Role of fascial collagen in stress urinary incontinence

Objectives: Our purpose was to determine whether collagen of the pubocervical fasciae that support the urethrovesical junction undergoes alterations that might contribute to incontinence. Study Design: Pubocervical fascia was collected as a residual tissue in 82 patients, aged 25 to 73 years, during...

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Veröffentlicht in:American journal of obstetrics and gynecology 1998-12, Vol.179 (6), p.1511-1514
Hauptverfasser: Rechberger, Tomasz, Postawski, Krzysztof, Jakowicki, Jerzy A., Gunja-Smith, Zeenat, Woessner, J.Frederick
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Sprache:eng
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Zusammenfassung:Objectives: Our purpose was to determine whether collagen of the pubocervical fasciae that support the urethrovesical junction undergoes alterations that might contribute to incontinence. Study Design: Pubocervical fascia was collected as a residual tissue in 82 patients, aged 25 to 73 years, during surgical treatment of cystocele (n = 26, no incontinence) or of stress urinary incontinence (n = 56). Measurements were made of collagen content, solubility, and cross-linking and of collagenase activity. Results: Patients treated for incontinence had the same mean age and parity as the control cystocele group. There was a highly significant (20%, P < .0005) decrease in collagen content in fascial tissue from incontinent women. There was no difference in the percentage of acid-soluble (0.7%) and pepsin-soluble (17%) collagen in the 2 groups of patients; this agrees with the lack of significant change in the degree of collagen cross-linking by pyridinoline. Collagenase activity was significant in fascia but did not change in incontinence. Incontinent women had an increased body mass index. Conclusions: The pubocervical fasciae of incontinent women show a diminished content of collagen, but this is not accompanied by changes in collagen solubility or cross-linking or in collagenase activity. This decrease in collagen may contribute to the weakening of support of the bladder neck. (Am J Obstet Gynecol 1998;179:1511-4.)
ISSN:0002-9378
1097-6868
DOI:10.1016/S0002-9378(98)70017-1