Randomized comparison of 1-hour topical method vs. amoxycillin plus omeprazole for eradication of Helicobacter pylori in duodenal ulcer patients.

BACKGROUND: A novel 1-h topical method eradicated Helicobacter pylori in 96% of dyspeptic patients. The eradication rate of amoxycillin/omeprazole therapy varies from 0 to 93%. AIM: To compare both methods in patients with endoscopically proven duodenal ulcer. METHODS: Eighty patients (59 males, 21 females; median age 43 years) were randomized into two therapeutic groups. The first group (group A) was treated with a 6-week course of ranitidine 300 mg/day, then omeprazole 20 mg b.d. with pronase 36000 units/day for 2 days, followed by 1-h topical therapy with a solution of bismuth, metronidazole, amoxycillin and pronase. The second group (group B) consisted of patients treated with omeprazole 20 mg b.d. and amoxycillin 2 g/day for 2 weeks, followed by a 4-week course of ranitidine 300 mg/day. Eradication of H. pylori was assessed by urease test, histology, a polymerase chain reaction and a 13C-urea breath test, all of which were performed 4 weeks after discontinuation of the antibacterial treatment. RESULTS: Eradication rates in groups A and B were 2.5% and 35% in an intention-to-treat analysis, respectively. Side-effects were encountered in 40.5% and 12.5% of subjects in groups A and B, respectively. Treatment tolerance was rated as poor by 54% of patients in group A and 2.5% of patients in group B. CONCLUSIONS: Both treatment regimens, the 1-h topical method and amoxycillin with omeprazole, have low eradication rates in patients with duodenal ulcer. In addition, the topical treatment is characterized by a high rate of side-effects and poor tolerance. Based on the results of our study, neither method can be recommended for eradication of H. pylori in patients with duodenal ulcer.

The role of nitric oxide in portal hypertensive systemic and portal vascular pathology.

Hypotension, low systemic vascular resistance and reduced sensitivity to vasoconstrictor are features of hyperdynamic syndrome in portal hypertension (PH) and are pathogenetic factors triggering most serious clinical complications of liver cirrhosis. Nitric oxide (NO) is a powerful vasodilating agent, released from vascular endothelium cell and effecting relaxation of vascular smooth muscle. An increased release of NO has been proposed to play a role in the pathogenesis of vasodilation and vascular hypocontractility associated with PH. In agreement with this hypothesis, the whole-body production of NO has been found to be increased in PH, and the measurement of NOS mRNA expression in different organs suggest that the splanchnic vascular system is a major source of NO release. Consequently, NO could play a role in the development of the splanchnic hyperaemia, collateral circulation and portal hypertensive gastropathy. Furthermore, increased generation of NO in central circulation likely accounts for pulmonary vasorelaxation and cardiac dysfunction found in cirrhosis. By contrast, PH-associated endothelial dysfunction seems to invalidate the capability of intrahepatic and intrarenal vasculature to produce NO. A deficient NO release in these vascular territories might contribute to enhancement of PH and development of the hepatorenal syndrome. Overall NO hyperproduction is either the cause (induction of iNOS) or the consequence (stimulation of ecNOS) of the hyperdynamic syndrome. This incertitude results from the yet undefined significance of mild and transitory activation of the endotoxin-cytokines axis for iNOS induction and contradictory data on specific iNOS and ecNOS activities. A contribution of each isoform of NOS to pathogenesis of the hyperdynamic syndrome probably depends on the model of PH in animal studies and the aetiology or severity of cirrhosis in human studies.

[Isotope methods in diagnosis of portal vein occlusion]. / Metody izotopowe w diagnostyce niedroznosci zyly wrotnej.

The dynamic intravenous hepato-scintigraphy with pertechnetate Tc-99m enables a quantitative evaluation of portal and arterial blood flow in the liver. A case is presented of thrombotic occlusion of the portal vein with rapidly growing oesophageal varices in which hepato-scintigraphy showed the absence of portal blood flow in the liver, being the decisive diagnostic method. Using the dynamic transrectal porto-scintigraphy an evaluation was done of the degree of collateral circulation development in the area of the inferior mesenteric vein, obtaining indirect information about localization and duration of portal vein occlusion.