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因隆突下淋巴结病导致食管外压性压迫引起吞咽困难的内镜、影像学及测压检查结果。

Endoscopic, radiographic, and manometric findings in dysphagia associated with sarcoid due to extrinsic esophageal compression from subcarinal lymphadenopathy.

作者信息

Cappell M S

机构信息

Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick.

出版信息

Am J Gastroenterol. 1995 Mar;90(3):489-92.

PMID:7872293
Abstract

Esophageal dysphagia associated with sarcoid has been attributed to dysmotility from neuropathy, dysmotility from myopathy, mechanical obstruction from esophageal mural involvement, and mechanical obstruction from extrinsic compression by subcarinal lymphadenopathy. The relative importance of these etiologies has not been evaluated because of variable and nonstandardized analysis. In particular, manometry has not been performed to exclude esophageal dysmotility in dysphagia attributed solely to extrinsic compression. A 42-yr-old male with chronic sarcoid for 20 yr presented with mild dysphagia to solids. An upper gastrointestinal series revealed smooth narrowing of the esophageal lumen and transient hang-up of the barium column and a 1.3-cm diameter radiopaque pill at the level of the carina. Chest computerized tomography revealed esophageal narrowing at the level of the carina and splaying of the two mainstem bronchi from compression by subcarinal lymphadenopathy. Esophagogastroduodenoscopy revealed elliptical esophageal narrowing due to multiple, smooth, and nodular deformities at 29-32 cm from the incisors. Pathological examination of deep biopsies of the nodules revealed normal mucosa and submucosa without granulomas. Esophageal manometry revealed a highly localized high pressure zone of 39.8 +/- 6.1 mm Hg at 29-31 cm from the incisors (lab normal about -5 mm Hg). Esophageal muscle contractions were peristaltic and of normal amplitude above, within, and below this high pressure zone. This case report demonstrates that extrinsic compression from subcarinal lymphadenopathy is a sufficient mechanism for dysphagia with sarcoid, but it does not exclude a role for other mechanisms, such as nerve injury, in some cases.

摘要

结节病相关的食管吞咽困难被认为是由神经病变导致的运动障碍、肌病导致的运动障碍、食管壁受累引起的机械性梗阻以及隆突下淋巴结肿大引起的外部压迫导致的机械性梗阻所致。由于分析方法的不一致和不标准化,这些病因的相对重要性尚未得到评估。特别是,对于仅归因于外部压迫的吞咽困难,尚未进行测压以排除食管运动障碍。一名患有20年慢性结节病的42岁男性出现轻度固体食物吞咽困难。上消化道造影显示食管腔平滑狭窄,钡剂柱短暂滞留,隆突水平有一个直径1.3厘米的不透X线药丸。胸部计算机断层扫描显示隆突水平食管狭窄,隆突下淋巴结肿大压迫导致两个主支气管分开。食管胃十二指肠镜检查显示,在距门齿29 - 32厘米处,由于多个平滑和结节状畸形导致食管呈椭圆形狭窄。结节深部活检的病理检查显示黏膜和黏膜下层正常,无肉芽肿。食管测压显示,在距门齿29 - 31厘米处有一个高度局限的高压区,压力为39.8±6.1毫米汞柱(实验室正常约为 - 5毫米汞柱)。在这个高压区上方、区内及下方,食管肌肉收缩呈蠕动性,幅度正常。本病例报告表明,隆突下淋巴结肿大引起的外部压迫是结节病导致吞咽困难的一个充分机制,但在某些情况下并不排除其他机制(如神经损伤)的作用。

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