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Dyspepsia is a disorder characterized by dyspeptic symptoms which are located in the epigastrium and related to digestion of food in the initial part of the digestive system. In functional dyspepsia, unlike organic dyspepsia, there is no underlying organic disease that would cause dyspeptic symptoms. Immune and mucosal function changes, gastric dysmotility, different composition of the gastrointestinal microbiota, and altered central nervous system processing are considered responsible for the onset of the disorder. The diagnosis is based on history, clinical presentation, and exclusion of other organic diseases of the gastrointestinal tract manifested by dyspeptic symptoms. Therapy includes eradication of Helicobacter pylori infection, proton pump inhibitors, prokinetics, neuromodulators, and herbal preparations. Unfortunately, in some patients, this therapy leads to little or no improvement. The prevalence of functional dyspepsia is increasing. It has become one of the more common gastroenterological diagnoses. In order to reduce the costs associated with the diagnosis and treatment of the disorder itself, its mechanisms need to be fully elucidated and thus enable finding appropriate therapy for all patient subgroups.

Gastric cancer is the fourth most common type of cancer and the second leading cause of cancer-related death in the world. Although gastric cancer has a multifactorial etiology, infection with Helicobacter pylori is highly associated with gastric carcinogenesis. Carcinogenesis is also influenced by some environmental factors and host genetic diversity, which engenders differential host inflammatory responses that can influence clinical outcome. Chronic gastritis induced by H. pylori is the strongest known risk factor for adenocarcinoma of the distal stomach, but the effects of bacterial eradication on carcinogenesis have remained unclear up to now. Although eradication of H. pylori infection appears to reduce the risk of gastric cancer, several recent controlled interventional trials by H. pylori eradication to prevent gastric cancer have yielded disappointing results. To clarify this problem in a high-risk population, the investigators conducted a prospective, randomized, double-blind, placebo-controlled, population-based studies. The results of previous studies highlight the importance of longer and careful follow-up after eradication therapy. It seems that eradication treatment is effective in preventing gastric cancer if it is given before preneoplastic conditions/lesions, gastric atrophy, metaplasia, and dysplasia, have had time to develop. Furthermore, the significant efficacy of treatment observed in younger patients suggests the need to eradicate H. pylori as early as possible. This consensus aimed to propose guidelines for the diagnosis, management and control of individuals with chronic gastritis, atrophy, intestinal metaplasia, or dysplasia.

In the last year, different diseases possibly linked to Helicobacter pylori infection but localized outside of the stomach have been investigated. There are, in fact, several studies concerning cardiovascular diseases, hematologic disorders, neurologic diseases, metabolic, hepatobiliary diseases, and other conditions. Some of those studies, such as those on sideropenic anemia and idiopathic thrombocytopenic purpura, are quite large and well conducted, while in other cases there are just small or isolated studies or even case reports. Nonetheless, there is much interest among researchers all over the world for such a topic as demonstrated by the large number of studies published in the last year., (© 2012 Blackwell Publishing Ltd.)

In this article we reviewed experiences in approach and procedure with dyspepsia, with special accent on non-ulcer dyspepsia and Helicobacter pylori infection. Dyspepsia makes around 50% of gastroenterology cases. In 20% of cases it is caused by peptic ulcer disease and in 50% of cases non-ulcer dyspepsia. Around 50% of non-ulcer dyspepsia is followed by coexistent Helicobacter pylori positive gastritis. Dyspepsia followed by alarming symptoms in patients who are over 55 years old or in patients who are using NSAID indicated urgent endoscopic procedure--gastroscopy. In other patients non-invasive testing on Helicobacter pylori infection is recommended where eradication therapy should be applied in Helicobacter pylori positive and empirical cure by antisecreting drugs or prokinetics in Helicobacter pylori negative patients. Final gastroscopic evaluation is indicated after unsuccessful therapy. Ceasing of non-ulcer dyspeptic symptoms could be predicted in 20% of patients with cured Helicobacter pylori infection.

