Cameron lesions: A still overlooked diagnosis. Case report and systematic review of literature.

Cameron lesions are erosive-ulcerative alterations of gastric mucosa occurring in patients with large hiatal hernia, potentially causing gastrointestinal bleeding and iron deficiency anaemia. Diagnosis may be challenging, and not infrequently erosions are overlooked at endoscopy, so that repeated and unnecessary diagnostic procedures are performed, particularly in those patients with chronic anaemia. We described two peculiar cases of patients with iron deficiency anaemia in whom Cameron lesions were either overlooked or misinterpreted. By reviewing data of 22publications reporting endoscopic and clinical data of 140patients, we noted a large prevalence of females (75%). The most frequent presenting symptoms were anaemia (62%) and overt gastrointestinal bleeding (36%). Noteworthy, as many as 69% of patients underwent one or more previous upper endoscopy before diagnosis of Cameron lesion was achieved. Patients were mainly treated with proton pump inhibitor (PPI) therapy and iron supplementation. Moreover, endoscopic haemostasis was performed in 10% of case, blood transfusion was required in one third of cases, and a similar quote of patients underwent a surgical approach for hiatal hernia repair. The observation that as many as 60% patients were already receiving standard PPI therapy when diagnosis was performed would suggest that either long-term treatment with adequate dose PPI or surgical approach for hiatal hernia repair is required. In conclusion, Cameron lesion is still an overlooked diagnosis in patients with iron deficiency anaemia in whom a 5-9.2% prevalence has been reported.

Triple therapies plus different probiotics for Helicobacter pylori eradication.

The Helicobacter pylori (H. pylori) cure rate following standard triple therapies is decreasing worldwide. Therefore, further approaches aimed to improve standard triple therapy efficacy should be attempted. This prospective, pilot study aimed to evaluate the therapeutic role of either Lactobacillus reuteri (L. reuteri) or a high concentration of probiotics in addition to standard triple therapies for H. pylori eradication. The study enrolled 65 consecutive dyspeptic patients with H. pylori infection. All patients underwent upper endoscopy with gastric biopsies. Patients were assigned to receive one of the following therapies: (a) standard 7-day triple; (b) the same 7-day triple therapy plus L. reuteri supplementation; (c) the same 7-day triple therapy plus a probiotic mixture; and d) a 14-day standard triple therapy plus a probiotic mixture. H. pylori eradication was checked by using a 13C-urea breath test performed 4-6 weeks after treatment. No therapy regimen achieved > 80% eradication rate at both intention-to-treat (ITT) and per protocol (PP) analyses. Although the 14-day therapy plus a probiotic mixture tended to achieve higher eradication rate (71%), no statistically significant difference emerged among the different therapy regimens tested (range: 53-71%). The lowest incidence of side-effects was observed following the 7-day therapy plus L. reuteri (6%) and highest with the 14-day triple therapy plus probiotic mixture (33%), although the difference failed to reach the statistically significance. In conclusion, our data found that 7-14 days triple therapy with or without probiotic supplementation failed to achieved acceptable H. pylori eradication rates.

Q&A on diagnosis, screening and follow-up of colorectal neoplasia.

The impressive and brisk evolution of medical science prevents many physicians from a thorough update on all the research fields. Colorectal cancer diagnosis, screening and follow-up is well known to require a multi-disciplinary approach, as it is faced by several specialties such as primary care physicians, gastroenterologists, non-gastroenterologist internists, radiologists and surgeons. To address this issue in a mutual perspective, we focused on the main points of the epidemiology, diagnosis, screening and follow-up of colorectal neoplasia by using a simple "Question & Answers" structure.

Antibiotic treatment strategies for Helicobacter pylori infection.

In the third decade of the Helicobacter pylori era several informations are available on its pathogenetic mechanisms, as well as on therapeutic approaches. A 7-14 day triple or quadruple regimens (proton pump inhibitor together with 2 antibiotics) are currently suggested as first-line treatment, but the success rate following these therapy is constantly decreasing worldwide. Therefore, new drugs are needed to treat such a widespread infection. Several patents of new antibiotics have been claimed in the last 5 years, and some of them showed a very powerful antibacterial activity in vitro, even against clarithromycin and metronidazole resistant strains. Among the new compounds, thienylthiazole derivatives, benzamide derivatives and pyloricidins should be regarded as very promising molecules.

Sequential treatment for Helicobacter pylori eradication in duodenal ulcer patients: improving the cost of pharmacotherapy.

