Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “gene polymorphism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources

Angiotensin-converting enzyme gene polymorphism in patients with systemic lupus.

The renin-angiotensin-aldosterone system (RAAS) has been considered one of the probable pathophysiologic mechanisms involved in disease progression. Genetic polymorphism of the RAAS has been associated with the clinical course of renal disease. One of the genetic polymorphisms is a deletion or insertion of a 287 base pair fragment in intron 16 of the angiotensin-converting enzyme (ACE) gene. It is known that ACE gene polymorphism is present in humans and that it is associated with an increased risk of cardiovascular diseases, renal disease progression and sarcoidosis. In this study, the potential significance of ACE gene polymorphism in patients with systemic lupus erythematosus (SLE) was investigated. ACE gene polymorphism was determined in 18 patients with SLE and in 21 healthy volunteers as a control group. The mean age of patients was 38.5 years. All patients had a mean follow-up of 30.7 +/- 20.2 months (range 5-95 months). ACE genotypes were determined by the method of polymerase chain reaction. Proteinuria and creatinine were also followed. The frequency of DD, ID and II genotypes was 50%, 28% and 22% in SLE patients and 25%, 50% and 25% in healthy controls, respectively. DD genotype was more common in SLE patients than in the control group. The patients with II genotype had lower proteinuria and creatinine level than those with DD genotype (p < 0.05). The time to disease remission was shorter in patients with II genotype (p < 0.05). Study results indicated an increased frequency of D allele in SLE patients. The increased ACE activity in these patients pointed to the need of further studies of ACE gene polymorphism in SLE.

Adult↗

Effect of VDR gene polymorphisms on osteocalcin secretion in calcitriol-stimulated human osteoblasts.

BACKGROUND: The impact of vitamin D receptor (VDR) gene polymorphisms in bone metabolism remains controversial. Some authors have found a beneficial effect of some VDR gene polymorphisms, while others found no differences, or even a lower bone mass in subjects with the same type of polymorphisms. The aim of this study was to assess if the VDR gene polymorphisms could have an effect on the calcitriol-stimulated osteocalcin in human osteoblasts. METHODS: Osteoblasts were obtained from human femoral necks replaced because of osteoarthritis. Bones were cut into pieces of 1 to 2 mm and placed in a nylon mesh. After the migration of osteoblasts, the pieces were collected and cultured with different concentrations of calcitriol (10(-8), 10(-9), and 10(-1)0 mol/L). After 48 hours of incubation with calcitriol, the osteocalcin secreted into the medium (corrected by either total proteins or total DNA content) was measured. The DNA was extracted from the osteoblasts, amplified by polymerase chain reaction (PCR), and analyzed for target sequences sites of the BsmI, ApaI, TaqI, and FokI restriction enzymes. RESULTS: The response observed in osteocalcin secretion in the bb or TT genotypes doubled the response observed in the BB or tt genotypes (calcitriol 10(-8) and 10(-9) mol/L). A slight trend was also observed with the aa genotype. Men showed higher levels of osteocalcin secretion than women. Age did not show any influence in osteocalcin secretion. CONCLUSION: VDR alleles and gender demonstrated an effect on the osteocalcin secretion. BB or tt genotypes, and also the "A" allele, showed the lowest calcitriol-stimulated osteocalcin secretion.

Aged↗

[Parathyroid-related gene polymorphisms and their clinical significance].

To put the tailor-made medical care and treatment into practice, some gene polymorphisms related life-style diseases have been found. On this issue, candidate gene polymorphisms are now being searched in parathyroid related diseases. Regarding primary and secondary hyperparathyroidism, it has been suggested that some gene polymorphisms such as vitamin D receptor and parathyroid hormone might affect the condition and the seriousness of these diseases.

English Abstract↗

Estrogen receptor-alpha gene polymorphisms in patients with periodontitis.

