American Journal of BioScience

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Patent Foramen Ovale is Associated with an Increased NAFLD Risk for Health of Young Men

Received: 13 August 2014    Accepted: 19 August 2014    Published: 24 August 2014
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Abstract

Between March 2012 and July 2013, 1000 asymptomatic young military male underwent hepatic ultrasonography and echocardiography at Medical Check-up Center for general young health screening. Blood biochemistry, arterial blood pressure and anthropometric measurements were studied. All analyses were performed using the statistical package SPSS 15.0, where the statistical significance was assessed at the two-tailed 0.05 threshold. It was found that among 1000 persons, 60 had patent foramen ovale (PFO) and 110 subjects had symptoms of nonalcoholic fatty liver disease (NAFLD). The PFO-group consisted of 20 male with 33.3% of NAFLD symptoms, while the group without PFO consisted of 90 male with 9.6% of NAFLD symptoms only. There were significant differences between two groups: p<0.001. Moreover, such factors as the mean age, BMI, triglycerides, hemoglobin, and aspartate aminotransferase level, the mean HDL cholesterol, alanine aminotransferase, platelet count did not differ between the two groups. The main cause of the pathogenesis of nonalcoholic fatty liver disease (NAFLD) has not been sufficiently elucidated. Serotonin of plasma is removed from circulation in capillary beds, predominantly in the lung. Nevertheless, metabolism of serotonin can be by-passed by patent foramen ovale (PFO) that can lead to NAFLD. Therefore, the aim of this study was to test the hypothesis that echocardiographic diagnosed PFO predicts the subsequent NAFLD, which can be diagnosed by ultrasonography. The statistical analysis of the 1000 young male supports the hypothesis that PFO can be associated with increased NAFLD risk for the health of young men.

DOI 10.11648/j.ajbio.s.2014020601.16
Published in American Journal of BioScience (Volume 2, Issue 6-1, November 2014)

This article belongs to the Special Issue Chemical Biology

Page(s) 35-38
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Non-Alcoholic Fatty Liver Disease (NAFLD), Patent Foramen Ovale (PFO), Serotonin

References
[1] Tiniakos DG, Vos MB, Brunt EM. Nonalcoholic fatty liver disease: pathology and pathogenesis. Annu Rev Pathol 2010;5:145–71.
[2] Bae JC, Cho YK, Lee WY, Seo HI, Rhee EJ, et al. Impact of nonalcoholic fatty liver disease on insulin resistance in relation to HbA1c levels in nondiabetic subjects. Am J Gastroenterol 2010;105:2389–95.
[3] Targher G, Day CP, Bonora E. Risk of cardiovascular disease in patients with nonalcoholic fatty liver disease. N Engl J Med 2010;363: 1341–50.
[4] Bhatia LS, Curzen NP, Calder PC, Byrne CD. Non-alcoholic fatty liver disease: a new and important cardiovascular risk factor? Eur Heart J 2012;33: 1190– 200.
[5] Stefan N, Kantartzis K, Haring HU. Causes and metabolic consequences of Fatty liver. Endocr Rev 2008;29:939–60.
[6] Bae JC, Rhee EJ, Lee WY, Park SE, Park CY, et al. Combined effect of nonalcoholic fatty liver disease and impaired fasting glucose on the development of type 2 diabetes: a 4-year retrospective longitudinal study. Diabetes Care 2011;34:727–9.
[7] Fabbrini E, Sullivan S, Klein S . Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology 2010;51:679–89
[8] Nocito A, Dahm F, Jochum W, Jang JH, Georgiev P, Bader M, Renner EL,, et al. Serotonin mediates oxidative stress and mitochondrial toxicity in a murine model of nonalcoholic steatohepatitis. Gastroenterology 2007; 133:608-18.
[9] Jeremy D. Pearson, John L. Gordon Metabolism of serotonin and adenosine. Biology of Endothelial Cells Developments in Cardiovascular Medicine 1984;27: 330-342
[10] Hara H, Virmani R, Ladich E, Mackey-Bojack S, Titus J, Reisman M, Gray W, et al. Patent foramen ovale: current pathology, pathophysiology, and clinical status. J Am Coll Cardiol 2005; 46:1768-76.
[11] Wu LA, Malouf JF, Dearani JA, Hagler DJ, Reeder GS, Petty GW, Khandheria BK. Patent foramen ovale in cryptogenic stroke: current understanding and management options. Arch Intern Med 2004; 164:950-6.
[12] Kerut EK, Norfleet WT, Plotnick GD, Giles TD. Patent foramen ovale: a review of associated conditions and the impact of physiological size. J Am Coll Cardiol 2001; 38:613-23.
[13] Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984; 59:17-20.
[14] Meissner I, Whisnant JP, Khandheria BK, Spittell PC, O'Fallon WM, Pascoe RD, Enriquez-Sarano M, et al. Prevalence of potential risk factors for stroke assessed by transesophageal echocardiography and carotid ultrasonography: the SPARC study. Stroke Prevention: Assessment of Risk in a Community. Mayo Clin Proc 1999; 74:862-9.
[15] Cheng TO. Platypnea-orthodeoxia syndrome: etiology, differential diagnosis, and management. Catheter Cardiovasc Interv 1999; 47:64-6.
[16] Karacı M., Tanyeri B., Tekin D., TorosluE., Baysal K. Clinical Course And Prognosis At Patent Foramen Ovale. Journal of Clinical and Analytical Medicine. Published Online: 18.05.2013 DOI: 10.4328/JCAM.1886
[17] Mehta SR, Thomas EL, Bell JD, Johnston DG, Taylor-Robinson SD.Non-invasive means of measuring hepatic fat content. World J Gastroenterol 2008;14: 3476–83.
Author Information
  • Family Physician, Dicle University Hospital, Yeni?ehir, Diyarbakir, Turkey

