The relationship between circulating TRAIL and endothelial dysfunction in subclinical hypothyroidism

Guangda Xiang1, Ling Yue, Junxia Zhang

  • 1Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan, 430070, Hubei, People's Republic of China, guangda64@hotmail.com.

Endocrine
|October 9, 2014
PubMed

Insights

Circulating Tumor Necrosis Factor (TNF)-Related Apoptosis-Inducing Ligand (TRAIL) levels are lower in subclinical hypothyroidism (sHT) patients. Higher TRAIL levels are linked to improved endothelial function, suggesting TRAIL may protect against dysfunction in sHT.

Area of Science:

  • Endocrinology
  • Cardiovascular Medicine
  • Immunology

Background:

  • Subclinical hypothyroidism (sHT) is linked to increased atherosclerosis and cardiovascular events.
  • Tumor Necrosis Factor (TNF)-Related Apoptosis-Inducing Ligand (TRAIL) plays a role in atherosclerosis.
  • Endothelial dysfunction is a key factor in cardiovascular disease development.

Purpose of the Study:

  • To investigate the association between circulating TRAIL levels and endothelial dysfunction in patients with newly diagnosed sHT.
  • To determine if TRAIL levels correlate with flow-mediated dilation (FMD) in sHT patients.

Main Methods:

  • Recruited 204 patients with newly diagnosed sHT and 52 healthy controls.
  • Measured circulating TRAIL concentration using ELISA.
  • Assessed brachial artery flow-mediated dilation (FMD) via high-resolution ultrasound.

Main Results:

  • Mean TRAIL levels were significantly lower in sHT patients (67.2 pg/ml) compared to controls (78.5 pg/ml).
  • TRAIL levels positively correlated with FMD, increasing with higher FMD quartiles.
  • Multivariate analysis confirmed TRAIL was independently associated with FMD (p = 0.007).

Conclusions:

  • Circulating TRAIL levels are decreased in patients with newly diagnosed sHT.
  • TRAIL concentration is positively associated with endothelial function (FMD) in sHT patients.
  • TRAIL may serve as a protective biomarker for endothelial function in the context of sHT.

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