BACKGROUND: Recent studies have shown that estrogen receptor-alpha (ER-alpha) gene polymorphisms are associated with alterations in bone mineral density and osteoporosis. It is unclear whether ER-alpha gene polymorphisms are associated with alveolar bone loss in patients with periodontitis. OBJECTIVE: The aim of this study was to investigate the relationship between ER-alpha gene polymorphisms and periodontitis. METHODS: Ninety patients with aggressive periodontitis, 34 patients with chronic periodontitis and 91 healthy controls were recruited in this study. All these subjects belonged to the Han Chinese race. DNA was extracted from peripheral blood of each subject. The ER-alpha gene was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) with PvuII and XbaI restriction endonucleases. RESULTS: The detection frequency of XX genotype was significantly higher in the chronic periodontitis patients than in the healthy controls (11.8% vs. 4.4%, p < 0.05). The difference between the female chronic periodontitis patients and healthy controls (26.7% vs. 2.1%, p < 0.01) was statistically significant, but no difference was found between the male patients and controls (p > 0.05). The detection frequency of PvuII ER genotypes was not statistically different among the three groups (p > 0.05). CONCLUSIONS: In female Han Chinese population, the XX genotype may be a risk indicator for chronic periodontitis.

Acute Disease↗

Influence of Serum Amyloid A (SAA1) and SAA2 gene polymorphisms on renal amyloidosis, and on SAA/C-reactive protein values in patients with familial mediterranean fever in the Turkish population.

OBJECTIVE: To evaluate the effect of serum amyloid A (SAA) 1 and SAA2 gene polymorphisms on SAA levels and renal amyloidosis in Turkish patients with familial Mediterranean fever (FMF). METHODS: SAA1 and SAA2 gene polymorphisms and SAA levels were determined in 74 patients with FMF (39 female, 35 male; median age 11.5 yrs, range 1.0-23.0). All patients were on colchicine therapy. SAA1 and SAA2 gene polymorphisms were analyzed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). SAA and C-reactive protein (CRP) values were measured and SAA/CRP values were calculated. RESULTS: The median SAA level was 75 ng/ml (range 10.2-1500). SAA1 gene polymorphisms were: a/a genotype in 23 patients (31.1%), a/beta genotype in 30 patients (40.5%), a/g genotype in one patient (1.4 %), beta/beta genotype in 14 patients (18.9%), beta/g genotype in 5 patients (6.8 %), and g/g genotype in one patient (1.4%). Of the 23 patients who had a/a genotype for the SAA1 polymorphism, 7 patients had developed renal amyloidosis (30.4%) compared to only one patient without this genotype (1/51; 2.0%); p < 0.001. SAA2 had no effect on renal amyloidosis. SAA1 and SAA2 genotypes had no significant effect on SAA levels. SAA/CRP values were significantly lower in patients with the SAA1a/a genotype, compared to other SAA1 genotypes: 0.16 (0.025-1.96) versus 0.23 (0.012-28.20), p < 0.05. CONCLUSION: SAA1a/a genotype is one genetic factor that confers a significant risk for amyloidosis in the Turkish FMF population. Neither the SAA1 nor SAA2 genotypes had a significant effect on SAA level.

Adolescent↗

Relationship of large multifunctional proteasome 7 gene polymorphism with susceptibility to type 1 diabetes mellitus and DR3 gene.

OBJECTIVE: To study the relationship of the large multifunctional proteasome 7 (LMP7) gene polymorphism with susceptibility to type 1 diabetes mellitus (DM-1) and the DR3 gene in south Chinese Han population. METHODS: LMP7 genotypes and the DR3 gene were identified in 71 DM-1 patients and 86 healthy persons (as controls) by polymerase chain reaction-restriction fragment length polymorphism. DM-1 patients and controls were divided into DR3-positive and DR3-negative subjects. The frequencies of LMP7 genotypes and alleles were compared between DM-1 patients and controls respectively in the random subjects and in the DR3-matched subjects. Furthermore, DM-1 patients were divided into 3 groups according to the age of diabetic onset: group A < or = 14 years, group B 15-30 years, group C > or = 31 years. RESULTS: In the random subjects, the frequency of LMP7-B/B was lower (39% vs 58%, P < 0.05) and that of LMP7-B/A was higher (54% vs 31%, P < 0.01) in DM-1 patients than that in controls. In DR3-positive subjects, the frequencies of LMP7 genotypes and alleles showed no differences between DM-1 patients and controls. In DR3-negative subjects, the frequency of LMP7-B/B was decreased (40% vs 61%) and that of LMP7-B/A was increased (55% vs 28%, P < 0.01) in DM-1 patients. The frequencies of LMP7 genotypes and alleles showed no significant differences among different ages of diabetic onset. CONCLUSIONS: LMP7-B/B may be the protective genotype, and LMP7-B/A may be the susceptible genotype of DM-1, and this may not be affected by the DR3 gene. Persons with LMP7-B/B may have a decreased risk, and those with LMP7-B/A have an increased risk suffering from DM-1. The LMP7 gene may not be associated with the age of diabetic onset.

