (P=0.022) or control group (P=0.017). CONCLUSION: Our findings indicate that there are marked differences in the genetic background of type 1 diabetes and LADA. The low presence of TNF2 allele (known to be associated with high amount of TNF alpha production) in LADA could be one of the factors responsible for the relatively slow progression.

Adult↗

Variation in Severity of Symptoms Associated With Two Snow Mountain Virus Inocula.

Snow Mountain Virus (SMV), the prototype of genogroup II and genotype II Norovirus (NoV), was used in human challenge studies to examine the infectivity, pathogenicity, and immune response to NoV. Clinical and laboratory data from two previously completed SMV human challenge trials using two different inocula (primary and secondary) were analyzed to compare the infectivity, illness, viral shedding, and serum IgG conversion. The primary and secondary SMV inocula were sequenced for detecting single nucleotide mutations. Of 15 subjects challenged with the primary inoculum between 2000 and 2002, nine were infected, and seven presented with acute gastroenteritis. Of 33 subjects challenged with the secondary inoculum between 2016 and 2018, 25 were infected, and nine presented with acute gastroenteritis. There were no statistically significant differences in overall infection and illness rates between subjects challenged with the primary inoculum versus the secondary inoculum. However, subjects infected with the primary inoculum experienced more severe clinical symptoms of acute gastroenteritis, showing higher severity scores (6.00 vs. 2.94, p&#x2009;=&#x2009;0.003) compared with those infected with the secondary inoculum. We also observed that infection with the secondary inoculum resulted in longer viral shedding compared with the primary inoculum. Partial sequencing of the SMV genome identified three mutations in both inocula. Understanding the differences between these two SMV inocula is critical for NoV vaccine evaluation and using a less pathogenic inoculum for a vaccine trial will require more participants to meet the target reduction in illness when evaluating the efficacy of candidate vaccines.

Humans↗

Influence of angiotensin-converting enzyme polymorphism gene, IGF-1, and other factors in the response rate of hematocrit to enalapril treatment in patients with posttransplant erythrocytosis.

A significant relationship between hematocrit values and serum parameters such as the insulin like growth factor (IGF-1) and calcium was observed in patients with posttransplant erythrocytosis (PTE). Since angiotensin-converting enzyme inhibitors (ACEI) decrease hematocrit (Ht) levels in these patients, ACE genotype should play an important role. We designed this study to investigate whether ACE genotype or baseline concentrations of IGF-1, IGF-blood binding protein 3 (BP3), growth hormone (GH), or Ca influenced the response of Ht to ACEI treatment. Twenty-one kidney graft recipients with PTE were treated with enalapril (2.5 to 5 mg/d) for 1 year. IGF-1, BP3, GH, Ca, and Ht were determined before as well as 15, 30, 90, 180, and 365 days after enalapril treatment. ACE polymorphism was also determined. Enalapril treatment significantly decreased Ht levels. Only IGF-1 baseline levels showed a positive correlation to the decreased Ht (P < .025). ACE genotype as determined in 18 patients, showed no correlation with the response to enalapril. Patients with ACE genotype II showed a tendency to an earlier display of PTE. We conclude that low doses of enalapril decrease Ht levels in PTE patients; that PTE begins earlier in patients with II ACE genotype; and that only IGF-1 baseline levels influence the Ht decrease after treatment. These observations suggest that ACEI decrease the Ht via an inhibitory effect on IGF-1, which has a stimulary effect on erythropoiesis.

Angiotensin-Converting Enzyme Inhibitors↗

Left ventricular hypertrophy, blood pressure and ACE genotype in untreated hypertension.

It has been suggested that the deletion polymorphism of the angiotensin-converting enzyme (ACE) genotype may be important in the development of left ventricular hypertrophy (LVH). In order to test this hypothesis we investigated the interaction between blood pressure (BP), LVH and ACE genotype in 86 previously untreated hypertensive patients. Each underwent two-dimensional and Doppler echocardiography and ACE genotyping. There were no significant differences in BP, the parameters of left ventricular structure (including left ventricular mass index) or diastolic function between the three genotype groups. Additionally, there were no significant differences in the relationship between systolic BP and left ventricular mass index among the three genotype groups (II genotype, r = 0.46, P = 0.02; ID genotype, r = 0.42, P = 0.01; DD genotype, r = 0.34, P = 0.10; F = 0.38). In contrast to some previous studies, we have found in this group of previously untreated hypertensive subjects no evidence to suggest that the deletion polymorphism of the ACE genotype is important in the development of LVH.

Adult↗

Clonal infection with Actinobacillus actinomycetemcomitans following periodontal therapy.

