Autoimmune or Chronic Infectious Disease in B-CLL at Diagnosis: Association with Unmutated VH Gene Status and Unfavorable Cytogenetics.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3092-3092
Author(s):  
Katrina Vanura ◽  
Trang Le ◽  
Harald Esterbauer ◽  
Florentin Spaeth ◽  
Edith Porpaczy ◽  
...  

Abstract It is well known that chronic stimulation of the immune system (chronic infection, autoimmune disease) confers an increased risk of developing cancer. B-CLL represents an interesting model for the association of chronic antigenic stimulation with neoplastic transformation. We investigated the incidence of pre-existing chronic stimulation in patients with B-CLL at diagnosis. Chronic stimulation (CS) was defined as suffering from autoimmune disease or chronic or recurrent infection. The B-CLL control group consisted of patients without known chronic stimulation or concomitant diseases (non-CS). 187 unselected patients with known VH status diagnosed at our department were included in the study. Baseline characteristics were typical for a representative CLL patient cohort. Median age was 63 ranging from 25 to 83 years. Female:male ratio was 1:1,7. 87% of patients were staged Binet A, 13% Binet B or C. 63% of patients had mutated IgVH genes, 37% had unmutated genes (cut-off ≤ 98%). Normal karyotype was found by FISH in 25.8% of patients, 13q− in 46,1%, 11q− in 21,3%, +12 in 18%, and 17p− in 7,9% of patients. Of these 187 patients, 23,5% had a history of chronic stimulation (10,7% AI, 12,8% Inf). Age and Binet stage were similar between CS and non-CS patients. CS patients included a higher percentage of women (43.3 vs. 33.3%), and a higher percentage of CD38 positive (cut-off = 30%) patients (43,8 vs. 27,9%) compared to the non-CS subgroup, although both not statistically different. CS patients had a significantly higher percentage of unmutated clones (53%) compared to non-CS patients (28%) (p=0,002). Unfavorable cytogenetics (11q−, 17p−, +12) were more pronounced in CS patients compared to the non-CS group (77,8% vs 26,4%). The 4 most frequently used VH genes were 1–69, 3–30, 4–34, and 5–51 for the CS group, and 1–69, 2–5, 3–23, and 3–7 for the non-CS group. VH 1-69, the most frequently used VH gene overall, was unmutated in all CS patients, in non-CS patients several mutated cases were found. Several VH genes (2–26, 2–5, 3–7, 3–9) were exclusively unmutated in CS patients while they were mutated in non-CS patients. Several genes were exclusively used in either CS group (3–13, 3–15, 4–31, 4–39, 4–61, 5–51) or non-CS group (3–64, 3–65, 3–71, 3–74, 4–30, 7–4). They were mutated in most cases. Despite the drawbacks of our study (classification based on patients history and medical records), we provide unique and novel data on the frequency of chronic antigenic stimulation in an unselected cohort of newly diagnosed CLL patients. We noted considerable discrepancies between CS and non-CS patients regarding mutational status and VH gene usage. Our data warrant further evaluation of the role of CS in the development and course of B-CLL.

2016 ◽  
Vol 56 (1-2) ◽  
pp. 76-85
Author(s):  
Saddiq Qazi ◽  
Benedict Kjaergaard ◽  
Fei Yang ◽  
Hong Shen ◽  
Shenguo Wang ◽  
...  

Background: The fusing of the epicardium and sternum due to adhesion is a common problem during repeated cardiac surgery and carries with it an increased risk of bleeding. The use of barriers and patches has been tested to prevent the formation of adhesions, but the very presence of a patch can provoke adhesion formation. The objective of this study was, therefore, to investigate both biodegradable and bioresorbable polylactone patches [(polycaprolactone-poly(ethylene oxide)-polycaprolactone tri-block copolymer (PCE)]. The patches were also tested with a controlled release of rapamycin, which prevents cell migration and extracellular matrix deposition. The clinical effectiveness of rapamycin in pericardial patches has not previously been examined. Materials and Methods: Three groups of 6 female Danish Landrace pigs underwent sternotomy and abrasion of the epicardium, before being randomized to either group 1 - the control group (with no patch), group 2 - PCE patch implanted between the sternum and epicardium, or group 3 - PCE patch and slow-release 1.6-mg rapamycin. After a median time period of 26 days, the pigs were euthanized and their hearts removed en bloc with the sternum, for macroscopic, histological and pathological examination. Results: Upon macroscopic examination, a significantly lower degree of adhesion in group 2, as compared to group 1 (p < 0.05), was found. Histological analysis of the tissues showed significantly more fibrosis, inflammation and foreign body granulomas (p < 0.05) in both group 2 and group 3, when compared to group 1. Conclusion: A PCE patch following sternotomy in animal subjects reduces postoperative macroscopic adhesions without reducing microscopic fibrosis or inflammation. Loading the patch with rapamycin was found not to increase the antifibrotic effect.