Adolescent↗

Gene polymorphisms of folate metabolizing enzymes and the risk of gastric cancer.

Multiple studies have reported an association between disturbances of folate metabolism and increased risk of gastric cancer, including low intake of folate, low levels of folate in blood or genetic factors affecting folate metabolism. Among the genetic factors, in particular a common polymorphism in the gene encoding for 5,10-methylenetetrahydrofolate reductase (MTHFR C677T) has been linked to gastric cancer. Other polymorphisms in folate-metabolising genes have been less frequently investigated. Therefore, we analyzed this polymorphism, the glutamate carboxypeptidase (GCP) II C1561T and the reduced folate carrier (RFC) G80A in a case-control study involving 106 patients with histologically confirmed and characterized gastric cancer with adjustment for other established risk factors for gastric cancer in comparison to 106 age- and sex-matched controls. Neither the MTHFR nor the GCP gene polymorphisms showed an association to cancer diagnosis, to tumor stage, grade of differentiation or Lauren type. However, non-cardia cancers were more likely to exhibit the 80GA and 80AA RFC genotypes, compared to cancers of the gastric cardia (adjusted OR 0.28; 95% CI=0.11-0.71). Thus, gene polymorphisms of the RFC gene might contribute to an increased risk of developing distal gastric cancer.

Aged↗

CTLA4 gene polymorphisms in Dutch and Chinese patients with inflammatory bowel disease.

BACKGROUND: Inflammatory bowel diseases (IBDs) are characterized by chronic intestinal inflammation as a result of an exaggerated T-cell response. CTLA4, a receptor of activated T cells, has an inhibitory function in regulating T-cell activation. Since CTLA4 gene polymorphisms have been associated with several autoimmune diseases, the aim was to study these gene polymorphisms in patients with IBD in two different populations. METHODS: The C-318T polymorphism in the promoter region and A+49G polymorphism in exon I of the CTLA4 gene were investigated by a PCR-SSP method. We studied 139 unrelated patients with ulcerative colitis (UC), 163 patients with Crohn disease (CD) and 174 healthy controls of Dutch Caucasian origin as well as 35 patients with UC and 62 healthy controls from the Chinese Han population. RESULTS: No significant differences in the distribution of allele, genotype and haplotype frequencies were observed between C-318T and A+49G gene polymorphisms and IBD in Dutch Caucasians and UC in the Chinese Han population. Although the haplotypes of the C-318T and A+49G polymorphisms were distributed differently between Dutch Caucasian and Chinese Han populations, there were no differences in the subgroups of patients with CD classified according to age, localization and behaviour in the Vienna classification and in those with UC classified according to age at onset, disease extension and presence of colectomy in the Dutch patients. However, the CTLA4-318 genotype CC was more frequent in patients with CD over 40 years (93%) than in younger patients (74%) (P = 0.045). CONCLUSION: C-318T and A+49G CTLA4 gene polymorphisms and their haplotypes are not associated in Dutch Caucasian patients with IBD and in Chinese patients with UC.

Abatacept↗

Lack of evidence for association between endothelial nitric oxide synthase gene polymorphisms and coronary artery disease in the Australian Caucasian population.

BACKGROUND: Genetic polymorphism in the gene for endothelial nitric oxide synthase (eNOS) has been identified as a potential risk factor for the development of premature coronary artery disease (CAD). We determined whether the eNOS 4ab, G894T, and T-786C polymorphisms are associated with premature coronary artery disease. DESIGN: A case-control study. METHODS: PCR-based assays were used to compare the frequency of eNOS gene polymorphisms in 573 Caucasian subjects aged under 50 years presenting with symptomatic CAD and documented by coronary angiography, with or without myocardial infarction, to that of 624 similarly aged community controls without a history of symptomatic CAD. RESULTS: We found no difference in the frequency of 4ab genotypes between cases and controls: in the CAD subjects, the 4aa, 4ab, and 4bb genotype frequencies were 1.9%, 24.3% and 73.8% respectively, compared to 2.2%, 25.5% and 72.3% respectively for the controls. There was also no significant difference between cases and controls in the frequency of any allele (4a/4b, 894G/894T, -786C/-786T), or genotype for any of the polymorphisms. Similarly, logistic regression analysis showed no evidence for an association of the polymorphisms with premature CAD or myocardial infarction or any indication of an interaction between the polymorphisms and other CAD risk factors, including smoking. CONCLUSIONS: In a large case-control study, and in contrast to some earlier positive findings by others, we have found no evidence for an association between several eNOS gene polymorphisms and premature CAD in an Australian Caucasian population.