  • Family Physician, Diyarbakir Military Hospital, Yeni?ehir, Diyarbakir, Turkey

  • Family Physician, Presidential Guard Regiment, Ankara, Turkey

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    Erkan Kibrisli, Sinan Işcen, Salim Ozenc, Adem Parlak. (2014). Patent Foramen Ovale is Associated with an Increased NAFLD Risk for Health of Young Men. American Journal of BioScience, 2(6-1), 35-38. https://doi.org/10.11648/j.ajbio.s.2014020601.16

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    ACS Style

    Erkan Kibrisli; Sinan Işcen; Salim Ozenc; Adem Parlak. Patent Foramen Ovale is Associated with an Increased NAFLD Risk for Health of Young Men. Am. J. BioScience 2014, 2(6-1), 35-38. doi: 10.11648/j.ajbio.s.2014020601.16

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    AMA Style

    Erkan Kibrisli, Sinan Işcen, Salim Ozenc, Adem Parlak. Patent Foramen Ovale is Associated with an Increased NAFLD Risk for Health of Young Men. Am J BioScience. 2014;2(6-1):35-38. doi: 10.11648/j.ajbio.s.2014020601.16

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  • @article{10.11648/j.ajbio.s.2014020601.16,
      author = {Erkan Kibrisli and Sinan Işcen and Salim Ozenc and Adem Parlak},
      title = {Patent Foramen Ovale is Associated with an Increased NAFLD Risk for Health of Young Men},
      journal = {American Journal of BioScience},
      volume = {2},
      number = {6-1},
      pages = {35-38},
      doi = {10.11648/j.ajbio.s.2014020601.16},
      url = {https://doi.org/10.11648/j.ajbio.s.2014020601.16},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ajbio.s.2014020601.16},
      abstract = {Between March 2012 and July 2013, 1000 asymptomatic young military male underwent hepatic ultrasonography and echocardiography at Medical Check-up Center for general young health screening. Blood biochemistry, arterial blood pressure and anthropometric measurements were studied. All analyses were performed using the statistical package SPSS 15.0, where the statistical significance was assessed at the two-tailed 0.05 threshold. It was found that among 1000 persons, 60 had patent foramen ovale (PFO) and 110 subjects had symptoms of nonalcoholic fatty liver disease (NAFLD). The PFO-group consisted of 20 male with 33.3% of NAFLD symptoms, while the group without PFO consisted of 90 male with 9.6% of NAFLD symptoms only. There were significant differences between two groups: p<0.001. Moreover, such factors as the mean age, BMI, triglycerides, hemoglobin, and aspartate aminotransferase level, the mean HDL cholesterol, alanine aminotransferase, platelet count did not differ between the two groups. The main cause of the pathogenesis of nonalcoholic fatty liver disease (NAFLD) has not been sufficiently elucidated. Serotonin of plasma is removed from circulation in capillary beds, predominantly in the lung. Nevertheless, metabolism of serotonin can be by-passed by patent foramen ovale (PFO) that can lead to NAFLD. Therefore, the aim of this study was to test the hypothesis that echocardiographic diagnosed PFO predicts the subsequent NAFLD, which can be diagnosed by ultrasonography. The statistical analysis of the 1000 young male supports the hypothesis that PFO can be associated with increased NAFLD risk for the health of young men.},
     year = {2014}
    }
    

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  • TY  - JOUR
    T1  - Patent Foramen Ovale is Associated with an Increased NAFLD Risk for Health of Young Men
    AU  - Erkan Kibrisli
    AU  - Sinan Işcen
    AU  - Salim Ozenc
    AU  - Adem Parlak
    Y1  - 2014/08/24
    PY  - 2014
    N1  - https://doi.org/10.11648/j.ajbio.s.2014020601.16
    DO  - 10.11648/j.ajbio.s.2014020601.16
    T2  - American Journal of BioScience
    JF  - American Journal of BioScience
    JO  - American Journal of BioScience
    SP  - 35
    EP  - 38
    PB  - Science Publishing Group
    SN  - 2330-0167
    UR  - https://doi.org/10.11648/j.ajbio.s.2014020601.16
    AB  - Between March 2012 and July 2013, 1000 asymptomatic young military male underwent hepatic ultrasonography and echocardiography at Medical Check-up Center for general young health screening. Blood biochemistry, arterial blood pressure and anthropometric measurements were studied. All analyses were performed using the statistical package SPSS 15.0, where the statistical significance was assessed at the two-tailed 0.05 threshold. It was found that among 1000 persons, 60 had patent foramen ovale (PFO) and 110 subjects had symptoms of nonalcoholic fatty liver disease (NAFLD). The PFO-group consisted of 20 male with 33.3% of NAFLD symptoms, while the group without PFO consisted of 90 male with 9.6% of NAFLD symptoms only. There were significant differences between two groups: p<0.001. Moreover, such factors as the mean age, BMI, triglycerides, hemoglobin, and aspartate aminotransferase level, the mean HDL cholesterol, alanine aminotransferase, platelet count did not differ between the two groups. The main cause of the pathogenesis of nonalcoholic fatty liver disease (NAFLD) has not been sufficiently elucidated. Serotonin of plasma is removed from circulation in capillary beds, predominantly in the lung. Nevertheless, metabolism of serotonin can be by-passed by patent foramen ovale (PFO) that can lead to NAFLD. Therefore, the aim of this study was to test the hypothesis that echocardiographic diagnosed PFO predicts the subsequent NAFLD, which can be diagnosed by ultrasonography. The statistical analysis of the 1000 young male supports the hypothesis that PFO can be associated with increased NAFLD risk for the health of young men.
    VL  - 2
    IS  - 6-1
    ER  - 

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