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Popovic D, Lalic K, Jotic A, et al. The Inflammatory and Hemostatic Cardiovascular Risk Markers During Acute Hyperglycemic Crisis in Type 1 and Type 2 Diabetes. J Med Biochem. 2019;38(2):126-133doi: 10.2478/jomb-2018-0024.
Popovic, D., Lalic, K., Jotic, A., Milicic, T., Bogdanovic, J., Đorđevic, M., Stankovic, S., Jeremic, V., & Lalic, N. M. (2019). The Inflammatory and Hemostatic Cardiovascular Risk Markers During Acute Hyperglycemic Crisis in Type 1 and Type 2 Diabetes. Journal of medical biochemistry, 38(2), 126-133. https://doi.org/10.2478/jomb-2018-0024
Popovic, Dragana, et al. "The Inflammatory and Hemostatic Cardiovascular Risk Markers During Acute Hyperglycemic Crisis in Type 1 and Type 2 Diabetes." Journal of medical biochemistry vol. 38,2 (2019): 126-133. doi: https://doi.org/10.2478/jomb-2018-0024
Popovic D, Lalic K, Jotic A, Milicic T, Bogdanovic J, Đorđevic M, Stankovic S, Jeremic V, Lalic NM. The Inflammatory and Hemostatic Cardiovascular Risk Markers During Acute Hyperglycemic Crisis in Type 1 and Type 2 Diabetes. J Med Biochem. 2019 Mar 03;38(2):126-133. doi: 10.2478/jomb-2018-0024. eCollection 2019 Apr. PMID: 30867640; PMCID: PMC6410996.
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J Med Biochem. 2019 Mar 03;38(2):126-133. doi: 10.2478/jomb-2018-0024. eCollection 2019 Apr.

The Inflammatory and Hemostatic Cardiovascular Risk Markers During Acute Hyperglycemic Crisis in Type 1 and Type 2 Diabetes.

Journal of medical biochemistry

Dragana Popovic, Katarina Lalic, Aleksandra Jotic, Tanja Milicic, Jelena Bogdanovic, Maja Đorđevic, Sanja Stankovic, Veljko Jeremic, Nebojsa M Lalic

Affiliations

  1. Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Centre of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
  2. Emergency Center, Clinical Centar of Serbia, Clinical Center of Serbia, Belgrade, Serbia.
  3. Center for Medical Biochemistry, Clinical Center of Serbia, Belgrade, Serbia.
  4. Department for Operations Research and Statistics, Faculty of Organizational Sciences, University of Belgrade, Belgrade, Serbia.

PMID: 30867640 PMCID: PMC6410996 DOI: 10.2478/jomb-2018-0024

Abstract

BACKGROUND: We analyzed cardiovascular inflammatory (C-reactive protein (CRP), interleukin 6 (IL-6)), haemostatic (homocysteine) risk markers in lean and obese patients at admission and acute hyperglicemic crisis (AHC) resolving, involving diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).

METHODS: In that context, we included group A: N = 20 obese, B: N=20 lean patients with DKA; C: N = l0 obese, D: N=10 lean patients with HHS; E: N = 15 obese, F: N=15 lean controls. CRP IL-6, homocysteine were determined by ELISA.

RESULTS: Our results showed that CRP IL-6, and homocysteine levels decreased in all groups: (A: p<0.001; B: p<0.001, C: p<0.05; D: p<0.001 mg/L), (A: p<0.001 B: p<0.001, C: p<0.001, D: p<0.01 pg/mL), (A: p<0.001, B: p <0.001; C: p<0.05, D: p=0.001 μmol/L), respectively, at resolving AHC. However, CRP persisted higher (p<0.001, p<0.01), IL-6 lower (p<0.05, p<0.001), while homocysteine levels turned out to be similar to controls.

CONCLUSIONS: AHC is associated with increased inflammatory and hemostatic cardiovascular risk markers. Also, insulin therapy in AHC has had more pronounced favorable effect on IL-6 and homocystein than on CRP.

Keywords: acute hyperglycemic crisis; cardiovascular risk markers; haemostatic markers; inflammatory markers

Conflict of interest statement

Conflict of interest Conflict of interest statement: The authors stated that they have no conflicts of interest regarding the publication of this article.

References

  1. Am J Clin Nutr. 2000 Jul;72(1):22-9 - PubMed
  2. Endocrinology. 2000 Jul;141(7):2582-8 - PubMed
  3. Life Sci. 2000 Jun 8;67(3):291-300 - PubMed
  4. Diabetes Care. 2000 Dec;23(12):1816-22 - PubMed
  5. World Health Organ Tech Rep Ser. 2000;894:i-xii, 1-253 - PubMed
  6. JAMA. 2001 Jul 18;286(3):327-34 - PubMed
  7. Diabetes Care. 2001 Aug;24(8):1403-10 - PubMed
  8. Diabetologia. 2001 Aug;44(8):1011-4 - PubMed
  9. Am J Epidemiol. 2002 Jan 1;155(1):65-71 - PubMed
  10. J Clin Endocrinol Metab. 2002 Mar;87(3):1419-22 - PubMed
  11. Drugs. 2002;62(4):605-16 - PubMed
  12. Circulation. 2002 Oct 15;106(16):2067-72 - PubMed
  13. J Clin Endocrinol Metab. 2003 Mar;88(3):1082-8 - PubMed
  14. Diabetes Care. 2003 May;26(5):1535-9 - PubMed
  15. Clin Immunol. 2003 Sep;108(3):175-81 - PubMed
  16. Ann Clin Lab Sci. 2003 Fall;33(4):435-42 - PubMed
  17. Biochem Biophys Res Commun. 2004 Mar 5;315(2):404-7 - PubMed
  18. Diabetes. 2004 Aug;53(8):2079-86 - PubMed
  19. Int J Obes Relat Metab Disord. 2004 Sep;28 Suppl 2:S3-7 - PubMed
  20. Diabetes. 2005 Jan;54(1):85-91 - PubMed
  21. Eur Heart J. 2005 Feb;26(4):328-31 - PubMed
  22. Diabetologia. 2005 Jun;48(6):1038-50 - PubMed
  23. Nutr Metab Cardiovasc Dis. 2005 Apr;15(2):118-24 - PubMed
  24. Biochem Biophys Res Commun. 2005 Sep 23;335(2):491-5 - PubMed
  25. J Am Soc Nephrol. 2006 Mar;17(3):863-70 - PubMed
  26. Eur J Endocrinol. 2006 Dec;155(6):887-93 - PubMed
  27. Diabetes Care. 2007 Apr;30(4):854-60 - PubMed
  28. J Am Coll Cardiol. 2009 Feb 3;53(5 Suppl):S14-20 - PubMed
  29. Diabetes Care. 2009 Jul;32(7):1335-43 - PubMed
  30. N Am J Med Sci. 2012 Apr;4(4):180-4 - PubMed
  31. BMC Genomics. 2013 Dec 10;14:867 - PubMed
  32. Cardiovasc J Afr. 2014 May-Jun;25(3):137-41 - PubMed
  33. J Diabetes Complications. 2014 Sep-Oct;28(5):662-6 - PubMed
  34. PLoS One. 2015 Aug 27;10(8):e0136840 - PubMed
  35. J Med Biochem. 2017 Jul 14;36(3):211-215 - PubMed
  36. J Med Biochem. 2018 Jul 01;37(3):373-378 - PubMed
  37. Metabolism. 1998 Jun;47(6):686-9 - PubMed
  38. Circulation. 1998 Jul 21;98(3):204-10 - PubMed

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