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Background <p>Diabetic urinary incontinence is a multifactorial condition involving neuropathy, oxidative stress, and epithelial dysfunction. Serum biomarkers—cathelicidin (LL-37), elafin, vitamin D receptor (VDR), 4-hydroxynonenal (4-HNE), and amyloid-β1–42 (Aβ1–42) may provide insight into underlying mechanisms.</p> Methods <p>We conducted a cross-sectional, single-centre observational study including 120 adults: type II diabetes with urinary incontinence (DI; <i>n</i> = 40), non-diabetic urinary incontinence (Non-DI; <i>n</i> = 40), and healthy controls (<i>n</i> = 40). Serum biomarker levels were measured by ELISA. Group differences were analysed using Kruskal–Wallis, with pairwise Mann–Whitney U tests and Bonferroni adjustment (m = 3) where appropriate.</p> Results <p>Among profiled biomarkers, 4-HNE was lower in DI than in both Non-DI and controls, while LL-37, elafin, VDR, and Aβ1–42 showed no Bonferroni-corrected pairwise differences.</p> Conclusion <p>In diabetic urinary incontinence, 4-HNE showed the most consistent group-level separation—lower in DI compared with both Non-DI and healthy controls—whereas LL-37, elafin, VDR, and Aβ1–42 did not demonstrate Bonferroni-corrected pairwise differences. These preliminary findings highlight oxidative and neuroimmune alterations in diabetic incontinence and warrant validation in larger longitudinal studies.</p>

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Inflammatory and neuroimmune imbalance in diabetic incontinence: insights from serum biomarker profiling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月26日

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  • Ali Can Albaz,
  • Funda Kosova,
  • Gökhan Temeltaş,
  • Oktay Üçer,
  • Talha Müezzi̇noğlu

摘要

Background

Diabetic urinary incontinence is a multifactorial condition involving neuropathy, oxidative stress, and epithelial dysfunction. Serum biomarkers—cathelicidin (LL-37), elafin, vitamin D receptor (VDR), 4-hydroxynonenal (4-HNE), and amyloid-β1–42 (Aβ1–42) may provide insight into underlying mechanisms.

Methods

We conducted a cross-sectional, single-centre observational study including 120 adults: type II diabetes with urinary incontinence (DI; n = 40), non-diabetic urinary incontinence (Non-DI; n = 40), and healthy controls (n = 40). Serum biomarker levels were measured by ELISA. Group differences were analysed using Kruskal–Wallis, with pairwise Mann–Whitney U tests and Bonferroni adjustment (m = 3) where appropriate.

Results

Among profiled biomarkers, 4-HNE was lower in DI than in both Non-DI and controls, while LL-37, elafin, VDR, and Aβ1–42 showed no Bonferroni-corrected pairwise differences.

Conclusion

In diabetic urinary incontinence, 4-HNE showed the most consistent group-level separation—lower in DI compared with both Non-DI and healthy controls—whereas LL-37, elafin, VDR, and Aβ1–42 did not demonstrate Bonferroni-corrected pairwise differences. These preliminary findings highlight oxidative and neuroimmune alterations in diabetic incontinence and warrant validation in larger longitudinal studies.