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Homocysteine and pro-inflammatory cytokine concentrations in acute heart disease

Cahide Gokkusu1, Feti Tulubas, Yesim Unlucerci

  • 1Department of Biochemistry, Istanbul University, Turkey. cahgok@istanbul.edu.tr

Cytokine
|February 5, 2010
PubMed

Insights

This study found higher levels of total homocysteine (tHcy), interleukin-2 (IL-2), and interleukin-6 (IL-6) in acute coronary syndrome (ACS) patients, suggesting inflammation is linked to tHcy-related cardiovascular disease.

Area of Science:

  • Cardiovascular Science
  • Inflammation Research
  • Biochemistry

Background:

  • Atherosclerosis development and progression are linked to inflammation.
  • Interleukin-2 (IL-2) and Interleukin-6 (IL-6) are implicated in cardiovascular diseases.
  • Hyperhomocysteinemia (elevated homocysteine) is a significant risk factor for atherosclerosis and thrombosis, with homocysteine (Hcy) shown to promote pro-inflammatory cytokine production.

Purpose of the Study:

  • To investigate the relationship between pro-inflammatory cytokines IL-2 and IL-6 and total homocysteine (tHcy) in patients with acute coronary syndrome (ACS).

Main Methods:

  • A study cohort included 102 patients diagnosed with ACS and 90 healthy control subjects.
  • Measurements included total homocysteine (tHcy), IL-2, IL-6, and folic acid levels.
  • Receiver Operating Characteristic (ROC) curve analysis was used to evaluate the sensitivity of IL-2.

Main Results:

  • Patients with ACS exhibited significantly higher levels of tHcy, IL-2, and IL-6 compared to healthy controls.
  • Folic acid levels were found to be lower in the ACS patient group.
  • ROC plot analysis indicated that IL-2 demonstrated higher sensitivity in distinguishing ACS patients.

Conclusions:

  • Elevated inflammation, as indicated by increased IL-2 and IL-6 levels, is associated with total homocysteine in acute coronary syndrome.
  • These findings suggest a potential link between homocysteine-related pathways and inflammatory processes in cardiovascular disease development.

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