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Beta2 Glycoprotein 1

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Huriye Balci – 1st expert on this subject based on the ideXlab platform

  • hereditary thrombophilia anti Beta2 Glycoprotein 1 igm and anti annexin v antibodies in recurrent pregnancy loss
    American Journal of Reproductive Immunology, 2012
    Co-Authors: Suat Karata, Yavuz Aydin, Fahri Öçer, Aysenur Buyru, Huriye Balci

    Abstract:

    Citation Karata S, Aydin Y, Ocer F, Buyru A, Balci H. Hereditary Thrombophilia, anti-Beta2 Glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss. Am J Reprod Immunol 2012; 67: 251–255

    Problem We investigated the Beta2Glycoprotein I and anti-annexin V antibodies as anti-phospholipid–cofactor antibodies; and factor V G1691A Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations as hereditary thrombophilia in recurrent pregnancy losses (RPL).

    Method of study Study group consisted of 84 women with recurrent pregnancy loss and control group consisted of 84 women having at least one live birth.

    Results Methylenetetrahydrofolate reductase C677T homozygous mutation was detected in 28.5% of the study group and in 14.2% of the controls, and the difference was highly significant (P < 0.001). Heterozygous mutation of this gene was found in 64.3% of the study population and in 38.1% of the controls, and difference in heterozygous mutation frequency was also significant (P < 0.001). Both homozygous and heterozygous mutations of PT G20210A and factor V G1691A were not different between the groups. There was no significant difference in anti-annexin V levels and anti-Beta2-gp 1 levels of the groups.

    Conclusion We concluded that both homozygous and heterozygous mutations of MTHFR C677T were related with RPL in Caucasian women.

  • Hereditary thrombophilia, anti-Beta2 Glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss.
    American Journal of Reproductive Immunology, 2011
    Co-Authors: Suat Karata, Yavuz Aydin, Fahri Öçer, Aysenur Buyru, Huriye Balci

    Abstract:

    Citation Karata S, Aydin Y, Ocer F, Buyru A, Balci H. Hereditary Thrombophilia, anti-Beta2 Glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss. Am J Reprod Immunol 2012; 67: 251–255

    Problem We investigated the Beta2Glycoprotein I and anti-annexin V antibodies as anti-phospholipid–cofactor antibodies; and factor V G1691A Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations as hereditary thrombophilia in recurrent pregnancy losses (RPL).

    Method of study Study group consisted of 84 women with recurrent pregnancy loss and control group consisted of 84 women having at least one live birth.

    Results Methylenetetrahydrofolate reductase C677T homozygous mutation was detected in 28.5% of the study group and in 14.2% of the controls, and the difference was highly significant (P 

Suat Karata – 2nd expert on this subject based on the ideXlab platform

  • hereditary thrombophilia anti Beta2 Glycoprotein 1 igm and anti annexin v antibodies in recurrent pregnancy loss
    American Journal of Reproductive Immunology, 2012
    Co-Authors: Suat Karata, Yavuz Aydin, Fahri Öçer, Aysenur Buyru, Huriye Balci

    Abstract:

    Citation Karata S, Aydin Y, Ocer F, Buyru A, Balci H. Hereditary Thrombophilia, anti-Beta2 Glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss. Am J Reprod Immunol 2012; 67: 251–255

    Problem We investigated the Beta2Glycoprotein I and anti-annexin V antibodies as anti-phospholipid–cofactor antibodies; and factor V G1691A Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations as hereditary thrombophilia in recurrent pregnancy losses (RPL).

    Method of study Study group consisted of 84 women with recurrent pregnancy loss and control group consisted of 84 women having at least one live birth.

    Results Methylenetetrahydrofolate reductase C677T homozygous mutation was detected in 28.5% of the study group and in 14.2% of the controls, and the difference was highly significant (P < 0.001). Heterozygous mutation of this gene was found in 64.3% of the study population and in 38.1% of the controls, and difference in heterozygous mutation frequency was also significant (P < 0.001). Both homozygous and heterozygous mutations of PT G20210A and factor V G1691A were not different between the groups. There was no significant difference in anti-annexin V levels and anti-Beta2-gp 1 levels of the groups.

    Conclusion We concluded that both homozygous and heterozygous mutations of MTHFR C677T were related with RPL in Caucasian women.

  • Hereditary thrombophilia, anti-Beta2 Glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss.
    American Journal of Reproductive Immunology, 2011
    Co-Authors: Suat Karata, Yavuz Aydin, Fahri Öçer, Aysenur Buyru, Huriye Balci

    Abstract:

    Citation Karata S, Aydin Y, Ocer F, Buyru A, Balci H. Hereditary Thrombophilia, anti-Beta2 Glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss. Am J Reprod Immunol 2012; 67: 251–255

    Problem We investigated the Beta2Glycoprotein I and anti-annexin V antibodies as anti-phospholipid–cofactor antibodies; and factor V G1691A Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations as hereditary thrombophilia in recurrent pregnancy losses (RPL).

    Method of study Study group consisted of 84 women with recurrent pregnancy loss and control group consisted of 84 women having at least one live birth.

    Results Methylenetetrahydrofolate reductase C677T homozygous mutation was detected in 28.5% of the study group and in 14.2% of the controls, and the difference was highly significant (P 

Elisabet Svenungsson – 3rd expert on this subject based on the ideXlab platform

  • Risk factors for cardiovascular mortality in patients with systemic lupus erythematosus, a prospective cohort study
    Arthritis Research & Therapy, 2012
    Co-Authors: Johanna T Gustafsson, Julia F Simard, Iva Gunnarsson, Kerstin Elvin, Ingrid E Lundberg, Lars-olof Hansson, Anders Larsson, Elisabet Svenungsson

    Abstract:

    Introduction Systemic lupus erythematosus (SLE) is a chronic autoimmune disease. Cardiovascular disease (CVD) is common and a major cause of mortality. Studies on cardiovascular morbidity are abundant, whereas mortality studies focusing on cardiovascular outcomes are scarce. The aim of this study was to investigate causes of death and baseline predictors of overall (OM), non-vascular (N-VM), and specifically cardiovascular (CVM) mortality in SLE, and to evaluate systematic coronary risk evaluation (SCORE). Methods 208 SLE patients were included 1995-1999 and followed up after 12 years. Clinical evaluation, CVD risk factors, and biomarkers were recorded at inclusion. Death certificates and autopsy protocols were collected. Causes of death were divided into CVM (ischemic vascular and general atherosclerotic diseases), N-VM and death due to pulmonary hypertension. Predictors of mortality were investigated using multivariable Cox regression. SCORE and standardized mortality ratio (SMR) were calculated. Results During follow-up 42 patients died at mean age of 62 years. SMR 2.4 (CI 1.7-3.0). 48% of deaths were caused by CVM. SCORE underestimated CVM but not to a significant level. Age, high cystatin C levels and established arterial disease were the strongest predictors for all- cause mortality. After adjusting for these in multivariable analyses, only smoking among traditional risk factors, and high soluble vascular cell adhesion molecule-1 (sVCAM-1), high sensitivity C-reactive protein (hsCRP), anti-Beta2 Glycoprotein1 (aBeta2GP1) and any antiphospholipid antibody (aPL) among biomarkers, remained predictive of CVM. Conclusion With the exception of smoking, traditional risk factors do not capture the main underlying risk factors for CVM in SLE. Rather, cystatin C levels, inflammatory and endothelial markers, and antiphospholipid antibodies (aPL) differentiate patients with favorable versus severe cardiovascular prognosis. Our results suggest that these new biomarkers are useful in evaluating the future risk of cardiovascular mortality in SLE patients.