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Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi

Year 2019, Volume: 46 Issue: 2, 369 - 377, 11.06.2019
https://doi.org/10.5798/dicletip.528618

Abstract

Özet



Amaç: Yaptığımız bu çalışmada Kardiyopulmoner bypass (KPB)
sırasında homosistein, vitamin B12 ve folik asit parametrelerinin değişimlerine
bakılarak birbirleri ile olan ilişkilerinin araştırılması amaçlanmıştır.



Materyal ve Metod: Göğüs Kalp Damar Cerrahisi bölümünde
çeşitli sebeplerden dolayı KPB cerrahisi ile ameliyat olan hastalardan ameliyat
öncesi, pompaya (kalp akciğer makinesi) giriş, kross klemp sonrası ve protamin
verilmesi sonrası olmak üzere 4 jelsiz tüpe kan alınarak bir çalışma grubu
oluşturuldu. Alınan kanlarda serum Vitamin B12 düzeyi ve serum Folik asit
düzeyi Kemilüminesans yöntemi ile serum Homosistein düzeyi ise Kolorimetrik
yöntem ile ölçülmüştür.



Bulgular: Vitamin B12, pg/MI değeri; Ameliyat öncesi
206.30 ±64.76, Pompaya Giriş108.03 ± 35.75, Kross Klemp Sonrası 128.53 ± 38.43,
Protamin Sonrası 141.33 ± 39.21, p<0,001 olarak bulunmuştur. Folik Asit,
ng/MI değeri sırasıyla; 10.04 ± 2.89, 6.53 ± 1.84, 6.53 ± 1.95,  9.02 ± 2.83 ve p<0,001 olarak bulunmuştur.
Homosistein, μmol/L         değeri
sırasıyla;14.40 ± 4.48, 7.63 ± 2.30, 9.44 ± 2.62, 9.15 ± 2.55 ve p<0,001
olarak bulunmuştur.



Sonuç: Pompaya girişte
homosistein, vitamin B12 ve folik asit düzeyi prime solüsyondan dolayı sayısal
olarak düşerken; pompa girişinden kross klemp sonrasına kadar homosisteinde
anlamlı artış olmuş, folik asit düzeyinde artış olmamış, vitamin B12 oranındaki
artış ise homosistein kadar olmamıştır. Bu durum Vitamin B12 ve Folik asit
düzeyi ile serum homosistein konsantrasyonu arasında negatif bir korelasyon
göstermiştir. Kross klemp sonrasından protamin sonrasına kadarki dönemde homosistein
seviyesinde düşüş olmasına rağmen, Vitamin B12 ve folik asit seviyesinde
yükselmeler olmuştur. Bu yükseklik homositeinin Vitamin B12 ve folik asit ile
negatif ilişkisine destek olmaktadır. Perfüzyon süresi uzadıkça artan
inflamatuar yanıt ve kullanılan ilaçlar ile homosistein seviyesinde değişimlere
neden olmuş fakat bu etkileşimlerin homosistein, Vitamin B12 ve folik asit
düzeyi ile ilişkisi istatistiksel olarak gösterilememiştir.



 



INVESTIGATION OF THE RELATIONSHIP BETWEEN HOMOCYSTEINE, VITAMIN B12 AND
FOLIC ACID LEVELS AND THEIR RELATIONSHIP BETWEEN THE CARDIOPULMONARY BYPASS



ABSTRACT



Background: The aim of this study was to investigate the
association between homocysteine, vitamin B12 and folic acid parameters in
cardiopulmonary bypass (CPB).



Methods: In the thoracic cardiovascular surgery
department, a study group was formed by taking 4 gel-free scales from
pre-operative, pump (heart lung machine), after cross-clamp and protamine
administration from patients who underwent surgery with CPB surgery for various
reasons. Serum vitamin B12 level and serum Folic acid level were measured by
chemiluminescence method and serum homocysteine level by Colorimetric method.



Results: Vitamin B12, pg / mL value; Preoperatively
206.30 ± 64.76, Pump Entry 108.03 ± 35.75, Post Cross Clamp 128.53 ± 38.43,
Post Protamine 141.33 ± 39.21, p <0.001. Folic Acid, ng / ml value
respectively; 10.04 ± 2.89, 6.53 ± 1.84, 6.53 ± 1.95, 9.02 ± 2.83 and p
<0.001 respectively. Homocysteine, μmol / L values were found to be 14.40 ±
4.48, 7.63 ± 2.30, 9.44 ± 2.62, 9.15 ± 2.55 and p <0.001 respectively.