Adult↗

Interleukin-12B gene polymorphism does not confer susceptibility to Graves' ophthalmopathy in Japanese population.

Graves' disease (GD) is an autoimmune disorder with genetic predisposition and frequently associated with Graves' ophthalmopathy (GO). Interleukin 12 (IL-12) is an important mediator of inflammatory immune responses and is expressed in the thyroid and orbit. IL-12B gene, which encodes the p40 subunit of IL-12, is located at chromosome 5q31-33. The aim of the present study was to investigate whether IL-12B gene polymorphism is associated with the development of GD or GO. IL-12B gene polymorphism was studied in Japanese GD patients (n = 329) and healthy control subjects without anti-thyroid autoantibodies or a family history of autoimmune disorders (n = 226). The A/C polymorphism at position 1188 of the 3' untranslated region (3'UTR) of the IL-12B gene was analyzed using the polymerase chain reaction--restriction fragment length polymorphism method. There was no difference in allele or genotype frequency of the IL-12B gene polymorphism (1188A/C) between GD patients and control subjects. There was no association of the IL-12B gene polymorphism with ophthalmopathy, severity of hyperthyroidism or serum IgE levels. There was no association of the IL-12B gene polymorphism with serum IL-12 levels, which were significantly elevated in hyperthyroid phase of GD. In conclusion, IL-12B gene 1188A/C polymorphism is not associated with GD or GO susceptibility in Japanese.

Adolescent↗

Genetic dissection of psychopathological symptoms: insomnia in mood disorders and CLOCK gene polymorphism.

We investigated the possible effect of the 3111T/C CLOCK gene polymorphism on sleep disorders in a sample of 620 patients affected by major depressive disorder (MDD) and bipolar disorder (BP). We detected a significantly higher recurrence of initial (P = 0.0001), middle (P = 0.0009), and early (P = 0.0008) insomnia in homozygotes for the C variant and a similar trend concerning decreased need of sleep in BP (P = 0.0074). Other demographic and clinical features were found not related with CLOCK polymorphisms. This preliminary observation leads to hypothesize a possible involvement of the CLOCK gene polymorphism in the sleep disregulations in MDD and BP.

Adult↗

[Gene polymorphisms in Uighur patients with Abnormal Savda].

OBJECTIVE: To investigate gene polymorphisms in Uighur patients with Abnormal Savda. METHODS: Polymorphisms of genomic fingerprints generated by arbitrarily primed PCR(AP-PCR) can be used for distinguishing between strains of almost any organism. The authors of this article applied the technique to the polymorphism analysis on the DNA of Uighur patients suffering from four kinds of Abnormal Savda (n=116), and on the DNA of a control group(n=50). RESULTS: From the patients, 42 fragments were obtained, among them 27(64.2%) fragments did not show gene polymorphisms. On the 220-344 bp regions, the authors detected 6 AP-PCR products showing individual specificity. CONCLUSION: The polymorphisms may serve as a molecular marker for gene diagnosis in the patients with Abnormal Savda.

Asthma↗

Glucosyltransferase gene polymorphism among Streptococcus mutans strains.

Genetic polymorphisms in genes coding for the glucosyltransferases were detected among Streptococcus mutans serotype c strains by Southern blot analysis with DNA probes located within the gtfB gene (H. Aoki, T. Shiroza, M. Hayakawa, S. Sato, and H. K. Kuramitsu, Infect. Immun. 53:587-594, 1986). Restriction endonucleases were used to examine genomic DNAs isolated from serotype a to h strains. The variations were readily detected among 33 strains of serotype c by EcoRI and PstI restriction enzyme digestions. Serotypes e and f, which are genetically similar to serotype c, also had comparable polymorphism; however, serotypes a, b, d, g, and h did not hybridize to the same DNA probes in parallel experiments. Further analysis of enzymatic activities for glucan synthesis and sucrose-dependent adherence revealed no significant differences among the serotype c strains. Our results suggested that genetic polymorphisms existing in S. mutans serotype c strains may reflect a complexity in genes coding for the glucosyltransferases, which are produced ubiquitously in members of the S. mutans group.