2021 ◽  
Vol 28 (2) ◽  
pp. 185-192
Author(s):  
Neha SAHAY ◽  
◽  
Felice FAIZAL ◽  

Background: Glucose tolerance testing in pregnancy identifies many women with glycaemic responses that exceed normal range but that do not meet the threshold required to diagnose Gestational Diabetes Mellitus. It is controversial whether maternal hyperglycemia less severe than in diabetes is associated with increased risk of adverse pregnancy outcome or not. Materials and methods: All women were subjected to Glucose Challenge Test(GCT) with 50 gram glucose either at first visit or between 24-28 weeks on the basis of risk profile. High risk cases were screened at first visit and the rest between 24-28 weeks. Patients with a GCT value ≥200mg/dl were not subjected for GTT and were diagnosed as GDM.Value of GCT <140 mg/dl was taken as normal. Irrespective of GCT result, women were subjected to Oral Glucose Tolerance Test (OGTT) as recommended by WHO with 75 gram glucose using WHO criteria. Study group was identified with 4 categories with abnormal glucose homoeostasis as defined by the following criteria: 1. Abnormal GCT (>140 mg/dl) with normal OGTT; 2. Normal GCT with only Impaired Fasting Glucose(IFG) in OGTT; 3. Normal GCT with Gestational Glucose Intolerance(GGI); 4. Patients diagnosed as GDM: a. If fasting is >126mg/dl; b. If 2hr OGTT ≥ 140mg/dl & ≤ 199 mg/dl; c. If value of either GCT or OGTT >200 mg/dl. The control group comprised of women with normal GCT and normal OGTT. In all the above groups, adverse prenatal outcome and maternal outcomes were evaluated by the primary and secondary outcome measures. Results: There were 10 cases (15.3%) of hypertensive disorder of pregnancy in the study group (3 cases of gestational hypertension in abnormal GCT, 3 cases of pre eclampsia in each GGI and GDM and 1 antepartum eclampsia in GGI category) and 2 cases in control group (3%) (p=0.03). There were 2 cases of Fetal Growth Reduction (FGR) and 5 cases of Premature Rupture Of Membranes(PROM) in both study and control group. There was 1 case of cholestasis of pregnancy in study group. Term inductions were 11 and 13 in the study and control group respectively.Within the study group number of cases induced were more in GGI(n=7) and GDM(n=4) category. There were 14 caesarean sections (21.5%) and 2 (3%) instrumental deliveries among the study group. However there were 6 caesarean sections (9.2%) and no instrumental deliveries among control groups. The rate of elective LSCS is more in GDM (n=5) vs other 3 categories and the difference is significant (p=0.04) The overall number of LSCS (14 cases) was significantly higher in GDM. Conclusion: Cases with abnormal glucose homeostasis of lesser degree than GDM, like only abnormal GCT, IFG and GGI also were observed to have adverse maternal outcomes than controls, in form of hypertensive disorders of pregnancy, significantly higher LSCS rates, and increased risk of macrosomia. Instead of 2 step procedure, single step screening cum diagnostic test with 75 gm OGTT for diagnosing GDM could be an option to be universally practiced.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3935-3935
Author(s):  
Sandra Grass ◽  
Klaus-Dieter Preuss ◽  
Alexandra Wikowicz ◽  
Evangelos Terpos ◽  
Marita Ziepert ◽  
...  

