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BACKGROUND: Although Barrett's esophagus (BE) is the precursor of esophageal adenocarcinoma (ACA), most patients with ACA present outside of a BE surveillance program. This could be due to undiagnosed symptomatic GER and BE or BE/ACA occurring in patients without reflux symptoms. We have, therefore, studied the prevalence of BE and symptom status in older patients referred for colonoscopy. METHODS: All patients referred for outpatient colonoscopy were eligible if they were at least 65 yr old and had not previously undergone esophagoscopy. After informed consent, the patients completed detailed GER questionnaires. During the research endoscopy, the endoscopist recorded the squamocolumnar junction (SCJ) as either long-segment BE (LSBE), short-segment BE (SSBE), or normal. If the SCJ was felt to be "irregular" the endoscopist was asked to predict, in their judgment, if BE was present. All patients had biopsies below the SCJ, which were examined by a gastrointestinal pathologist who was blinded to the endoscopic findings. RESULTS: BE esophagus was present in 50 of the 300 patients studied (16.7%). BE was more common in men (35 of 161, 21.7%) than in women (15 of 139, 10.8%) (p < 0.025). GERD symptoms were reported in 106 patients (35%) and BE was present in 19.8% of symptomatic and 14.9% of asymptomatic cases (NS). The majority of the BE in this study was less than 3 cm in length (92%). The questionnaires did not predict the presence of BE. CONCLUSIONS: BE is common in unscreened male and female patients at least 65 yr of age who are referred for colonoscopy. Men were more likely than women to have BE although it occurred in both sexes. Reflux symptoms were fairly common but a poor predictor of BE.  相似文献   
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The pharmacokinetics, pharmacodynamics, and safety of pravastatin, a new selective 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, were evaluated during monotherapy and with subsequent concomitant cholestyramine therapy in 33 patients with primary hypercholesterolemia in this randomized study. After 4 weeks, pravastatin monotherapy (5 mg, 10 mg, and 20 mg twice daily) significantly decreased total cholesterol by 17% to 24% (p less than 0.001 versus baseline) and low-density lipoprotein cholesterol by 23% to 35% (p less than 0.001). High-density lipoprotein cholesterol increased by 8% to 9%, and triglycerides decreased by 6% to 9%. The area under the serum concentration-time curve and maximum serum concentration of pravastatin showed dose-proportionality; time to maximum serum concentration and serum elimination half-life were independent of dose. When added to pravastatin therapy, cholestyramine enhanced the lipid-lowering effects of pravastatin. After 4 weeks of combination therapy, total cholesterol was reduced by 32% to 38% (p less than 0.001 versus baseline), and low-density lipoprotein cholesterol was reduced by 47% to 56% (p less than 0.001). High-density lipoprotein cholesterol increased by 11% to 18% (p less than 0.05). Pravastatin was well tolerated; no clinical adverse events directly attributable to the drug were reported.  相似文献   
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A case of aplastic anemia quickly followed therapy with intravenous chloramphenicol and cimetidine and rapidly resulted in death. This is the second such case reported and the 10th case of fatal aplastic anemia complicating therapy with parenteral chloramphenicol. The patient died 19 days (and the previously reported patient 18 days) after the initiation of intravenous therapy with chloramphenicol and cimetidine; the interval from the start of treatment to death was 414 +/- 683 days (mean +/- SD) in the total of nine evaluatable cases of aplastic anemia following parenteral administration of chloramphenicol. Chloramphenicol and cimetidine, each a rare cause of aplastic anemia, should be used--separately or together--with caution. The case described herein is consistent with reports of liver disease, uremia, or bone marrow dysfunction influencing the toxicities of these drugs. The potential for aplastic anemia must be considered whenever chloramphenicol is used, regardless of the route of administration.  相似文献   
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Contaminant body burdens in lake trout (Salvelinus namaycush) from the Upper Great Lakes have been monitored since 1970 on Lake Michigan and since 1977 and 1978 on Lakes Superior and Huron by United States Environmental Protection Agency (USEPA), Great Lakes National Program Office and U.S. Fish and Wildlife Service (USFWS), Great Lakes Fishery Laboratory. Analysis of the Lake Michigan data shows that mean polychlorobiphenyl (PCB) concentrations declined from a maximum of 22.91 mg/kg in 1974 to 5.63 mg/kg in 1982. Mean total DDT concentrations declined from 19.19 mg/kg in 1970 to 2.74 mg/kg in 1982. The decline in both contaminants closely followed first order loss kinetics. If the current declines continue, PCB concentrations will decline to the U.S. Food and Drug Administration (USFDA) tolerance of 2.0 mg/kg in 1988. Mean total DDT concentrations will fall to the International Joint Commission (IJC) objective of 1.0 mg/kg by 1991. Mean dieldrin concentrations increased significantly from 0.20 mg/kg in 1971 to 0.58 mg/kg in 1979 before declining to 0.21 mg/kg in 1982. The decline from 1979–1982 followed first order loss kinetics. As this decline is not reflected in other species (bloater chubs, smelt) it will require additional years of monitoring to determine if dieldrin concentrations between 1979 and 1982 truly represents a declining trend. The only statistically significant trend other than in Lake Michigan was for total DDT which declined significantly in Lake Superior lake trout. Large data variance and the short time frame covered (1977–1982) interfered with detection of trends on Lakes Superior and Huron.  相似文献   
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