SUMMARYBackground: Eradication rates of Helicobacter pylori with standard triple therapy are disappointing, and studies from several countries confirm this poor performance. Aim: To assess the eradication rate of a new sequential treatment regimen compared with conventional triple therapy for the eradication of H. pylori infection. Methods: One thousand and forty-nine dyspeptic patients were studied prospectively. H. pylori-infected patients were randomized to receive 10-day sequential therapy [rabeprazole (40 mg daily) plus amoxicillin (1 g twice daily) for the first 5 days, followed by rabeprazole (20 mg), clarithromycin (500 mg) and tinidazole (500 mg) twice daily for the remaining 5 days]

Gastric cancer remains the second most frequent cause of cancer-related mortality in the world. Screening programs in some Asian countries are impractical in the majority of other countries worldwide. Therefore, follow-up of precancerous lesions is advisable for secondary gastric cancer prevention. Intestinal metaplasia (IM) is recognized as a precancerous lesion for gastric cancer, increasing the risk by 6-fold. IM is highly prevalent in the general population, being detected in nearly 1 of every 4 patients undergoing upper endoscopy. The IM prevalence rate is significantly higher in patients with Helicobacter pylori (H. pylori) infection, in first-degree relatives of gastric cancer patients, in smokers and it increases with patient age. IM is the "breaking point" in the gastric carcinogenesis cascade and does not appear to regress following H. pylori eradication, although the cure of infection may slow its progression. Gastric cancer risk is higher in patients with incomplete-type IM, in those with both antral and gastric body involvement, and the risk significantly increases with IM extension over 20% of the gastric mucosa. Scheduled endoscopic control could be cost-effective in IM patients, depending on the yearly incidence of gastric cancer in IM patients, the stage of gastric cancer at diagnosis discovered at surveillance, and the cost of endoscopy. As a pragmatic behavior, yearly endoscopic control would appear justified in all IM patients with at least one of these conditions: (1) IM extension > 20%; (2) the presence of incomplete type IM; (3) first-degree relative of gastric cancer patients; and (4) smokers. In the remaining IM patients, a less intensive (2-3 years) could be proposed.

Background : Following standard triple therapy, up to 20% of patients require further Helicobacter pylori eradication treatment. Data regarding the efficacy of re‐treatment in these patients are scarce. Aim : To evaluate the efficacy of a triple therapy after one or more consecutive treatment failures. Methods : A total of 51 patients with persistent H. pylori infection after at least one unsuccessful standard 1‐week regimen were enrolled in the study. H. pylori infection at entry was assessed by rapid urease test and histology on biopsies from the antrum and the corpus. Patients were given a 2‐week triple therapy, comprising ranitidine bismuth citrate 400 mg b.d., tetracycline 500 mg t.d.s., and tinidazole 500 mg b.d. Ranitidine bismuth citrate was given during meals, whilst tetracycline and tinidazole was given after meals. Bacterial eradication was assessed by endoscopy (36 patients) or 13C‐urea breath test (15 patients) 4–6 weeks after therapy had ended. Results : All 51 patients completed the study and H. pylori eradication was achieved in 46, with an eradication rate of 90% (95% CI: 82–98). In detail, bacterial eradication was obtained in 96% of patients who had previously failed one course of clarithromycin–amoxicillin based triple therapy, in 88% patients who had failed a clarithromycin–tinidazole based triple therapy, in 83% patients who had failed both treatment schedules, and in the only patient who had failed three consecutive therapeutic attempts. Two patients took the therapy for 9 and 10 days instead of the full 14 day‐course. No major side‐effects were reported, whilst six (12%) patients complained of mild side‐effects. Conclusion : This study demonstrates that this triple therapy regimen is effective for re‐treatment of H. pylori infection.

The prevalence of diverticulosis and colorectal cancer (CRC) is markedly increased in the last century. Both diseases are highly frequent in Western countries and in aged people. Western diet--low in fiber and rich in dietary fat--has been largely regarded to play a major role in the pathogenesis of both conditions. A causal relationship between diverticulosis and CRC has been suggested in different studies. Epidemiologic series found a more frequent rectosigmoid localization of neoplastic lesions (advanced adenoma and CRC) in patients with diverticulosis as compared with controls, particularly in those with a previous diverticulitis episode or with an extensive disease. However, data are still controversial, with other studies failing to confirm this observation. Such discrepancy could be referred to the highly heterogeneous study design and setting in the different epidemiologic series. Pathologic studies showed that either macroscopic and microscopic chronic inflammation--which is regarded as risk factor for CRC development--is present in the colonic mucosa of some patients with diverticula. Moreover, alterations in the extracellular matrix, also involved in colorectal carcinogenesis, have been depicted in diverticulosis. In addition, an upward shifting of cell proliferation occurs in diverticular mucosa, and in nondiverticular patients with advanced adenomas. Finally, aberrant crypt foci--which are considered potential markers of CRC risk in ulcerative colitis--have been detected in colonic mucosa of patients with diverticulosis. Despite this substantial amount of evidence, however, the available data are not yet strong enough to suggest a more aggressive CRC prevention in diverticular as compared with nondiverticular subjects.

Hepatic encephalopathy (HE) is the second most common major complication in cirrhotics and it significantly impacts quality of life. Therapeutic approaches for HE treatment and prevention mainly continue to rely on ammonia-lowering strategies and non-absorbable disaccharides are currently considered the cornerstone therapy. Non-absorbable antibiotics, such as neomycin and paramomycin, are effective in treatment of acute HE episodes but their prolonged use for recurrence prevention is hampered by possible side-effects. To overcome these limitations, rifaximin use has been proposed. Rifaximin has been shown to be not superior to non-absorbable disaccharides for either HE treatment or prevention, with a similar incidence of side-effects. Cirrhosis significantly increases rifaximin absorption and this could be a cause for concern. Following long-term rifaximin therapy, Clostridium difficile colitis has been observed and Candida albicans has been isolated from 20% of patients. In addition, selection of resistant mutants of both Gram-negative and -positive bacteria in the gastrointestinal tract cannot be definitely ruled out. Electrolyte alterations (sodium and potassium) have been reported during rifaximin therapy, a warning for its long-term use in cirrhotics. Moreover, a potential interference with vitamin K production should be considered which could further impair the already altered clotting status of these patients. The therapeutic cost of rifaximin is markedly higher than non-absorbable disaccharides. While waiting for further safety data, caution should be used to limit the use of rifaximin therapy for a very short-term period in selected HE cirrhotics not responding to non-absorbable disaccharides.