2000
DOI: 10.1016/s0016-5107(00)70289-6
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Nonmalignant obstruction is a common problem with metal stents in the treatment of esophageal cancer

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Cited by 120 publications
(68 citation statements)
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“…Tissue overgrowth is caused by tumor tissue from progressive tumor growth or by nonmalignant hyperplastic tissue growth at the end of the stent. Mayoral et al [21] reported that recurrent dysphagia was caused by nonmalignant obstructive tissue such as granulation tissue, reactive hyperplasia, and fibrosis at the proximal or distal end of the stent in 32% of patients after a mean interval of 22 weeks.…”
Section: Discussionmentioning
confidence: 99%
“…Tissue overgrowth is caused by tumor tissue from progressive tumor growth or by nonmalignant hyperplastic tissue growth at the end of the stent. Mayoral et al [21] reported that recurrent dysphagia was caused by nonmalignant obstructive tissue such as granulation tissue, reactive hyperplasia, and fibrosis at the proximal or distal end of the stent in 32% of patients after a mean interval of 22 weeks.…”
Section: Discussionmentioning
confidence: 99%
“…This hyperplastic tissue reaction can be clinically manifest as early as 2 weeks after stent placement and also at a later stage. 28 Moreover, tissue inand ⁄ or overgrowth may complicate removal of PSEMS in patients, resulting in a second oesophageal perforation.…”
Section: (98)mentioning
confidence: 99%
“…The application of DXM to coronary or peripheral arteries has been investigated to reduce neointimal hyperplasia by the following plausible mechanisms; i.e., reduction of inflammatory cells at the site of vessel wall trauma, inhibition of leukocyte adhesion to endothelial cells, decrease of plateletderived growth factor (PDGF) expression, inhibition of smooth muscle cell proliferation, and inhibition of the expression of the fibroblast-and macrophage-bound metal- loproteinase which influences the synthesis of extracellular matrix [12,16,19]. Since granulation tissue is histologically highly vascularized connective tissue composed of newly formed capillaries, numerous fibroblasts, and inflammatory cells [20,21], and vascular proliferation is usually followed by division of the endothelial cells and an increase in the number of cells as a response to chronic inflammation [20], we surmise that similar mechanisms of DXM will apply to the tissue reaction secondary to stent placement in non-vascular luminal organs such as the tracheobronchial tree, urethra or esophagus. This conjecture is also supported by previous reports that subepithelial fibrosis or smooth muscle cell proliferation is significantly suppressed by locally administered DXM in bovine and mouse airway models [22,23].…”
Section: Discussionmentioning
confidence: 99%