Bacterial Adhesion↗

Interleukin-13 gene polymorphisms confer the susceptibility of Japanese populations to Graves' disease.

Graves' disease (GD) is an autoimmune disorder with genetic predisposition. IL-13 is an important mediator of antiinflammatory immune responses and is expressed in the thyroid and orbit. The aim of the present study was to investigate whether IL-13 gene polymorphisms are associated with the development of GD. IL-13 gene polymorphisms were studied in Japanese GD patients (n = 310) and healthy control subjects without antithyroid autoantibodies or a family history of autoimmune disorders (n = 244). A C/T polymorphism at position -1112 of the promoter region was measured using the direct sequencing method, and an Arg(130)Gln (G2044A) polymorphism in exon 4 was examined using the PCR-restriction fragment length polymorphism method. There was a significant decrease in -1112T allele frequency in GD patients compared with controls (16% vs. 23%; P = 0.0019). The frequency of the 2044A allele on exon 4 also appeared lower in GD patients compared with controls. Haplotype analysis showed a significant decrease in the -1112T/2044A haplotype in GD patients. There was no association between IL-13 gene polymorphisms and ophthalmopathy, severity, or serum IgE levels. In conclusion, IL-13 gene polymorphisms are associated with GD susceptibility in Japan.

Adolescent↗

Toll-like receptor 4 gene polymorphisms and susceptibility to juvenile idiopathic arthritis.

OBJECTIVES: To determine if polymorphisms within the Toll-like receptor 4 (TLR4) gene are associated and linked with juvenile idiopathic arthritis (JIA). To investigate any possible gene-gene (epistatic) interaction between TLR4 and macrophage migration inhibitory factor (MIF) gene polymorphisms. METHODS: 313 simplex families (each containing one affected JIA proband) were genotyped. Two known functionally important single nucleotide polymorphisms (SNPs) within the TLR4 gene (Asp299Gly and Thr399Ile) were typed by SNaPshot ddNTP primer extension and capillary electrophoresis. Single point and multipoint transmission disequilibrium tests (TDT) were carried out through the extended TDT and TDT phase packages for the two TLR4 SNPs. Epistatic interaction between TLR4 haplotypes and the previously JIA associated MIF CATT(7)-MIF-173*C promoter haplotype was investigated by chi(2) test and unconditional logistic regression in Stata version 7. RESULTS: No distortion from random inheritance was observed by single point analysis for TLR4 Asp299Gly (p = 0.89) or TLR4 Thr399Ile (p = 0.40). Similarly, no distortion in transmission was seen when the TLR4 haplotypes were studied (p = 0.54). Additionally, no evidence for gene-gene interaction between TLR4 polymorphisms and the previously associated MIF gene polymorphisms was found (p = 0.40). CONCLUSIONS: No linkage or association was seen for Asp299Gly or Thr399Ile SNPs of TLR4 with JIA susceptibility. No evidence of an epistatic interaction between these TLR4 polymorphisms and MIF polymorphisms was found.

Adolescent↗

Gene polymorphisms and serological markers of patients with active Crohn's disease in a clinical trial of antisense to ICAM-1.

Serological profiles for anti-Saccharomyces cerevisiae antibodies (ASCA)/ perinuclear antineutrophil cytoplasmic antibodies (pANCA) and gene polymorphisms in tumour necrosis factor (TNF)-alpha and intercellular adhesion molecule-1 (ICAM-1) are associated with occurrence and/or outcome in Crohn's disease. The aim of the study was to characterize the ASCA/pANCA profile, soluble ICAM-1 expression and single nucleotide gene polymorphisms (SNPs) in TNF-alpha and ICAM-1 genes. Crohn's patients with moderate disease activity were enrolled in a clinical trial of Alicaforsen (ISIS 2302). Peripheral blood samples were collected prospectively for serum studies and for potential analysis of gene polymorphisms. A multivariate analysis was performed to compare treatment effect with the biomarkers studied. Serological testing for ASCA/pANCA was obtained for 257 patients at baseline: 37% were ASCA(+)/pANCA(-) (Crohn's pattern), 9% had both markers, 15% were ASCA(-)/pANCA(+) and 39% had neither marker. When the data were analysed by multiple regression analysis, a trend was found within the Alicaforsen-treated groups for greater rates of remission in the ASCA(+)/pANCA(-) subgroup versus all other serological profiles (25 versus 14%, P = 0.068), but not versus the placebo remission rate (18.8%). Gene polymorphisms were assessed in 64 patients, 21 from the placebo group. ICAM-1 assessment revealed no over-representation. However, three unique TNF-alpha SNPs were identified that correlated significantly with remission; sites 290 (P = 0.0253), -2735 (P = 0.0317) and -3090 (P = 0.0067). Although the overall clinical trial was negative, we have identified a trend towards clinical remission with Alicaforsen therapy in a subgroup of patients with Crohn's disease expressing ASCA(+)/pANCA(-). Furthermore, we have identified three TNF-alpha SNPs that may also predict a positive therapeutic outcome.

