[Croatian guidelines for gastric cancer prevention by eradication of Helicobacter pylori infection]. / Hrvatski postupnik za prevenciju zelucanog raka eradikacijom infekcije Helicobacterom pylori.

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.

[Croatian guidelines for diagnostics and treatments of Helicobacter pylori infection]. / Hrvatski postupnik za dijagnostiku i terapiju infekcije Helicobacterom pylori.

In the past 30-year period of investigations, the crucial role of Helicobacter pylori in chronic gastritis, gastric and duodenal ulcer development, and subsequently in gastric cancer and MALT lymphoma pathogenesis, has been recognized. During the first meeting of European Helicobacter Study Group in 1996 in Maastricht, the first recommendations for diagnostics and treatments of Helicobacter pylori infection were published, later reviewed in 2000, 2007 and 2010. The first meeting of Croatian doctors focusing on the same topics, but suitable to specific national circumstances, was held as early as 1998. The need for updating the old guidelines has emerged during the last years. The working expert group of gastroenterologists was formed and gathered on Consesus Conference in December 2012 in Zagreb, to arrive to current guidelines for the clinical management of Helicobacter pylori infection in Croatia. The following topics relating to Helicobacter pylori infection were examined: 1. indications and contraindications for diagnostics and treatments; 2. diagnostic methods and 3. treatments applicable in our country.

[Croatian consensus on the treatment of inflammatory bowel diseases with biologic therapy]. / Hrvatski konsenzus o lijecenju upalnih bolesti crijeva bioloskom terapijom.

Introduction of biologic therapy in clinical practice represented significant progress in the treatment of inflammatory bowel diseases (IBD) because of its proven efficacy and due to the fact that biologics are the first drugs used in the treatment of IBD that can change the natural course of this diseases. At the same time, biologics are very expensive drugs with complex mechanism of action and important side effects and their use requires evidence-based clinical guidelines. These were the reasons that Referral Center of the Croatian Ministry of Health for IBD and the IBD Section of the Croatian Society of Gastroenterology organised Croatian consensus conference that defined guidelines for the treatment of IBD with anti-TNF drugs. The text below includes definitions of IBD, general principles of IBD therapy, comments on the importance of mucosal healing, analysis of reasons for nonresponse and loss of response to anti-TNF drugs, recommendation for the duration of anti-TNF therapy, rules of screening for opportunistic infections prior to anti-TNF therapy, comments on the problems with reproduction in IBD and finally guidelines for the treatment of various phenotypes of IBD including extraintestinal manifestations with anti-TNF therapy.

[Activity indices in IBD]. / Indeksi aktivnosti upalnih bolesti crijeva.

Inflammatory bowel disease (IBD) encompasses two medical conditions, Crohn's disease (CD) and ulcerative colitis (UC). These are chronic idiopathic conditions, marked by recurrent episodes of inflammation of the gastrointestinal tract, interspersed with periods of remission. An important feature of both disorders is that patients vary significantly in their clinical, endoscopic, biochemikal and histologic features. The heterogeneity in disease activity makes objective assessment of disease activity a prerequisite for rationale choice of therapy. At present, a number of activity indices are available for both conditions. These indices may be distinguished in more subjective (clinical), more objective (endoscopic-histological, biochemical) or a combination of the two. All these indices are rather complex and time-consuming; therefore their use is limited to clinical trials. Despite the different indices available, there is no consensus in the literature as to which is the most valid. In everyday clinical practice most gastroenterologists rely on their global clinical judgement, which is less reproducible, but simpler for decision-making in patients treatment. The aim of this article is to provide an overview of the disease activity indices (with a focus on the most frequently used), with analysis of their utilities, strengths and limitations.

Helicobacter pylori and nonmalignant diseases.

The incidence of peptic ulcer disease has declined over the last few decades, particularly in Western populations, most likely as a result of the decrease in Helicobacter pylori infection and the widespread use of proton-pump inhibitors (PPI) in patients with dyspepsia. The hospital admission rate for uncomplicated duodenal and gastric ulcers has significantly decreased worldwide. In contrast, admissions for complicated ulcer disease, such as bleeding peptic ulcers and perforation, remained relatively stable. Prophylactic H. pylori eradication was found to be associated with a reduced risk of both gastric and duodenal ulcers and their complications, including bleeding in chronic users of nonsteroidal anti-inflammatory drugs. The recent Helicobacter Eradication Relief of Dyspeptic Symptoms trial presented important data relating to symptoms and quality of life of H. pylori-positive patients with functional dyspepsia (FD) and also demonstrated significant benefits from eradication compared with the control group. The new Asian consensus report on FD recommended that dyspepsia accompanied by H. pylori infection should be considered a separate disease entity from FD and that H. pylori infection should be eradicated before diagnosing FD. The association of H. pylori with gastroesophageal reflux disease (GERD) is still controversial. Treatment for H. pylori does not seem to increase GERD symptoms or reflux esophagitis. However, documented eradication of H. pylori appears to significantly improve GERD symptoms. Additional long-term intervention studies are needed to provide more information on which to base clinical decisions.