Conclusions: While homocysteine, vitamin B12 and folic
acid levels were decreased by prime solu- tion in the pump, there was a
significant increase in homocysteine from the pump inlet to the end of the
cross clamp, no increase in folic acid level, and no increase in vitamin B12 as
homocysteine. This showed a negative correlation between Vitamin B12 and Folic
acid level and serum homocysteine concentration. Although there was a decrease
in homocysteine levels after the crosstalk after protamine, there was a rise in
vitamin B12 and folic acid levels. This elevation supports the negative
association of homocyte with Vitamin B12 and folic acid. Increased duration of
perfusion resulted in increased inflammatory response and changes in
homocysteine levels with drugs used, but these interactions were not
statistically related to homocysteine, Vitamin B12 and folic acid levels.

References

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  • 2. Cumming AM, Olujohungbe A, Keeney S, Singh H, Hay CR, Serjeant GR. The methylenetetrahydrofolate reductase gene C677T polymorphism in patients with homozygous sickle cell disease and stroke. Br J Haematol. 1999;107(3):569-71.
  • 3. Markus HS, Ali N, Swaminathan R, Sankaralingam A, Molloy J, Powell J. A common polymorphism in the methylenetetrahydrofolate reductase gene, homocysteine, and ischemic cerebrovascular disease. Stroke. 1997;28(9):1739-43.
  • 4. Utku U, Çelik Y. Serebrovasküler hastalıklar. In: Balkan S, ed. Ankara: Güneş Kitapevi. 2002:49-61.
  • 5. Hademenos GJ, Alberts MJ, Awad I, Mayberg M, Shepard T, Jagoda A, et all. Advances in the genetics of cerebrovascular disease and stroke. Neurology. 2001: 24;56(8):997-1008. Review.
  • 6. Kostulas K, Crisby M, Huang WX, Lannfelt L, Hagenfeldt L, Eggertsen G, et all. A methylenetetrahydrofolate reductase gene polymorphism in ischaemic stroke and in carotid artery stenosis. Eur J Clin Invest. 1998;28(4):285-9.
  • 7. Engbersen AM, Franken DG, Boers GH, Stevens EM, Trijbels FJ, Blom HJ. Thermolabile 5,10-methylenetetrahydrofolate reductase as a cause of mild hyperhomocysteinemia. Am J Hum Genet. 1995;56(1):142-50.
  • 8. Sucu M, Karadere A, Toprak N. Homosistein ve kardiyovasküler hastalıkları. Türk Kardiyol Dern Arş. 2001; 29:181-90.
  • 9. Schmitz C, Lindpaintner K, Verhoef P, Gaziano JM, Buring J. Genetic polymorphism of methylenetetrahydrofolate reductase and myocardial infarction. A case-control study. Circulation. 1996; 15;94(8):1812-4.
  • 10. Dekou V, Whincup P, Papacosta O, Ebrahim S, Lennon L, Ueland PM, et all. The effect of the C677T and A1298C polymorphisms in the methylenetetrahydrofolate reductase gene on homocysteine levels in elderly men and women from the British regional heart study. Atherosclerosis. 2001; 15;154(3):659-66.
  • 11. Tice JA, Ross E, Coxson PG, Rosenberg I, Weinstein MC, Hunink MG, et all. Cost-effectiveness of vitamin therapy to lower plasma homocysteine levels for the prevention of coronary heart disease: effect of grain fortification and beyond. JAMA. 2001; 22-29;286(8):936-43.
  • 12. Fallon UB, Ben-Shlomo Y, Elwood P, Ubbink JB, Smith GD. Homocysteine and coronary heart disease in the Caerphilly cohort: a 10 year follow up. Heart. 2001;85(2):153-8.
  • 13. Jacques PF, Bostom AG, Williams RR, Ellison RC, Eckfeldt JH, Rosenberg IH, Selhub J, Rozen R. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation. 1996: 1;93(1):7-9.
  • 14. Nygård O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997: 24;337(4):230-6.
  • 15. Sakurabayashi T, Fujimoto M, Takaesu Y, Haginoshita S, Goto S, Aoike I, et all. Association between plasma homocysteine concentration and carotid atherosclerosis in hemodialysis patients. Jpn Circ J. 1999;63(9):692-6.
  • 16. Clarke R, Daly L, Robinson K, Naughten E, Cahalane S, Fowler B, Graham Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med. 1991: 25;324(17):1149-55.
  • 17. Ranucci M, Ballotta A, Frigiola A, Boncilli A, Brozzi S, Costa E, et all. Pre-operative homocysteine levels and morbidity and mortality following cardiac surgery. Eur Heart J. 2009 Apr;30(8):995-1004. doi: 10.1093/eurheartj/ehp015. Epub 2009;17.
  • 18. Nygård O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997: 24;337(4):230-6.
  • 19. McCully KS. Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am J Pathol. 1969;56(1):111-28.
  • 20. McCully KS. Atherosclerosis, serum cholesterol and the homocysteine theory: a study of 194 consecutive autopsies. Am J Med Sci. 1990;299(4):217-21.
  • 21. McCully KS, Ragsdale BD. Production of arteriosclerosis by homocysteinemia. Am J Pathol. 1970;61(1):1-11.
  • 22. Dhamija RK, Gaba P, Arora S, Kaintura A, Kumar M, Bhattacharjee J. Homocysteine and lipoprotein (a) correlation in ischemic stroke patients. J Neurol Sci. 2009 Jun 15;281(1-2):64-8. doi: 10.1016/j.jns.2009.02.341. Epub 2009;13.
  • 23. Prathapasinghe GA, Siow YL, O K. Detrimental role of homocysteine in renal ischemia reperfusion injury. Am J Physiol Renal Physiol. 2007;292(5):F1354-63. Epub 2007 Jan 30.
  • 24. Chen YF, Li PL, Zou AP. Effect of hyperhomocysteinemia on plasma or tissue adenosine levels and renal function. Circulation. 2002: 3;106(10):1275-81.
Year 2019, Volume: 46 Issue: 2, 369 - 377, 11.06.2019
https://doi.org/10.5798/dicletip.528618

