Rosch R, Junge K, Knops M, Lynen P, Klinge U, Schumpelick V
Department of Surgery, University Hospital, RWTH, Pauwelsstrasse 30, 52074, Aachen, Germany.
Langenbecks Arch Surg. 2003 Feb;387(11-12):427-32. doi: 10.1007/s00423-002-0345-3. Epub 2003 Jan 15.
In recent years a disorder of the collagen metabolism has been suggested for the pathogenesis of abdominal wall hernias. Previous investigations of skin specimens revealed a reduction in the collagen I/III ratio and alterations in matrix metalloproteinases in patients with incisional hernias. We investigated known collagen-interacting proteins to further characterize connective tissue in these patients.
Skin scars from patients with either primary or recurrent incisional and recurrent inguinal hernias, as a subgroup of incisional hernias, were analyzed for overall collagen content and for the distribution of collagen types I and III by crosspolarization microscopy. The expression of collagen type V, collagen receptor discoidin domain receptor 2, matrix metalloproteinase 1, connective tissue-like growth factor, and tenascin was determined by immunohistochemistry. Mature abdominal skin scars from patients without evident hernia served as controls.
Patients with recurrent incisional hernia showed lowest ratios of collagen types I to III. Contents of overall collagen and of collagen type V did not differ between the groups. In patients with either primary or recurrent incisional hernias the proportion of collagen receptor discoidin domain receptor 2 positive cells was increased. Matrix metalloproteinase 1 expression was more pronounced in patients with recurrent incisional or inguinal hernias than in controls. Connective tissue-like growth factor was significantly increased in recurrent inguinal hernia patients. The expression of tenascin was notably decreased in all hernia groups.
The observed alterations in the expression of collagen-interacting proteins again indicate the possibility of a fundamental connective tissue disease as the causal factor in the pathogenesis of (recurrent) incisional hernias.
近年来,有人提出胶原代谢紊乱与腹壁疝的发病机制有关。先前对皮肤标本的研究显示,切口疝患者的I型/III型胶原比例降低,基质金属蛋白酶也有改变。我们研究了已知的胶原相互作用蛋白,以进一步明确这些患者结缔组织的特征。
分析原发性或复发性切口疝以及复发性腹股沟疝(作为切口疝的一个亚组)患者的皮肤瘢痕,通过交叉偏振显微镜观察总胶原含量以及I型和III型胶原的分布情况。采用免疫组织化学法测定V型胶原、胶原受体盘状结构域受体2、基质金属蛋白酶1、结缔组织生长因子样蛋白和腱生蛋白的表达。无明显疝的患者成熟腹部皮肤瘢痕作为对照。
复发性切口疝患者的I型/III型胶原比例最低。各组之间的总胶原含量和V型胶原含量无差异。原发性或复发性切口疝患者中,胶原受体盘状结构域受体2阳性细胞的比例增加。复发性切口疝或腹股沟疝患者的基质金属蛋白酶1表达比对照组更明显。复发性腹股沟疝患者的结缔组织生长因子样蛋白显著增加。所有疝组的腱生蛋白表达均明显降低。
观察到的胶原相互作用蛋白表达改变再次表明,存在一种基本的结缔组织疾病作为(复发性)切口疝发病机制中的致病因素的可能性。