BACKGROUND: Several studies have shown that Helicobacter pylori eradication rates with standard 7-day triple therapy are unsatisfactory. A novel 10-day sequential treatment regimen recently achieved a significantly higher eradication rate. To improve the pharmacotherapeutic cost, we evaluated whether an acceptable eradication rate could be achieved in peptic ulcer patients by halving the dose of clarithromycin. METHODS: In a prospective, open-label study, 152 duodenal ulcer patients with H. pylori infection, assessed by rapid urease test and histology, were enrolled. Patients were randomized to receive either a 10-day sequential treatment comprising rabeprazole 20 mg b.d. plus amoxicillin 1 g b.d. for the first 5 days, followed by rabeprazole 20 mg b.d., clarithromycin 500 mg b.d. and tinidazole 500 mg b.d. for the remaining 5 days (high-dose therapy), or a similar schedule with the clarithromycin doses halved to 250 mg b.d. (low-dose therapy). No further antisecretory drugs were offered. Four to six weeks after therapy, H. pylori eradication and ulcer healing rates were assessed by endoscopy. RESULTS: Similar H. pylori eradication rates were observed following high- and low-dose regimens for both per protocol (97.3% vs. 95.9%; P = N.S.) and intention-to-treat (94.7% vs. 92.2%; P = N.S.) analyses. No major side-effects were reported. At repeat endoscopy, peptic ulcer healing was observed in 93% and 93% of patients following high- and low-dose therapy, respectively. CONCLUSION: The cheaper low-dose sequential regimen may be suggested for H. pylori eradication in duodenal ulcer patients, even without continued proton pump inhibitor therapy after eradication treatment.

Zinc supplementation reduces blood ammonia and increases liver ornithine transcarbamylase activity in experimental cirrhosis.

Zinc deficiency is common in cirrhosis and may be involved in the alteration of ammonia metabolism. Rats with carbon tetrachloride-induced cirrhosis have high plasma ammonia and low serum and tissue zinc levels. We used this model to examine the effects of oral zinc supplementation on activities of plasma ammonia and liver ornithine transcarbamylase (a key enzyme in the urea cycle). These parameters were examined in two consecutive experiments. Each experiment included two groups of rats treated with carbon tetrachloride; one group received zinc in the drinking water during the induction of cirrhosis, and another served as a control group. Regardless of zinc supplementation, all carbon tetrachloride-treated rats exhibited similar micronodular cirrhosis, with similar histological appearance and liver function impairment. Cirrhotic rats without zinc supplementation showed high plasma ammonia and low serum and hepatic zinc levels and reduced liver ornithine transcarbamylase activity. Serum, hepatic zinc and liver ornithine transcarbamylase activity increased significantly in the zinc-supplemented group, and these rats' plasma ammonia levels became normal. Plasma ammonia level was significantly inversely correlated with liver ornithine transcarbamylase activity and positively correlated with serum and hepatic zinc content. Our results suggest that zinc deficiency may modify hepatic ornithine transcarbamylase activity and, therefore, ammonia disposal.

Short-term oral zinc supplementation does not improve chronic hepatic encephalopathy. Results of a double-blind crossover trial.

The effect of short-term oral zinc supplementation (zinc sulfate 600 mg/day) on hepatic encephalopathy, was assessed in a double-blind, crossover trial. Fifteen cirrhotic patients with stable, chronic hepatic encephalopathy were randomized to receive either oral zinc or a placebo for 10 days. Following a two-week washout period, these were crossed over to the alternate treatment. Conn's index, which comprises the evaluation of the mental state, asterixis, number connection test, EEG record, and plasma ammonia, was used to score the degree of hepatic encephalopathy, both at the beginning and end of each treatment period. Serum zinc was significantly raised after oral zinc administration and reached the levels observed in cirrhotics without hepatic encephalopathy. Despite this, however, no modification in the parameters included in Conn's index were observed. In conclusion, this study failed to confirm that short-term oral zinc supplementation improves chronic hepatic encephalopathy.

Zinc and other trace elements in liver cirrhosis.

Alterations in trace element concentrations may be observed in patients with chronic liver disease. Notably, selenium and zinc levels are reduced both in serum and in liver tissue of cirrhotic patients. Low selenium levels have been involved in the pathogenesis of liver damage as this element is important in controlling the levels of toxic oxygen radicals in the cells. Zinc deficiency has been involved in the pathogenesis of a number of clinical findings in chronic liver disease. These include the possible role of zinc deficiency in the pathogenesis of hepatic encephalopathy, by inducing alterations in urea metabolism. In CC14 cirrhotic rats oral zinc supplementation reduces ammonia levels and increases OCT activity in the liver. Oral zinc supplementation has been also proposed in the treatment of cirrhotic patients with chronic hepatic encephalopathy, the results however are not yet conclusive.