Abstract Abstract 3935 Poster Board III-871 Background Antigenic targets of paraproteins in MGUS, multiple Myeloma (MM) and WM might play a role in the pathogenesis of these neoplasms by chronic antigenic stimulation, but very few have been identified, of which most were specific for one individual paraprotein only. In contrast, we recently described paratarg-7, a protein of unknown function which is expressed in all human tissues as the target of 15% of IgA and IgG paraproteins in MGUS and MM (Grass et al.; Lancet Oncology 2009 in press). Methods To determine if and how frequently paratarg-7 functions as the antigenic target of the IgM paraproteins in MGUS/WM, sera from patients with IgM-MGUS/WM were tested for reactivity with recombinant paratarg-7 by ELISA. The specificity of the paraprotein-mediated reaction was demonstrated by absorption studies with recombinant paratarg-7 and by cloning the B-cell receptor from bone marrow cells of patients with a paratarg-7 specific paraprotein. Lysates of peripheral blood from patients and controls were tested by gel electrophoresis and isoelectric focusing before and after phosphatase treatment. Moreover, paratarg-7 cDNA was sequenced to exclude SNPs and mutations. Results The paraproteins of 18 (9 WM and 9 IgM-MGUS) of 161 (11%) sera from patients in Germany, USA and Greece reacted specifically with paratarg-7, proving paratarg-7 as the first antigen identified as a paraprotein target in a significant proportion of patients with IgM-MGUS/WM. Mutations or polymorphisms of paratarg-7 were not found. However, 2D-gelelectrophoresis, isoelectric focusing and phosphatase treatment revealed that paratarg-7 was hyperphosphorylated in all patients with an anti-paratarg-7 specific IgM-paraprotein tested. In contrast, only 4 of 200 (2%) healthy blood donors were carriers of hyperphosphorylated paratarg-7. Thus, carriers of hyperphosphorylated paratarg-7 have a significantly increased risk (odds ratio= 6.5; 95%-CI: 2.1-19.6; p=0.001) for developing IgM-MGUS/MW. Moreover, family analyses of relatives of IgM-MGUS/WM patients with an anti-paratarg-7 specific paraprotein revealed that the hyperphosphorylated state of this protein is inherited as a dominant trait. The results obtained in IgM-MGUS/WM are similar to recent observations made in 252 patients with IgG- or IgA-MGUS/MM where hyperphosphorylated paratarg-7 was also associated with a significantly increased risk of developing IgG- and IgA-MGUS (odds ratio: 7.9; 95% CI, 2.8-22.6; p=0.0001). Conclusions Hyperphosphorylated paratarg-7 is a highly significant risk factor for MGUS, WM and MM, with the highest odds ratio of any risk factor reported to date for these diseases. Hyperphosphorylated paratarg-7 is the first molecularly defined and dominantly inherited risk factor identified for any hematological neoplasm reported to date. The carrier state of hyperphosphorylated paratarg-7 explains cases with familial MGUS, MM and WM and enables the identification of family members of patients at increased risk for MGUS/WM/MM. That only MGUS/WM/MM patients who are carriers of hyperphosphorylated paratarg-7 had a paratarg-7 specific paraprotein suggests that the hyperphosphorylation of paratarg-7 induces auto-immunity and is involved in the pathogenesis of these diseases, e.g. by chronic antigenic stimulation. The identification of paratarg-7 as a frequent antigenic target enables the more detailed analysis of tumor-host interactions in these patients and its role in the pathogenesis of these diseases. Moreover, its dominant inheritance and the identification of familial cases with MGUS/MM/WM and hyperphosphorylated paratarg-7 carrier state facilitate genome-wide screens for the identification of the SNP responsible for hyperphosphorylation of this molecule. Disclosures: No relevant conflicts of interest to declare.


PEDIATRICS ◽  
1989 ◽  
Vol 83 (3) ◽  
pp. 364-368
Author(s):  
Joseph Oren ◽  
Dorothy H. Kelly ◽  
Daniel C. Shannon

