den Braber-Ymker M, Vonk M C, Grünberg K, Lammens M, Nagtegaal I D
Department of Pathology 824, Radboud University Medical Center, PO Box 9101, 6500, HB, Nijmegen, The Netherlands.
Department of Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands.
Clin Rheumatol. 2021 Mar;40(3):981-990. doi: 10.1007/s10067-020-05325-8. Epub 2020 Aug 18.
The pathogenesis of intestinal involvement in systemic sclerosis (SSc) is thought to be a sequential process (vascular, neuronal, and consecutive muscular impairment), but understanding of the underlying histological changes and how they translate to symptoms, is still lacking. Therefore, we systematically investigated histological characteristics of SSc in the intestines, compared to controls.
Autopsy material from the small bowel and colon was used for histological semiquantitative evaluation of the vasculature, enteric nervous system, interstitial cells of Cajal (ICC), and muscle layers, using a combination of histochemical and immunohistochemical stainings, according to guidelines of the Gastro 2009 International Working Group.
Vascular changes were most frequently encountered, represented by intima fibrosis in both arteries and small vessels, and represented by venous dilatation. Second, generalized fibrosis of the circular muscle layer was significantly more found in SSc patients than in controls. Third, reduction of submucosal nerve fibers and myenteric neurons was shown in the colon of four SSc patients, which may explain severe symptoms of intestinal dysmotility. The density of myenteric ICC network was decreased in the small bowel of SSc patients.
The postulated sequential processes of intestinal involvement in SSc could not be supported by our histological evaluation. The interpatient diversity suggests that parallel processes occur, explaining the variety of histological features and clinical symptoms. Key Points • Histological analysis showed vascular changes, fibrosis in the muscularis propria, and reduction of the ENS and ICC network in the intestines of SSc patients. • Pathophysiological mechanisms leading to intestinal dysmotility in SSc may be parallel rather than sequential. • The interpatient diversity suggests parallel pathophysiological processes, explaining the variety of histological features and clinical symptoms.
系统性硬化症(SSc)肠道受累的发病机制被认为是一个连续的过程(血管、神经及随后的肌肉损伤),但对潜在的组织学变化及其如何转化为症状仍缺乏了解。因此,我们系统地研究了SSc患者肠道的组织学特征,并与对照组进行比较。
根据2009年胃肠病国际工作组指南,使用组织化学和免疫组织化学染色相结合的方法,对小肠和结肠的尸检材料进行血管系统、肠神经系统、 Cajal间质细胞(ICC)和肌层的组织学半定量评估。
血管变化最为常见,表现为动脉和小血管内膜纤维化以及静脉扩张。其次,SSc患者环形肌层的广泛性纤维化明显多于对照组。第三,4例SSc患者的结肠显示黏膜下神经纤维和肌间神经元减少,这可能解释了严重的肠道动力障碍症状。SSc患者小肠中肌间ICC网络的密度降低。
我们的组织学评估无法支持SSc肠道受累的假定连续过程。患者间的差异表明存在并行过程,这解释了组织学特征和临床症状的多样性。要点 • 组织学分析显示SSc患者肠道存在血管变化、固有肌层纤维化以及肠神经系统和ICC网络减少。 • SSc导致肠道动力障碍的病理生理机制可能是并行的而非连续的。 • 患者间的差异表明存在并行的病理生理过程,这解释了组织学特征和临床症状的多样性。