Helicobacter pylori infection is linked to conditions of the upper gastrointestinal tract, including peptic ulcer and gastric adenocarcinoma na MALT lymphoma. It has also been associated with wide variety of extragastric and non-gastrointestinal conditions. However, the evidence in support of Helicobacter pylori infection as a cause of the non-gastrointestinal tract diseases is not widely understood. We reviewed the medical literature in regard to putative association of Helicobacter pylori infection and non-gastrointestinal tract condition, notably cardiovascular, autoimmune and dermatological diseases. The majority of published papers examining the potential causal relationship were case-control studies, cross-sectional and cohort studies while only a few recent articles that did not confirm the evidence of causal relationship represent well designed population-based prospective studies. The lack of clear evidence for etiopathogenetic associations of Helicobacter pylori infection and non-gastrointestinal tract conditions should focus our attention on appropriate testing and treatment of Helicobacter pylori infection in patients with conditions that are of proven association such as peptic ulcer disease.

The clinical significance of Helicobacter pylori infection in the etiopathogenesis of many gastroduodenal disorders, especially peptic ulcer disease and current awareness of the benefits of its eradication has entirely changed the current treatment of these diseases. Eradication was already defined as the disappearance of Helicobacter pylori from the gastric mucosa (finding negativization) confirmed at least 4 weeks (or later) after completed antibiotic eradication therapy. The regimen has to be simple, cheap and tolerable so that the patient could carry it out completely and as easy as possible (good compliance is required). The success of Helicobacter pylori eradication, evaluated by the strict "intention-to-treat" criteria, has to be higher than 80%. Current modern therapy should be triple and not longer than 7 days. One of three proton pump inhibitors is recommended as the antisecretory component (omeprazole, pantoprazole or lansoprazole). Two of three following antibiotis is added to this therapy: metronidazole/tinidazole, clarithromycin or amoxicillin. Treatment failure and growing number of antimicrobial resistant Helicobacter pylori strains require new ways of therapy and more effective drugs. Our results of 7-, 10- and 14-day therapy consisting of omeprazole, amoxicillin and metronidazole are poorer than those of drug combination including clarithromycin instead of amoxicillin. The results of Clinical Hospital "Merkur" showed that combination of amoxicillin, metronidazole and pantoprazole was more effective than the same combination with omeprazole, and the opposite was true for metronidazole and azithromycin combined with omeprazole and pantoprazole, respectively. The results of other medical centers prescribing the same eradication protocols were completely different. The differences are probably caused by poor patient compliance.

Helicobacter pylori infection almost invariably results in chronic gastritis. The Sydney System (1990) emphasised the importance of combining topographical, morphological and etiological aspects in attempt to make clinical useful diagnosis of chronic gastritis. The aims of revised Sydney System in Houston (1994), Texas, were to improve terminology of chronic gastritis emphasising distinction between nonatrophic and atrophic gastritis, and in addition to determinate special forms of gastritis. The special forms of gastritis were described and diagnostic criteria were provided. Principles and grading of histological division of Sydney System were only slightly modified, grading being improved by the provision of a visual scale. Endoscopy and histological findings of 1062 patients from University Hospital Merkur were compared to evaluate the value of endoscopic division of Sydney System, and the modified grading proposed by Houston classification. There was no correlation between endoscopic and histological findings. Localisation of inflammatory cells was either 1) superficial or 2) diffuse in the mucosa, respectively. In Helicobacter pylori positive patients the most common finding was chronic active gastritis, and in Helicobacter pylori negative superficial and inactive chronic gastritis.

Histopathologic and clinical data strongly suggest a causal relation between Helicobacter pylori infection and gastritis, peptic ulcer disease, or both. However, little has been written about the potential association between H. pylori infection and Brunner's gland adenoma. Therefore, we carried out a prospective study to determine the presence of H. pylori infection among patients with Brunner's gland adenoma. From November 1996 till October 1999, 19100 patients who had undergone upper gastrointestinal endoscopy at two clinical centers in Zagreb, Croatia, were candidates for participation in the study. Brunner's gland adenoma was diagnosed on the basis of histologic samples taken from the polyp (four patients) or after the entire polyp was made available upon endoscopic removal (three patients). When all endoscopic examinations had been performed, biopsy samples were taken from the antrum and body of the stomach, so that gastritis could be classified and H. pylori determined by histology. Biopsy samples were also taken from the duodenal bulb to verify duodenitis. Two other samples were taken from the antrum for rapid urease test. The patients were considered positive for H. pylori when both histology and rapid urease test were positive. Brunner's gland adenoma was diagnosed in seven patients (five women and two men; median age, 49 yrs). Five (71%) patients with diagnosed Brunner's gland adenoma had concurrent H. pylori infection. Duodenitis associated with gastric metaplasia was observed in six patients. Complete eradication of H. pylori was achieved in only two patients. Symptoms disappeared or markedly diminished in all patients with significant improvement during therapy or immediately upon endoscopic removal of the polyp. Although limited by a very small number of patients, our results suggest that concurrent H. pylori infection is very common in patients with Brunner's gland adenoma. However, the role of H. pylori infection in the pathogenesis and development of Brunner's gland hyperplasia remains unclear.