Infants who sustained a spell of apnea of infancy during which they were resuscitated have been shown to be at increased risk for sudden infant death syndrome. To determine the value of the pneumogram as a predictor of outcome in this population, the first pneumogram obtained of 51 such infants was analyzed. The infants were grouped on the basis of subsequent outcome during a course of monitoring: group 1—infants who died during a subsequent event; group 2—infants who received resuscitation or vigorous stimulation to terminate a subsequent spell; group 3—infants who survived and did not have a significant subsequent episode. The results for these infants were compared with those of a control group matched for age and sex. A detailed, blinded computer analysis revealed no significant difference in the results of the pneumogram analysis between the three groups. It did not identify the infants in whom apneic spells necessitating resuscitation subsequently developed or those who died. However, when compared with the control group, infants with apnea of infancy had significantly higher mean respiratory rates, heart rates, and tachycardia indexes. It is concluded that, although the first pneumogram does not predict the risk of an adverse outcome in a population of infants with severe apnea of infancy, it does reveal subtle cardiorespiratory differences between study and control infants.


Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 26-26
Author(s):  
Klaus-Dieter Preuss ◽  
Natalie Fadle ◽  
Evi Regitz ◽  
Michael Pfreundschuh

Abstract Background Chronic antigenic stimulation might have a role in the pathogenesis of monoclonal gammopathy of unknown significance (MGUS) and multiple myeloma. We previously identified a group of 11 autoantigenic paraprotein targets (paratargs) of which paratarg-7 is the most frequent, found in ~15 % of all MGUS/MM/Waldenstrom patients. These paratarg autoantigens all have in common to be 1) recognised by patients paraprotein with an extreme high titer (>1:1011), 2) hyperphosphorylated in patients, and 3) their phosphorylation carrier state is autosomal-dominant inherited in patients families. The finding that all these paratargs were permanently hyperphosphorylated in patients in contrast to healthy controls brought up the assumption that abnormal posttranslational modification of autoantigens might be a frequent finding in those patients. Methods A RZPD macroarray representing more than 30.000 different human proteins was subjected to in-vitro posttranslational modification using sumoylation-competent recombinant enzymes followed by screening with paraprotein-containing sera at high dilution (1:107). Immunopositive signals were identified and characterized by DNA sequencing, SDS-PAGE, isoelectric focusing, western blotting and ELISA. Findings Twenty-seven of 226 (11.9%) paraproteins from European, 9/80 (11.2%) from African-American and 9/176 (5.1%) from Japanese patients reacted specifically with the sumoylated heat shock protein-90β isoform-α (HSP90-SUMO). No reactivity was detected in >800 controls. All patients with HSP90-SUMO-binding paraproteins carried HSP90-SUMO. HSP90-SUMO carrier state is autosomal-dominantly inherited and was sown to be caused by the inability of SENP2 to desumoylate HSP90-SUMO. Five of 550 (0.9%) European, 2/100 (2%) African-American and 2/178 (0.8%) Japanese controls carried HSP90-SUMO, resulting in odds ratios of 14.8, 6.2 and 7.4, respectively, of healthy carriers for MGUS/MM/WM. Only, but all MGUS/MM/WM patients who were HSP90-SUMO carriers had HSP90-SUMO-specific paraproteins suggesting that sumoylated HSP-90 is involved in the pathogenesis of MGUS/MM/WM by chronic antigenic stimulation. Demonstration of HSP90-SUMO carriership identifies family members of HSP90-SUMO patients at risk. Interpretation A significant proportion of MGUS/MM/WM are associated with a dominant inheritance of posttranslationally modified autoantigens as shown for members of the paratarg autoantigen family and for HSP90-SUMO, enabling family members at increased risk for MGUS/MMWM to be identified by simple analysis of their peripheral blood. That only patients with MGUS/MM/WM who are carriers of such modified autoantigens have target-specific paraproteins suggests that the posttranslational modification induces auto-immunity and is involved in the pathogenesis of MGUS/MM/WM, for example, by chronic antigenic stimulation. Supported by Deutsche Forschungsgemeinschaft DFG, Deutsche José Carreras Leukämie Stiftung, Wilhelm-Sander-Stiftung, Deutsche Krebshilfe e.V. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2003 ◽  
Vol 101 (3) ◽  
pp. 1087-1093 ◽  
Author(s):  
Stuart Lanham ◽  
Terry Hamblin ◽  
David Oscier ◽  
Rachel Ibbotson ◽  
Freda Stevenson ◽  
...  