Results of National Colorectal Cancer Screening Program in Croatia (2007-2011).

AIM: To study the epidemiologic indicators of uptake and characteristic colonoscopic findings in the Croatian National Colorectal Cancer Screening Program. METHODS: Colorectal cancer (CRC) was the second leading cause of cancer mortality in men (n = 1063, 49.77/100,000), as well as women (n = 803, 34.89/100,000) in Croatia in 2009. The Croatian National CRC Screening Program was established by the Ministry of Health and Social Welfare, and its implementation started in September, 2007. The coordinators were recruited in each county institute of public health with an obligation to provide fecal occult blood testing (FOBT) to the participants, followed by colonoscopy in all positive cases. The FOBT was performed by hypersensitive guaiac-based Hemognost card test (Biognost, Zagreb). The test and short questionnaire were delivered to the home addresses of all citizens aged 50-74 years consecutively during a 3-year period. Each participant was required to complete the questionnaire and send it together with the stool specimen on three test cards back to the institute for further analysis. About 4% FOBT positive cases are expected in normal risk populations. A descriptive analysis was performed. RESULTS: A total of 1,056,694 individuals (born between 1933-1945 and 1952-1957) were invited to screening by the end of September 2011. In total, 210,239 (19.9%) persons returned the envelope with a completed questionnaire, and 181,102 of them returned it with a correctly placed stool specimen on FOBT cards. Until now, 12,477 (6.9%), FOBT-positive patients have been found, which is at the upper limit of the expected values in European Guidelines for Quality Assurance in CRC Screening and Diagnosis [European Union (EU) Guidelines]. Colonoscopy was performed in 8541 cases (uptake 66%). Screening has identified CRC in 472 patients (5.5% of colonoscopied, 3.8% of FOBT-positive, and 0.26% of all screened individuals). This is also in the expected range according to EU Guidelines. Polyps were found and removed in 3329 (39% of colonoscopied) patients. The largest number of polyps were found in the left half of the colon: 64% (19%, 37% and 8% in the rectum, sigma, and descendens, respectively). The other 36% were detected in the proximal part (17% in the transverse colon and 19% in ceco-ascending colon). Small polyps in the rectum (5-10 mm in diameter), sigmoid and descending colon were histologically found to be tubular adenomas in 60% of cases, with a low degree of dysplasia, and 40% were classified as hyperplastic. Polyps of this size in the transverse or ceco-ascending colon in almost 20% had a histologically villous component, but still had a low degree of dysplasia. Polyps sized 10-20 mm in diameter were in 43% cases tubulovillous, and among them, 32% had areas with a high degree of dysplasia, especially those polyps in the ceco-ascending or transverse part. The characteristics of the Croatian CRC Screening National Program in the first 3 years were as follows: relatively low percentage of returned FOBT, higher number of FOBT-positive persons but still in the range for population-based programs, and higher number of pathologic findings (polyps and cancers). CONCLUSION: These results suggest a need for intervention strategies that include organizational changes and educational activities to improve awareness of CRC screening usefulness and increase participation rates.

The influence of the different morphological changes on gastric mucosa on somatostatin cell number in antrum mucosa and serum somatostatin.

The aim of our paper was to investigate the influence of the different morphological changes on gastric mucosa on somatostatin D-cell number in antral mucosa and serum Somatostatin. We analyzed according to Sydney classification to what extent the severity of gastritis affect the observed hormonal values. somatostatin D-cell number in antral mucosa and serum Somatostatin values were compared between three groups of patients; mild, moderate and severe chronic gastritis. The average number of somatostatin cell in biopsy sample of antrum mucosa was 30.41 +/- 35.38 (N = 17) in the case of middle form, 18.69 +/- 26.65 (N = 56) in moderate and in severe case of chronic gastritis 5.23 +/- 5.93 (N = 7) cells in mm2 of mucosa. The level of somatostatin in the serum of middle form gastritis were 26.43 +/- 28.76, moderate 19.95 +/- 35.93 and severe 17.88 +/- 17.66 pg/mL. In order to determine the number of somatostatin cells in antrum mucosa and serum somatostatin with present morphological changes of mucosa, it might helpful to exclude the patients with non-ulcer dyspepsia, but with the higher risk of premalignant and malignant changes.

