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Background <p>IntercellularAQ1 adhesion molecules (ICAMs) are released from the endothelium in response toshear stress. Their role in persistent pulmonary hypertension (PPHN) remains un-investigated.</p> Methodology <p>Sixty neonates (30 PPHN, 30 controls) underwent serum ICAM testing and echocardiography.</p> Results <p>Right and left ventricular function was depressed in PPHN cases. Tricuspid annular plane systolicexcursion was reduced (Cases 8±1 vs. Controls 11±3.5). ICAM was elevated in cases (332±96 vs. 208 ±36).</p> Conclusion <p>ICAM is a sensitive PPHN marker. Elevated ICAM may result from endothelial damage or contribute toPPHN pathogenesis. Further studies are needed to confirm these results and explore this relationship.</p>

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Circulating Intercellular Adhesion Molecule as a Novel Marker of Pulmonary Hypertension in Newborn

  • 期刊论文

  • 发表日期：

    2025年4月15日

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  • Antoine Fakhry AbdelMassih,
  • Sherif ElAnwary,
  • Nourhan Taha,
  • Noha Radwan,
  • Mahmoud Othman AbouDeif

摘要

Background

IntercellularAQ1 adhesion molecules (ICAMs) are released from the endothelium in response toshear stress. Their role in persistent pulmonary hypertension (PPHN) remains un-investigated.

Methodology

Sixty neonates (30 PPHN, 30 controls) underwent serum ICAM testing and echocardiography.

Results

Right and left ventricular function was depressed in PPHN cases. Tricuspid annular plane systolicexcursion was reduced (Cases 8±1 vs. Controls 11±3.5). ICAM was elevated in cases (332±96 vs. 208 ±36).

Conclusion

ICAM is a sensitive PPHN marker. Elevated ICAM may result from endothelial damage or contribute toPPHN pathogenesis. Further studies are needed to confirm these results and explore this relationship.