Abstract The mutational status of tumor immunoglobulin VHgenes is providing a powerful prognostic marker for chronic lymphocytic leukemia (CLL), with patients having tumors expressing unmutated VH genes being in a less favorable subset. However, the biologic differences correlating with VH gene status that could determine the clinical course of the disease are unknown. Here we show that differing responses to IgM ligation are closely associated with VH gene status. Specifically, 80% of cases with unmutated VH genes showed increased global tyrosine phosphorylation following IgM ligation, whereas only 20% of samples with mutated VH genes responded (P = .0002). There was also an association between response to IgM ligation and expression of CD38 (P = .015). The Syk kinase, critical for transducing B-cell receptor (BCR)– derived signals, was constitutively present in all CLL samples, and there was a perfect association between global phosphorylation and induction of phosphorylation/activation of Syk. Nonresponsiveness to anti-IgM could be circumvented by ligation of IgD (10 of 15 samples tested) or the BCR-associated molecule CD79α (12 of 15 samples tested). These results suggest that multiple mechanisms underlie nonresponsiveness to anti-IgM in CLL and that retained responsiveness to anti-IgM contributes to the poor prognosis associated with the unmutated subset of CLL. The prognostic power of the in vitro response to IgM ligation remains to be determined in a large series, but the simple technology involved may present an alternative or additional test for predicting clinical course.


2018 ◽  
Vol 27 (4) ◽  
pp. 363-369 ◽  
Author(s):  
Gintare Dargiene ◽  
Greta Streleckiene ◽  
Jurgita Skieceviciene ◽  
Marcis Leja ◽  
Alexander Link ◽  
...  

Background & Aims: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H.pylori infection, atrophic gastritis (AG) or GC in the European population.Methods: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time polymerase chain reaction. H. pylori status was determined by testing for anti-H. pylori IgG antibodies in the serum.Results: The study included 697 (59.2%) H. pylori positive and 481 (40.8%) H. pylori negative cases. We observed similar distribution of TLR1 and PRKAA1 alleles and genotypes in H. pylori positive and negative cases. TLR1 and PRKAA1 SNPs were not linked with the risk of AG. TC genotype of TLR1 gene was more prevalent in GC patients compared to the control group (29.7% and 22.3% respectively, p=0.002). Carriers of TC genotype had a higher risk of GC (aOR=1.89, 95% CI: 1.26–2.83, p=0.002). A similar association was observed in a dominant inheritance model for TLR1 gene SNP, where comparison of CC+TC vs. TT genotypes showed an increased risk of GC (aOR=1.86, 95% CI: 1.26–2.75, p=0.002). No association between genetic polymorphism in PRKAA1 gene and GC was observed.Conclusions: TLR1 rs4833095 SNP was associated with an increased risk of GC in a European population, while PRKAA1 rs13361707 genetic variant was not linked with GC. Both genetic polymorphisms were not associated with H. pylori infection susceptibility or the risk of AG.


2019 ◽  
pp. 50-54
Author(s):  
V.O. Golyanovskiy ◽  
◽  
Ye.O. Didyk ◽  

Pregnant women with intrauterine growth restriction (IUGR) have an increased risk of adverse perinatal and long-term complications compared with the birth of children with normal body weight. Thus, IUGR is one of the main challenges for the global health system, especially in poor and developing countries. Morpho-functional studies of the placentas help in determining the causes of IUGR, and therefore, timely prevent complications in pregnant women with IUGR. The objective: The purpose of this study is to investigate various morphometric and pathomorphological changes in the placenta, including inflammatory, in cases of IUGR, and to establish a correlation of these results with the etiology and complications for the fetus. Materials and methods. In the current study, 54 placentas of the fetuses with IUGR (the main group) were compared with 50 placentas of the fetuses with normal development (control group). The criteria for the inclusion of IUGR were gestational age more than 30 weeks and all fetuses with a weight less than 10th percentile for this period of pregnancy. The placenta material was studied pathomorphologically with laboratory screening for infection and inflammation. Similarly, the results were determined for placentas of the fetuses with normal development compared to placentas with IUGR. Results. The placenta study showed the presence of calcification in the case of IUGR, as well as in the case of prolonged pregnancy. However, calcification of the placenta in the case of IUGR was more progressive compared with placenta in the normal pregnancy. In addition, the presence of intrauterine infection and inflammation was observed, which could also lead to an adverse outcome for the further progression of pregnancy with IUGR. Conclusion. A comparative macro- and microscopic pathomorphological study of the placentas in the two groups has shown a significant increase in the pathological changes in all the anatomical structures of the fetuses with IUGR. Key words: Intrauterine growth restriction (IUGR), fetal weight, pathomorphological changes of the placenta.


