ABSTRACT
To assess the efficacy of the additional treatment of transcatheter arterial chemoembolization (TACE) to percutaneous ethanol injection (PEI) therapy for relatively small hepatocellular carcinomas (HCCs), a multicenter randomized control study (RCT) was performed. We conducted an RCT and follow-up study during the enrollment period from 1997 to 1999. Newly diagnosed patients with one to three HCC tumors measuring from 2 to 4 cm (4 cm maximum) in diameter were enrolled. A total of 30 patients initially underwent a combination TACE-PEI or PEI-alone therapies at eight randomly assigned Japanese hospitals. However, 3 patients withdrew. Of the 27 remaining patients, 13 were treated with the combination TACE-PEI therapy and 14 with PEI therapy alone. The patients were observed over several months [median (interquartile range) 33.2 (24.6) months]. There were no significant differences in the background of the patients between the two groups. Among the patients treated with TACE-PEI, the development of a local residual tumor was of significantly lower occurence, compared to the group receiving PEI alone (7.6 and 42.9%, respectively; P=0.024). However, the mean cancer-free time (absence of local or multiple nodule recurrence) or patient survival time was not significantly different between the two groups [PEI alone vs. TACE-PEI: cancer-free time 16.7 (95% CI 7.3-26.0) vs. 22.9 months (95% CI 12.4-33.4); survival time 57.2 (95% CI 37.2-77.2) vs. 42.4 months (95% CI 29.2-55.6)]. Although the combination of TACE and PEI had significant effects on the local tumor control, no efficacy of the addition of TACE to PEI was noted in the prognosis among patients with relatively small HCC tumors.
ABSTRACT
BACKGROUND: Whether or not the eradication of Helicobacter pylori is a risk factor for reflux esophagitis (RE) is a question at issue. To find an answer, it is necessary to clarify the influence of H. pylori eradication on the mechanism of RE. METHODS: The authors investigated the influence of H. pylori eradication on gastric acidity and gastroesophageal reflux in ten gastric ulcer (GU) patients and ten duodenal ulcer (DU) patients by 24-h simultaneous determination of pH in the stomach and esophagus. RESULTS: Though the results indicated enhanced gastric acidity in GU patients at night after H. pylori eradication, no such influence was observed in DU patients. No significant changes in gastroesophageal reflux occurred in GU or DU patients before and after H. pylori eradication. RE after H. pylori eradication occurred in only one patient, with GU. This patient had several risk factors for RE, such as obesity, male sex, and dietary habits to add to the increase in gastric acidity at night that occurred after H. pylori eradication. No increase in gastroesophageal reflux occurred in any DU patients or in the other GU patients that demonstrated enhanced gastric acidity at night after H. pylori eradication. CONCLUSIONS: The cure of H. pylori infection does not, by itself, cause RE in patients who have few other risk factors for RE.