Mechanical debridement results in a shift of the bacterial composition in the periodontal pocket on the species level. It is unknown, however, whether a clonal change within a species could lead to the emergence of strains with different levels of virulence. Therefore, in the present study, the genetic variability of Actinobacillus actinomycetemcomitans was assessed and strains identified which were associated with periodontal disease progression following periodontal therapy, i.e., refractory periodontitis. Twenty adult patients with untreated periodontitis and subgingival colonization of A. actinomycetemcomitans were randomly assigned to receive full-mouth scaling alone or scaling with an adjunctive antimicrobial therapy. Both groups received supportive periodontal therapy at 3, 6, 9, 12, 18, and 24 months. Subgingival plaque samples were taken at every visit; venous blood was obtained at 24 months only. A. actinomycetemcomitans isolates were typed by the RAPD method, and antibody reactivity against outer membrane proteins was assessed by immunoblot analysis. Eleven distinct RAPD patterns were found in 18 patients completing the study. All patients harbored only one A. actinomycetemcomitans genotype, and within each patient this genotype persisted throughout the 24-month observation period. No differences in the expression of antibody reactivity against outer membrane proteins were found between strains isolated at baseline and at 24 months. Three genotypes were associated with reduced survival rates of teeth without probing attachment loss of 2 mm or more. The results indicated that (i) most patients harbored only one A. actinomycetemcomitans genotype; (ii) the genotype persisted following therapy; and (iii) only some genotypes were associated with refractory periodontitis.

Adult↗

Lack of association between angiotensin-converting enzyme gene polymorphism and peripheral vascular disease in type 2 diabetic patients in Taiwan.

A total of 361 Chinese patients with type 2 diabetes were studied for the association between peripheral vascular disease (PVD) and the insertion/deletion polymorphism involving a 287-bp alu repeat sequence at intron 16 of the angiotensin-converting enzyme (ACE) gene. The patients were divided into PVD (+) (n=45) and PVD (-) (n=316) based on an ankle-brachial index <0.9 and > or =0.9, respectively. Polymerase chain reaction was used to identify gene polymorphism. Results showed that D allele frequency in the patients without and with PVD was 31.8% and 33.3%, respectively (p=NS). The prevalence rates of II, ID and DD genotypes in the PVD (-) group were 45.6%, 45.3% and 9.2%, respectively; and the respective values for the PVD (+) group were 44.4%, 44.4% and 11.1% (p=NS). Prevalence rates of PVD in genotypes II, ID, and DD were 12.2%, 12.3% and 14.7%, respectively (p=NS). In logistic regression analyses, the unadjusted and adjusted odds ratios for DD vs II and ID vs II genotypes for PVD were not statistically significant. The respective adjusted odds ratios were 1.88 (0.56-6.29) and 1.33 (0.63-2.80). In conclusion, there was not a significant association between the ACE genotype and PVD in Chinese type 2 diabetic patients. However, a type 2 error can not be ruled out.

Aged↗

Association of angiotensin I-converting enzyme gene polymorphism with susceptibility to antiproteinuric effect of angiotensin I-converting enzyme inhibitors in patients with proteinuria.

The antiproteinuric effect of angiotensin I-converting enzyme (ACE) inhibitors in patients with renal diseases of various origins has been well recognized. However, individual responses regarding the degree of decrease in urinary protein excretion appear to vary considerably. The mechanism underlying this variable response to ACE inhibitors has not been clarified yet. A possible role of ACE gene insertion/deletion (I/D) polymorphism in the responsiveness to antiproteinuric effect of ACE inhibitors is examined. Thirty-six patients with proteinuria (23 men and 13 woman; mean age, 47 +/- 13 yr) were studied. These patients were classified into two groups on the basis of the percent decrease in their urinary protein excretion: the effective group, those with a decrease in proteinuria (18 patients, -64 +/- 19%) and the noneffective group (18 patients, +13 +/- 40%). A 287-base pair (bp) I/D polymorphism in the ACE gene was examined by polymerase chain reaction. The allelic frequencies of the ACE gene were I/D = 0.53/0.47 in the effective group and I/D = 0.81/0.19 in the noneffective group. The difference in the allelic frequencies between the two groups was significant (chi 2 = 6.25, P = 0.0114 < 0.05). Furthermore, the difference in the responsiveness of proteinuria to ACE inhibition between genotype II versus genotype ID + DD was statistically significant (chi 2 = 4.05, P = 0.0442 < 0.05). There was no significant difference between the two groups with regard to initial urinary protein level, blood pressure, renal function, and daily sodium intake. The genetic susceptibility to the antihypertensive effect of ACE inhibitors was also studied, but no significant relation was observed. This study suggests the association of ACE gene I/D polymorphism with the antiproteinuric efficacy of ACE inhibitors in patients with proteinuria.

Adult↗

[The relationship between angiotensin converting enzyme gene polymorphism and hypertensive kidney lesion and PAI-1 in hypertension patients].

The work is to explore the relationship between the polymorphism of angiotensin converting enzyme (ACE) gene and hypertensive kidney lesion/PAI-1 in hypertension patients. ACE genotyping with polymorase chain reaction (PCR) was performed in 96 unrelated healthy controls, 67 hypertensives without kidney lesion and 70 hypertensives complicated with kidney lesion. The plasma PAI-1 were determined with ELISA. No significant differences could be detected between ACE gene I/D polymorphism and hypertension. However, the frequencies of DD genotype and deletion allele among the hypertensives complicated with kidney lesion were higher than those among the healthy controls and those among the hypertensives without kidney lesion."chi2" values were 6.8589,5.6162 and 5.9085,5.372 respectively. The plasma PAI-1 level showed significant differences among DD genotype,ID genotype and II genotype(P<0.05). The DD genotype of ACE gene may be a risk for hypertensive kidney lesion. The plasma PAI-1 level is associated with ACE gene polymorphism.

English Abstract↗