Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
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Clinical Trial
Ketoconazole and pulmonary failure after esophagectomy: a prospective clinical trial.
Thromboxane is a key mediator in pulmonary injury after esophageal resection. In this prospective trial we studied the clinical course and development of pulmonary alterations in patients undergoing esophagectomy and prophylactic treatment with a thromboxane synthase inhibitor. Thirty-eight consecutive patients undergoing esophageal resection were treated pre- and perioperatively with 3 x 200 mg ketoconazole. ⋯ However, in the ketoconazole group, more patients were at risk of pulmonary failure by receiving neoadjuvant radiochemotherapy (22/38) or undergoing thoracotomies (33/38) than control subjects (14/118 and 80/118, P < 0.05). Two out of 38 ketoconazole-treated patients developed acute lung injury after esophagectomy, as did 20/118 control patients (P < 0.05). This prospective non-randomized clinical study (in patients subjected to esophagectomy) provides further evidence that prophylactic thromboxane synthase inhibition by ketoconazole reduces the incidence of acute lung injury in patients at risk.
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Gastroesophageal reflux is a major postoperative problem in esophageal patients with cancer, and the principal cause is resection of the lower esophageal sphincter. Two new antireflux operations to solve this problem were investigated. The number of patients studied was 139, with a male to female ratio of 5. ⋯ Postoperative preanastomotic mean pressure was 14.2 mmHg. Postoperative mucosal biopsies revealed a remarkable reduction in esophagitis. The radiologic, manometric, and histologic findings as well as the patient satisfaction rate suggest that these antireflux operations are suitable and effective for patients undergoing esophageal resection and intrathoracic esophagogastric anastomosis.
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Post-operative chylothorax and chyloperitoneum resulting from a thoracic duct injury are possible complications of esophagectomy for carcinoma. Management of such conditions includes conservative methods (pleural drainage, chyle flow reduction and supportive nutrition) and surgery. ⋯ Etilefrine infusion allowed chyle flow resolution in a few days without any side-effects. As result of this experience, we believe that etilefrine deserves to be considered as an alternative therapy in the management of post-esophagectomy chylothorax/chyloperitoneum.
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Paraesophageal bronchogenic cysts are a rare developmental anomaly of the upper digestive tract. Although often asymptomatic, their growth can cause severe symptoms and complications because of the location. ⋯ The authors present a case of a paraesophageal bronchogenic cyst, of typical histologic structure (ciliated epithelium and hyaline cartilage) connected with the esophageal lumen by a narrow canal composed of stratified squamous epithelium. According to the available literature, only three cases of bronchogenic paraesophageal cysts with esophageal communication have been reported.
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Comparative Study
Influence of surgically induced gastric and gastroduodenal content reflux on esophageal carcinogenesis--experimental model in Wistar female rats.
Studies in human beings and animals have shown that esophageal exposure to duodenal and gastric contents may be important for the development of Barrett's esophagus and its complications, including adenocarcinoma and epidermoid carcinoma. Diethylnitrosamine (DEN) is a carcinogen that stimulates the development of epidermoid carcinoma in the esophagus of mice. The aim of this study was to evaluate the effect of gastroduodenal and gastric content reflux on induction of esophageal carcinogenesis. ⋯ Rats treated with DEN alone developed papillomas in 50.0% of the cases and remained histologically unchanged in 50.0%. There was no development of low- or high-grade dysplasia in any group. The conclusions are that (1) GDER is significantly more deleterious to esophageal mucosa than GER; (2) in this study, GER did not present carcinogenic potential in relation to the esophagus; (3) GDER in isolation is an esophageal carcinogen, producing Barrett's esophagus and esophageal adenocarcinoma; (4) esophageal oncogenesis caused by GDER is potentiated by DEN, inducing esophageal epidermoid carcinoma; (5) in this study, DEN in isolation did not generate tumors in the esophagus of rats.