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Background <p>Chronic inflammation plays a central role in the development of adenoid hypertrophy, and vasoactive peptides such as urotensin II may contribute to its pathogenesis.</p> Objectives <p>Adenoid hypertrophy (AH) is a prevalent, recurrent, and chronic inflammatory disease in pediatrics. This study sought to examine the inflammatory profile of AH by measuring urotensin II (UII) levels and to ascertain the correlation between the severity of adenoid hypertrophy and UII levels.</p> Methods <p>The study population comprised children with grade 3 and 4 adenoid hypertrophy who were scheduled for adenoidectomy. UII levels were quantified in samples obtained from adenoid tissue using ELISA. Furthermore, the expressions of LTR1 and TNF-α were evaluated through real-time PCR analysis.</p> Results <p>A significant elevation in UII levels was observed in the adenoid tissue of patients with Grade 4. A positive correlation was identified between UII levels and the severity of AH. Molecular studies revealed that the expression of TNF-α and leukotriene receptor 1 (LTR1) in the adenoid tissue of grade 4 patients was higher than that of grade 3 patients.</p> Conclusion <p>The study results indicate that the inflammatory profile of AH is linked to UII activity, suggesting that UII may contribute to the pathogenesis of AH. The measurement of UII levels has the potential to provide insight into the inflammatory status of AH. It may also serve as a promising avenue for advancing novel treatment strategies.</p>

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The role of urotensin II in the pathogenesis of adenoid hypertrophy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月29日

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  • Fatma Atalay,
  • Büşra Dincer,
  • İrfan Çınar,
  • Murat Yaşar

摘要

Background

Chronic inflammation plays a central role in the development of adenoid hypertrophy, and vasoactive peptides such as urotensin II may contribute to its pathogenesis.

Objectives

Adenoid hypertrophy (AH) is a prevalent, recurrent, and chronic inflammatory disease in pediatrics. This study sought to examine the inflammatory profile of AH by measuring urotensin II (UII) levels and to ascertain the correlation between the severity of adenoid hypertrophy and UII levels.

Methods

The study population comprised children with grade 3 and 4 adenoid hypertrophy who were scheduled for adenoidectomy. UII levels were quantified in samples obtained from adenoid tissue using ELISA. Furthermore, the expressions of LTR1 and TNF-α were evaluated through real-time PCR analysis.

Results

A significant elevation in UII levels was observed in the adenoid tissue of patients with Grade 4. A positive correlation was identified between UII levels and the severity of AH. Molecular studies revealed that the expression of TNF-α and leukotriene receptor 1 (LTR1) in the adenoid tissue of grade 4 patients was higher than that of grade 3 patients.

Conclusion

The study results indicate that the inflammatory profile of AH is linked to UII activity, suggesting that UII may contribute to the pathogenesis of AH. The measurement of UII levels has the potential to provide insight into the inflammatory status of AH. It may also serve as a promising avenue for advancing novel treatment strategies.