Adolescent↗

The effect of angiotensin converting enzyme gene polymorphism on chronic allograft dysfunction in living donor renal transplant recipients.

BACKGROUND: Chronic allograft dysfunction (CAD), the major cause of the failure of kidney allografts, may be caused by immunological and non-immunological haemodynamic factors. Renin-angiotensin system has been implicated in the development of intraglomerular hypertension and has a central role on progression in chronic renal disease. Polymorphism in 16th intron of the ACE gene has been reported to predict the circulating angiotensin II levels. The aim of this study was to investigate the effect of the both recipient and donor angiotensin converting enzyme (ACE) genotype on the development of CAD in renal allograft recipients. PATIENTS AND METHODS: A total of 143 renal transplant recipients (95 male, 48 female, mean age 32 +/- 10 yr) were included. In order to exclude the effect of cold ischaemia, only patients transplanted from living donors were selected. Factors analysed in the development of CAD were donor and recipient age, past history of acute rejection, presence of hypertension and hypercholesterolaemia, serum uric acid level and ACE gene polymorphism. RESULTS: Forty of the patients (28%) had CAD. Homozygous deletion type ACE gene polymorphism was detected in 59 renal transplant recipients (42%) and in 31 donors of the patients (37%). On comparing patients with and without CAD, donor age, rate of acute rejection and hypertension and serum uric acid levels were significantly higher in CAD (+) groups. Neither recipient nor donor ACE genotype was associated with time to CAD. Cox regression analysis revealed donor age (p < 0.001), presence of hypertension (p=0.002) and serum uric acid levels (p=0.009), but neither donor nor recipient ACE genotype as independent factors for predicting development of CAD. CONCLUSION: Donor age, presence of hypertension and serum uric acid levels was independent factors. Donor and recipient ACE genotype seemed to have no influence on the development of CAD in living donor transplanted patients.

Adult↗

Gene polymorphisms of the renin-angiotensin system and age-related changes in systolic and diastolic blood pressure in subjects with hypertension.

BACKGROUND: Few studies have examined to what extent genes might modulate the changes of systolic and diastolic blood pressure (BP) with age although, in older populations, systolic BP and diastolic BP vary with age in opposite directions. METHODS: This study involved 205 men and 99 women with either systolic-diastolic or isolated systolic hypertension. Age was > 50 years. Using polymerase chain reaction, four gene polymorphisms related to the renin-angiotensin system were independently investigated in men and women. Adjustments to cardiovascular and renal risk factors as well to the sodium/potassium extracellular space ratio were performed. RESULTS: Regarding the angiotensin-converting enzyme (ACE) gene polymorphism, in men > 50 years of age, the slope (mm Hg per unit of age) of the age-diastolic BP (and not age-systolic BP) relationships significantly (P = .0092) differed between genotypes: - 0.79 +/- 0.15 (P < .0001) for the DD genotype, -0.53 +/- 0.10 for the ID genotype (P < .0001), and -0.23 +/- 0.11 for II genotypes (P = NS). Such findings were not observed in the female population in which the age-diastolic BP curves were substantially flatter than in men. No comparable results were observed for gene polymorphisms related either to angiotensinogen or to angiotensin II type 1 receptor. CONCLUSIONS: In men > 50 years of age, the ACE gene polymorphism modulates the physiologic age-induced reduction of diastolic BP. The D allele might contribute to enhance this reduction, a finding that needs confirmation using prospective studies.

Adult↗