Serum Markers of Endothelial Dysfunction and Inflammation Increase in Hypertension with Prediabetes Mellitus

Zhouqing Huang1, Chen Chen1, Sheng Li1

  • 1Department of Cardiology, The Key Lab of Cardiovascular Disease of Wenzhou, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou, P.R. China .

Insights

Hypertension and prediabetes significantly increase inflammation and endothelial dysfunction markers. The combination of both conditions further elevates intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-α), worsening these effects.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Immunology

Background:

  • Hypertension and prediabetes are prevalent conditions associated with increased cardiovascular risk.
  • Endothelial dysfunction and chronic inflammation are key pathophysiological mechanisms in these diseases.

Purpose of the Study:

  • To investigate endothelial dysfunction and inflammation in patients with hypertension and prediabetes.
  • To analyze the levels of specific adhesion molecules and inflammatory factors in different patient groups.

Main Methods:

  • A study involving 133 outpatients categorized into control, hypertension-only, and hypertension with prediabetes groups.
  • Enzyme-linked immunosorbent assay (ELISA) was used to measure plasma concentrations of ICAM-1, TNF-α, P-selectin, and IL-6.

Main Results:

  • Patients with hypertension (H) and hypertension with prediabetes (HD) showed significantly higher levels of all four biomarkers compared to controls (N).
  • The HD group exhibited significantly higher levels of ICAM-1 and TNF-α compared to the H group.
  • No significant differences in P-selectin and IL-6 levels were found between the H and HD groups.

Conclusions:

  • Prediabetes and hypertension contribute to endothelial dysfunction and inflammation by increasing soluble adhesion molecules and inflammatory cytokines.
  • The comorbidity of hypertension and prediabetes exacerbates inflammation and endothelial dysfunction, particularly through enhanced ICAM-1 and TNF-α expression.
Abstract

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