Abstract

References

  • 1. Fattal-Valevski A, Bassan H, Korman SH, Lerman-Sagie T, Gutman A, Harel S. Methylenetetrahydrofolate reductase deficiency: importance of early diagnosis. J Child Neurol. 2000;15(8):539-43.
  • 2. Cumming AM, Olujohungbe A, Keeney S, Singh H, Hay CR, Serjeant GR. The methylenetetrahydrofolate reductase gene C677T polymorphism in patients with homozygous sickle cell disease and stroke. Br J Haematol. 1999;107(3):569-71.
  • 3. Markus HS, Ali N, Swaminathan R, Sankaralingam A, Molloy J, Powell J. A common polymorphism in the methylenetetrahydrofolate reductase gene, homocysteine, and ischemic cerebrovascular disease. Stroke. 1997;28(9):1739-43.
  • 4. Utku U, Çelik Y. Serebrovasküler hastalıklar. In: Balkan S, ed. Ankara: Güneş Kitapevi. 2002:49-61.
  • 5. Hademenos GJ, Alberts MJ, Awad I, Mayberg M, Shepard T, Jagoda A, et all. Advances in the genetics of cerebrovascular disease and stroke. Neurology. 2001: 24;56(8):997-1008. Review.
  • 6. Kostulas K, Crisby M, Huang WX, Lannfelt L, Hagenfeldt L, Eggertsen G, et all. A methylenetetrahydrofolate reductase gene polymorphism in ischaemic stroke and in carotid artery stenosis. Eur J Clin Invest. 1998;28(4):285-9.
  • 7. Engbersen AM, Franken DG, Boers GH, Stevens EM, Trijbels FJ, Blom HJ. Thermolabile 5,10-methylenetetrahydrofolate reductase as a cause of mild hyperhomocysteinemia. Am J Hum Genet. 1995;56(1):142-50.
  • 8. Sucu M, Karadere A, Toprak N. Homosistein ve kardiyovasküler hastalıkları. Türk Kardiyol Dern Arş. 2001; 29:181-90.
  • 9. Schmitz C, Lindpaintner K, Verhoef P, Gaziano JM, Buring J. Genetic polymorphism of methylenetetrahydrofolate reductase and myocardial infarction. A case-control study. Circulation. 1996; 15;94(8):1812-4.
  • 10. Dekou V, Whincup P, Papacosta O, Ebrahim S, Lennon L, Ueland PM, et all. The effect of the C677T and A1298C polymorphisms in the methylenetetrahydrofolate reductase gene on homocysteine levels in elderly men and women from the British regional heart study. Atherosclerosis. 2001; 15;154(3):659-66.
  • 11. Tice JA, Ross E, Coxson PG, Rosenberg I, Weinstein MC, Hunink MG, et all. Cost-effectiveness of vitamin therapy to lower plasma homocysteine levels for the prevention of coronary heart disease: effect of grain fortification and beyond. JAMA. 2001; 22-29;286(8):936-43.
  • 12. Fallon UB, Ben-Shlomo Y, Elwood P, Ubbink JB, Smith GD. Homocysteine and coronary heart disease in the Caerphilly cohort: a 10 year follow up. Heart. 2001;85(2):153-8.
  • 13. Jacques PF, Bostom AG, Williams RR, Ellison RC, Eckfeldt JH, Rosenberg IH, Selhub J, Rozen R. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation. 1996: 1;93(1):7-9.
  • 14. Nygård O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997: 24;337(4):230-6.
  • 15. Sakurabayashi T, Fujimoto M, Takaesu Y, Haginoshita S, Goto S, Aoike I, et all. Association between plasma homocysteine concentration and carotid atherosclerosis in hemodialysis patients. Jpn Circ J. 1999;63(9):692-6.
  • 16. Clarke R, Daly L, Robinson K, Naughten E, Cahalane S, Fowler B, Graham Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med. 1991: 25;324(17):1149-55.
  • 17. Ranucci M, Ballotta A, Frigiola A, Boncilli A, Brozzi S, Costa E, et all. Pre-operative homocysteine levels and morbidity and mortality following cardiac surgery. Eur Heart J. 2009 Apr;30(8):995-1004. doi: 10.1093/eurheartj/ehp015. Epub 2009;17.
  • 18. Nygård O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997: 24;337(4):230-6.
  • 19. McCully KS. Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am J Pathol. 1969;56(1):111-28.
  • 20. McCully KS. Atherosclerosis, serum cholesterol and the homocysteine theory: a study of 194 consecutive autopsies. Am J Med Sci. 1990;299(4):217-21.
  • 21. McCully KS, Ragsdale BD. Production of arteriosclerosis by homocysteinemia. Am J Pathol. 1970;61(1):1-11.
  • 22. Dhamija RK, Gaba P, Arora S, Kaintura A, Kumar M, Bhattacharjee J. Homocysteine and lipoprotein (a) correlation in ischemic stroke patients. J Neurol Sci. 2009 Jun 15;281(1-2):64-8. doi: 10.1016/j.jns.2009.02.341. Epub 2009;13.
  • 23. Prathapasinghe GA, Siow YL, O K. Detrimental role of homocysteine in renal ischemia reperfusion injury. Am J Physiol Renal Physiol. 2007;292(5):F1354-63. Epub 2007 Jan 30.
  • 24. Chen YF, Li PL, Zou AP. Effect of hyperhomocysteinemia on plasma or tissue adenosine levels and renal function. Circulation. 2002: 3;106(10):1275-81.
There are 24 citations in total.