Objective: Histopathological and clinical data strongly suggest that Helicobacter pylori is the cause of chronic gastritis and peptic ulceration. However, little has been written about the potential causal relation of H. pylori infection to hyperplastic and adenomatous gastric polyps. We therefore carried out a prospective study to determine the effect of eradicating H. pylori infection on the course of hyperplastic and adenomatous gastric polyps., Methods: From November 1996 to December 1997, 6700 patients who had undergone upper gastrointestinal endoscopy at the two centres in Zagreb, Croatia, were candidates for participation in the study. Hyperplastic and adenomatous polyps were diagnosed on a basis of at least three histological samples taken from the polyp. In seven patients endoscopy had to be repeated because forceps biopsy sampling either provided inadequate tissue for correct histological diagnosis, or accurate characterization of gastric polyp histology was not possible. Upon completion of all endoscopic examinations before and after treatment, biopsy samples were taken from the antrum (two) and the body of the stomach (two) so that gastritis could be graded and classified, and the presence of H. pylori sought by histology. Two other samples were taken from the antrum for a rapid urease test. Follow-up examinations were performed by using endoscopy. Control endoscopy was performed at least 4 weeks after the treatment of H. pylori infection had been completed, and then every 3-4 months. The follow-up ranged from 4 to 17 months, with a median of 14 months. The treatment of H. pylori infection consisted of a 1-week course of either omeprazole (20 mg twice daily) or pantoprazole 40 mg twice daily), and a 1-week course of amoxicillin 2g twice daily) and metronidazole (400 mg three times daily), and clarithromycin (500 mg twice daily). Eradication of H. pylori infection was assessed by repeated histology and rapid urease test., Results: Twenty-one patients (nine women, 12 men; median age 52 years) with histologically proven hyperplastic gastric polyps, and seven patients (two women, five men; median age, 67 years) with adenomatous gastric polyps were included in the study. Among 21 patients with hyperplastic gastric polyps, 16 patients (76%) were positive for H. pylori infection. Only two patients (29%) with adenomatous gastric polyps were positive for the infection. Complete eradication of H. pylori was initially achieved in all patients positive for H. pylori. Total regression of the gastric polyps was observed only among the patients with hyperplastic gastric polyps in whom H. pylori had been eradicated. Complete regression of the hyperplastic gastric polyps was observed in seven of the 16 evaluable patients (44%; 95% CI, 19-68%) after H. pylori eradication. The endoscopic snare polypectomy was carried out in nine patients with hyperplastic polyps and two patients with adenomatous gastric polyps in whom regression of the polyps was not observed after H. pylori eradication, as well as in five patients with hyperplastic and four with adenomatous gastric polyps who were negative for H. pylori. Exploratory laparotomy and gastrotomy with polyps excision were carried out in one patient with multiple adenomatous gastric polyps. In only one patient who was not positive for H. pylori recurrence of hyperplastic gastric polyp was recorded during follow-up, and no re-infection with H. pylori has been detected., Conclusions: Our results suggest that the development of hyperplastic gastric polyps may be directly related to chronic active gastritis and concomitant H. pylori infection. Cure of H. pylori infection associated with hyperplastic gastric polyps resulted in complete polyp regression in more than 40% of patients. Therefore, for patients with hyperplastic gastric polyps and concurrent H. pylori infection an antibiotic treatment designed to eradicate H. pylori appears to be recommended before further therapeutic options are consi