Randomized comparison of two rescue therapies for Helicobacter pylori infection.

BACKGROUND: Bismuth salts are not available worldwide. It remains unknown whether clarithromycin can replace bismuth salts as an adjuvant agent in the rescue regimens for Helicobacter pylori infection. We therefore designed the prospective study to compare the efficacies of two rescue therapies for H. pylori infection after standard triple therapies. PATIENTS AND METHODS: Ninety-three patients who failed H. pylori eradication using proton pump inhibitor plus clarithromycin and amoxicillin were randomly assigned to undergo rescue therapy with esomeprazole, clarithromycin, tetracycline and metronidazole (ECTM group, n = 46) or esomeprazole, bismuth subcitrate, tetracycline and metronidazole (EBTM group, n = 47). Follow-up endoscopy was performed at 8 weeks after the end of treatment to assess the treatment response. RESULTS: Intention-to-treat analysis demonstrated both groups had similar eradication rates (ECTM 74% vs. EBTM 77%; P = 0.76) and drug compliance (ECTM 94% vs. EBTM 96%; P = 0.68). However, the frequency of adverse events in the ECTM group was higher than that in EBTM group (ECTM 57% vs. EBTM 36%, P = 0.05). In the EBTM group, eradication rate of metronidazole-resistant strains was lower than that of metronidazole-susceptible strains (67%[8/12] vs. 100%[9/9], P = 0.05). However, eradication rates were similar between metronidazole-susceptible and metronidazole-resistant strains in ECTM group (69%[9/13] vs. 70%[7/10], P = 1.00). CONCLUSIONS: The new ECTM second-line therapy can achieve similar eradication rate as standard EBTM therapy. It may be very useful in countries where bismuth salts are not available.

[Study of color scale B-ultrasonography in syndrome differentiation of biliary tract diseases].

OBJECTIVE: To evaluate the relationship between modern medical detective method of imaging and Syndrome Differentiation of TCM. METHODS: Two hundred and sixteen biliary tract diseases patients were observed with color scale B-ultrasonography and fat meal tests. RESULTS: Eighty-four cases (38.89%) of damp-heat type in the Liver-gallbladder among the 216 patients had widened gallbladder, higher tension and weak bile echo-penetration through, 39 cases (18.06%) of type of Liver-Qi stagnation and Spleen deficiency had small transection, hypotension, slender type and low contraction rate, 13 cases (6.02%) of Blood-stasis type had small gallbladder volume and the contraction rate decrease significantly. There were 71 cases (32.87%) of Liver-Qi stagnation type and 9 cases (4.17%) of Liver Yin-Deficiency type, whose characters of the gallbladder were not prominent, so the identification of these cases depended largely on clinical differentiation. CONCLUSIONS: This study will facilitate the further extending the principle of inspection in the specific organs which may provide us with the objective basis for the differentiation of biliary tract diseases.

[Experimental observation of high portal venous resistance in dogs].

To study the relationship between portal resistance and formation of portal hypertension, we designed a high portal systemic resistance model by injecting bletilla hyacinthina into the intrahepatic portal venulae through the portal vein in 9 dogs. The portal pressure was measured and the portal hemodynamics studied by ultrasonic Doppler before operation, and the data were collected with re-laparotomy after 10, 20 days respectively. Liver function, portal collateral circulation and liver histology were also observed. Our results suggest that the portal high resistance could cause portal hypertension. The elevation of FPP was maintained and portal blood flow was increased constantly in different degrees. The veins of the abdominal wall and esophagus were dilated slightly. Histological study of the liver showed fibrotic hyperplasia in the portal area. Liver function was not markedly changed except elevation of ALP. It seems that the combination of portal resistance and portal hyperdynamics are the necessary pathogenic factor of formation of portal hypertension.