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贲门失弛缓症患者食管外膜的免疫组织化学研究。

Immunohistochemical study of the muscularis externa of the esophagus in achalasia patients.

机构信息

Department of Surgery, Jikei University School of Medicine, 3-19-18 Nishishinbashi, Minato-ku, Tokyo, Japan.

出版信息

Dis Esophagus. 2013 Jan;26(1):14-21. doi: 10.1111/j.1442-2050.2011.01318.x. Epub 2012 Feb 6.

Abstract

The etiology of achalasia is believed to be the neuropathy associated with chronic inflammation of the nerve plexus, but the cause of plexus inflammation is unknown. The purpose of this study was to evaluate the pathophysiology of achalasia by examining the muscularis externa of the esophagus. We used the muscularis externa of the esophagus of 62 patients with achalasia (median 44 years, male : female 32:30) who underwent surgical treatment (achalasia group) and of 10 patients (median 65.5 years, male : female 9:1) who underwent esophagectomy for thoracic esophageal cancer (control group) to perform immunohistochemical staining with S-100, CD43, c-kit (CD117), n-NOS, vasoactive intestinal polypeptide (VIP), and ubiquitin. The cell counts that were positive for S-100, n-NOS, VIP, and ubiquitin were significantly lower in the achalasia group compared with the control group (P < 0.001, P= 0.001, P < 0.001, and P= 0.001, respectively). There were no statistically significant differences with respect to CD43 and c-kit staining (P= 0.586 and P= 0.209, respectively). In conclusion, the pathophysiology of achalasia is therefore considered to be an impaired production of NO and VIP, which both affect interstitial cell of Cajal and smooth muscles, and this impairment is therefore considered to play a role in the pathophysiology of achalasia.

摘要

贲门失弛缓症的病因被认为是与神经丛慢性炎症相关的神经病变,但神经丛炎症的原因尚不清楚。本研究旨在通过检查食管外膜来评估贲门失弛缓症的病理生理学。我们使用了 62 例贲门失弛缓症患者(中位年龄 44 岁,男:女 32:30)和 10 例因胸段食管癌而行食管切除术的患者(中位年龄 65.5 岁,男:女 9:1)的食管外膜进行免疫组织化学染色,用 S-100、CD43、c-kit(CD117)、n-NOS、血管活性肠肽(VIP)和泛素进行染色。与对照组相比,贲门失弛缓症组 S-100、n-NOS、VIP 和泛素阳性细胞计数显著降低(P<0.001,P=0.001,P<0.001 和 P=0.001),而 CD43 和 c-kit 染色则无统计学差异(P=0.586 和 P=0.209)。总之,贲门失弛缓症的病理生理学被认为是一氧化氮和 VIP 产生受损,这两者均影响 Cajal 间质细胞和平滑肌,这种损害被认为在贲门失弛缓症的病理生理学中起作用。

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