Department of Surgery K, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Br J Surg. 2011 Feb;98(2):210-9. doi: 10.1002/bjs.7339.
The aetiology and pathogenesis of abdominal wall hernia formation is complex. Optimal treatment of hernias depends on a full understanding of the pathophysiological mechanisms involved in their formation. The aim of this study was to review the literature on specific collagen alterations in abdominal wall hernia formation.
A computer-assisted search of the medical databases PubMed and Embase was performed, together with a cross-reference search of eligible papers.
Fifty-two papers were included. Collagen alteration depended on the type of hernia; there were more pronounced changes in patients with a direct inguinal hernia than in those with an indirect inguinal hernia, recurrent inguinal hernia or incisional hernia. A consistent finding was a significant increase in immature type III collagen relative to the stronger type I collagen in patients with a hernia. This resulted in thinner collagen fibres with a correspondingly diminished biomechanical strength. It has been suggested that these alterations are due to variation in the synthesis, maturation or degradation of collagen by matrix metalloproteinases, in combination or alone.
Hernia formation and recurrence is associated with altered collagen metabolism manifested by a decreased type I:III collagen ratio.
腹壁疝形成的病因和发病机制较为复杂。疝的最佳治疗取决于对其形成相关病理生理机制的全面了解。本研究旨在综述腹壁疝形成中特定胶原改变的文献。
计算机辅助检索医学数据库 PubMed 和 Embase,并对符合条件的论文进行交叉参考检索。
共纳入 52 篇论文。胶原改变取决于疝的类型;与间接腹股沟疝、复发性腹股沟疝或切口疝患者相比,直接腹股沟疝患者的改变更为明显。一致的发现是疝患者的不成熟型 III 胶原相对较强的 I 型胶原显著增加。这导致胶原纤维变薄,生物力学强度相应降低。有人认为这些改变是由于基质金属蛋白酶对胶原的合成、成熟或降解的变化,单独或联合引起的。
疝的形成和复发与胶原代谢改变有关,表现为 I 型:III 型胶原比值降低。