Details

Primary Language Turkish
Subjects Health Care Administration
Journal Section Research Article
Authors

Hatice Bilge Açık This is me 0000-0003-1085-933X

Mustafa Göz This is me 0000-0003-1951-8881

Mehmet Salih Aydın This is me 0000-0002-6652-6035

Mahmut Padak 0000-0001-6863-1907

Reşat Dikme 0000-0001-9157-7830

Ömer Göç This is me 0000-0002-3047-6232

Publication Date June 11, 2019
Submission Date February 18, 2019
Published in Issue Year 2019 Volume: 46 Issue: 2

Cite

APA Açık, H. B., Göz, M., Aydın, M. S., Padak, M., et al. (2019). Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi. Dicle Medical Journal, 46(2), 369-377. https://doi.org/10.5798/dicletip.528618
AMA Açık HB, Göz M, Aydın MS, Padak M, Dikme R, Göç Ö. Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi. diclemedj. June 2019;46(2):369-377. doi:10.5798/dicletip.528618
Chicago Açık, Hatice Bilge, Mustafa Göz, Mehmet Salih Aydın, Mahmut Padak, Reşat Dikme, and Ömer Göç. “Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 Ve Folik Asit Seviyelerinin Değişimi Ve Birbirleri Ile Olan İlişkilerinin İncelenmesi”. Dicle Medical Journal 46, no. 2 (June 2019): 369-77. https://doi.org/10.5798/dicletip.528618.
EndNote Açık HB, Göz M, Aydın MS, Padak M, Dikme R, Göç Ö (June 1, 2019) Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi. Dicle Medical Journal 46 2 369–377.
IEEE H. B. Açık, M. Göz, M. S. Aydın, M. Padak, R. Dikme, and Ö. Göç, “Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi”, diclemedj, vol. 46, no. 2, pp. 369–377, 2019, doi: 10.5798/dicletip.528618.
ISNAD Açık, Hatice Bilge et al. “Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 Ve Folik Asit Seviyelerinin Değişimi Ve Birbirleri Ile Olan İlişkilerinin İncelenmesi”. Dicle Medical Journal 46/2 (June 2019), 369-377. https://doi.org/10.5798/dicletip.528618.
JAMA Açık HB, Göz M, Aydın MS, Padak M, Dikme R, Göç Ö. Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi. diclemedj. 2019;46:369–377.
MLA Açık, Hatice Bilge et al. “Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 Ve Folik Asit Seviyelerinin Değişimi Ve Birbirleri Ile Olan İlişkilerinin İncelenmesi”. Dicle Medical Journal, vol. 46, no. 2, 2019, pp. 369-77, doi:10.5798/dicletip.528618.
Vancouver Açık HB, Göz M, Aydın MS, Padak M, Dikme R, Göç Ö. Kardiyopulmoner Baypass Sırasında Homosistein, Vitamin B12 ve Folik Asit Seviyelerinin Değişimi ve Birbirleri ile Olan İlişkilerinin İncelenmesi. diclemedj. 2019;46(2):369-77.