Adenocarcinoma of the esophagogastric junction and Barrett's esophagus.

BACKGROUND & AIMS: Barrett's esophagus is associated with adenocarcinoma of the esophagus. The aim of this study was to find the prevalence of Barrett's esophagus in patients with adenocarcinoma of the esophagogastric junction. METHODS: Consecutive, freshly resected surgical esophagogastrectomy specimens were examined, and multiple histological sections were made around the tumor periphery. Barrett's esophagus was defined as specialized columnar epithelium above the esophagogastric junction. Tumors centered < or = 2 cm from the junction were defined as junction cancers. RESULTS: Barrett's esophagus was found in 9 of 9 (100%) esophageal adenocarcinomas compared with 0 of 8 (0%) squamous carcinoma controls (P < 0.001). Ten of 24 (42%) junction adenocarcinomas had a Barrett's esophagus. A Barrett's esophagus was found in 8 of 12 (67%) junction cancers < or = 6 cm in length but only 2 of 12 (17%) larger tumors (P < 0.05). Barrett's esophagus was significantly associated with junction tumors < 6 cm compared with squamous carcinoma controls (P < 0.02). In 5 specimens with junction cancer, the length of Barrett's esophagus was < 3 cm, and in 5 specimens it was > or = 3 cm. Specialized epithelium was often found below the esophagogastric junction in controls. CONCLUSIONS: Adenocarcinomas of the esophagogastric junction are associated with short and long segments of Barrett's esophagus. Larger cancers probably overgrow and conceal the underlying specialized columnar epithelium from which they arise.

Rest-redistribution thallium-201 scintigraphy to determine myocardial viability early after myocardial infarction.

OBJECTIVES: This study attempted to determine the utility of early rest-redistribution thallium-201 imaging in detecting residual myocardial viability after myocardial infarction. BACKGROUND: The early detection of myocardial viability after myocardial infarction would have clinical relevance. METHODS: Thirty-one patients with acute myocardial infarction had early (mean [+/- SD] 2 +/- 1 day) rest-redistribution thallium-201 imaging followed by radionuclide and coronary angiography. Late studies included stress-redistribution-reinjection thallium-201 imaging or radionuclide angiography, or both. Viability was defined by the rest thallium-201 scan as an initial mild rest defect or any defect that demonstrated redistribution. RESULTS: Group 1 (n = 15) was predicted to have viable and Group 2 (n = 16) nonviable myocardium in the infarct zone. Group 1 patients were more likely to have a patent infarct-related artery (15 of 15 vs. 10 of 16, p < 0.03), higher initial ejection fraction (61 +/- 12% vs. 53 +/- 9%, p < 0.05), higher infarct wall motion score (p < 0.0001) and fewer abnormal thallium-201 segments (p < 0.0001). On follow-up studies, ejection fraction improved in Group 1 (from 57 +/- 13% to 66 +/- 10%, p < 0.05, n = 9) and deteriorated in Group 2 (from 53 +/- 10% to 46 +/- 8%, p < 0.05, n = 13). On late stress testing with thallium-201 reinjection, Group 1 patients had fewer abnormal segments (p < 0.03) and higher infarct zone counts during exercise (p < 0.05) and after reinjection (p < 0.05) than Group 2 patients. CONCLUSIONS: If confirmed by larger studies, early rest-redistribution thallium-201 imaging may be a useful technique for identifying residual viability after myocardial infarction.

Portal vein thrombosis associated with pregnancy. A case report.

This report illustrates a case of portal vein thrombosis that developed in the second trimester of pregnancy. The patient did not have any of the known associations or predisposing factors for portal vein thrombosis or any past medical history of thrombosis or bleeding disorders. Antepartum and postpartum laboratory studies showed no evidence of a coagulation disorder; therefore, it seems that the sole cause of this thrombotic event was the hypercoagulable state of pregnancy.

Barrett's esophagus: age, prevalence, and extent of columnar epithelium.

The development of Barrett's esophagus was studied using data from 51,311 patients undergoing upper gastrointestinal endoscopy between 1976 and 1989. Three hundred seventy-seven patients had greater than or equal to 3-cm columnar epithelium in the esophagus and no carcinoma. The prevalence of Barrett's esophagus increased with age to reach a plateau by the seventh decade. Half of the maximum prevalence was reached by age 40 years, the estimated median age of development of the disorder. Unlike prevalence, the mean length of columnar epithelium did not increase with age. No significant change in length was found in 21 patients followed up for a mean of 7.3 years (mean initial length, 8.29 +/- 0.85 cm; mean final length, 8.33 +/- 0.77 cm). The length of columnar epithelium did not increase in the presence of esophagitis or decrease when esophagitis was absent. Mean age at diagnosis of Barrett's esophagus was 63 years without carcinoma and 64 years in a separate group of patients with adenocarcinoma. The data are consistent with a fairly rapid evolution of Barrett's esophagus to its full length with little subsequent change. Barrett's esophagus may develop more than 20 years before the mean age of clinical recognition or the development of esophageal adenocarcinoma.