Author(s):  
Iskander I. Zaidullin ◽  
Denis O. Karimov ◽  
Lilija K. Karimova ◽  
Milyausha F. Kabirova ◽  
Rasima R. Galimova ◽  
...  

The susceptibility to the development and progression of inflammatory periodontal diseases, which depends on genetic and external factors (smoking, stress, oral hygiene), varies widely. In the development of these diseases, an important role is played not only by the presence of periodontal pathogenic microorganisms, but also by the presence of congenital or acquired immunodeficiency, immunoregulatory defects. The immune system plays a key role in the physiological and pathological processes of periodontal tissues. In this regard, IL17, produced by CD4+ Th cells, which has both Pro-inflammatory and protective activity, is of particular interest in the pathogenesis of periodontitis. The aim of study was to identify the relationship between polymorphic loci of the IL-17A (rs2275913) and MMP-1 (rs1799750) genes and clinical manifestations of chronic periodontitis in petrochemical workers. Dental examination was performed in 92 ethylene oxide production workers with chronic periodontitis and 74 patients with chronic periodontitis who did not come into contact with chemical factors (control group). Genotyping of polymorphisms rs2275913 of the IL17A gene and rs1799750 of the MMP1 gene was performed by allele-specific real-time polymerase chain reaction (PCR). Hygienic assessment of the degree of air pollution of the working area with harmful substances was carried out by gas chromatography according to the guidelines for the determination of harmful substances in the air № 5098-89, № 3119-84. When comparing the results of studies of both groups, there were no statistically significant differences in the frequency distributions of allelic variants and genotypes of the IL-17A and MMP-1 genes. The AA/AG genotypes of the IL-17A gene were associated with an increased risk of severe disease compared to the GG genotype in workers in the main group (OR=6.1; 95% CI 1.33-28.5; p=0.021) and in the control group (OR=7.26; 95% CI 1.34-39.25; p=0.016). Carriers of the A allele in the control group increased the risk of severe chronic periodontitis by 2.4 times compared to carriers of the G allele (OR=2.41; 95% CI 1.19-4.87; p=0.014). During the dental examination of employees of the ethylene oxide plant, the clinical course of periodontal diseases was more severe in comparison with the control group, and the number of patients with severe periodontitis was twice as high. It was found that the AA/AG genotypes of the IL-17A gene and the carrier of the A allele are associated with increased susceptibility to the development of severe chronic periodontitis. The association between the MMP-1 gene polymorphism and the risk of severe forms of chronic periodontitis has not been established. A risk factor for the development of inflammatory periodontal diseases in employees of the petrochemical complex is a complex of harmful production factors.


2011 ◽  
pp. 119-125
Author(s):  
Thi Thuy Hang Nguyen

Objective: Prehypertensive individuals are at increased risk for developing hypertension and their complication. Many studies show that 2/3 prehypertensive individuals develop hypertension after 4 years. ECG and echocardiography are the routine tests used to assess LV mass. The objective of the research to determine the percentage of change in left ventricular morphology in the ECG, echocardiography, which explore the characteristics of left ventricular structural changes by echocardiography in pre-hypertensive subjects. Materials and method: We studied a total of 50 prehypertensive, 30 males (60%) and 20 females (40%), mean age 48.20±8.47years. 50 normotensive volunteers as control participants. These subjects were examined for ECG and echocardiography. Results: In prehypertensive group, with 18% of left ventricular hypertrophy on electrocardiogram, 12% of left ventricular hypertrophy on echocardiography; in the control group, we did not find any subjects with left ventricular hypertrophy. In the group with left ventricular hypertrophy, mostly eccentric left ventricular hypertrophy (83.33%), concentric left ventricular hypertrophy is 16.67%. Restructuring of left ventricular concentric for 15.9% of subjects without left ventricular hypertrophy on echocardiography. Conclusion: There have been changed in left ventricular morphology even in prehypertensive


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