[Post-transplant lymphoproliferative disease in liver transplant recipients--Merkur University Hospital single center experience]. / Post-transplantacijska limfoproliferativna bolest u bolesnika s transplantacijom jetre - iskustvo KB Merkur.

Post-transplant lymphoproliferative disorder (PTLD) is an increasingly recognized condition as the number of solid organ and bone marrow transplant recipients increases. It can be a life threatening fulminant disorder and affects approximately 8% of solid organ transplant recipients. Epstein-Barr virus (EBV) is closely involved in the pathogenesis of PTLD and the majority of PTLD cases arise in response to primary infection with EBV or to re-activation of previously acquired EBV. The principal risk factors underlying the development of PTLD are the degree of overall immunosuppression and EBV serostatus of the recipient. The most commonly used pathologic classification of PTLD is the World Health Organization classification, which divides PTLD into three categories: early lesions, polymorphic PTLD, and monomorphic PTLD. Early lesions are characterized by reactive plasmacytic hyperplasia. Polymorphic PTLD may be either polyclonal or monoclonal and is characterized by destruction of the underlying lymphoid architecture, necrosis, and nuclear atypia. In monomorphic PTLD, the majority of cases (>80%) arise from B cells, similar to non-Hodgkin's lymphoma in immunocompetent hosts. The most common subtype is diffuse large B-cell lymphoma, but Burkitt's/Burkitt's-like lymphoma and plasma cell myeloma are also seen. Rarely T-cell variants occur, which include peripheral T-cell lymphomas and, rarely, other uncommon types, including gamma/delta T-cell lymphoma and T-natural killer (NK) cell varieties. Hodgkin's disease-like lymphoma is very unusual. An accurate diagnosis of PTLD requires a high index of suspicion, since the disorder may present subtly and/or extranodally. Radiologic evidence of a mass or the presence of elevated serum markers (such as increased LDH levels) are suggestive of PTLD, with positive finding on ultrasonography, computed tomography, magnetic resonance and/or positron emission tomography scanning (possibly indicating metabolically active areas) also favoring the diagnosis. The management of PTLD poses a major therapeutic challenge and although there is reasonable agreement about the overall principles of treatment, there is still considerable controversy about the optimal treatment of individual patients. EBV-related PTLDs are a significant cause of mortality in patients undergoing orthotopic liver transplantation with the observed mortality rate of up to 50%. This paper presents the experience acquired at Merkur University Hospital in the diagnosis and treatment of patients with liver transplantation and PTLD.

Serum antibodies positivity to 12 Helicobacter pylori virulence antigens in patients with benign or malignant gastroduodenal diseases--cross-sectional study.

AIM: To investigate the association of gastric histological and endoscopic findings in patients with Helicobacter pylori (H. pylori), according to presence of seropositivity to 12 bacterial virulence antigens. METHODS: This is a cross-sectional single-center study of 360 consecutive outpatients referred in the period of one year to upper gastrointestinal endoscopy because of dyspeptic complaints. Patients sera were tested by Western blot method to determine the presence of serum antibodies to bacterial virulence antigens--p120 (CagA--cytotoxin-associated antigen), p95 (VacA - vacuolating cytotoxin), p67 (FSH--flagellar sheath protein), p66 (UreB--urease enzyme heavy subunit), p57 (HSP homologue--heath shock protein homologue), p54 (flagellin), p33, p30 (OMP--outer membrane protein), p29 (UreA--urease enzyme light subunit), p26, p19, and p17. Upper gastrointestinal endoscopy was performed, endoscopic diagnosis recorded, and 4 mucosal biopsy samples were obtained and assessed according to Updated Sydney protocol. RESULTS: The sera of 207 patients were analyzed. Thirty patients had gastric adenocarcinoma, 126 peptic ulcers, and 51 normal finding. p120 (CagA) seropositivity was significantly more often present in patients with higher activity grade in the antrum (P = 0.025), p30 in patients with greater inflammation in the antrum (P = 0.025) and the corpus (P = 0.010), p33 in patients with greater inflammation in the corpus (P = 0.050), and p19 (OMP) in patients with lower intestinal metaplasia grades in the corpus (P = 0.025). Seroreactivity to all other bacterial proteins showed no association with the histological status of the stomach mucosa. Except for the seropositivity to protein p95 (VacA), which was more often present in patients with duodenal ulcer (P = 0.006), there was no difference in seroreactivity to other bacterial proteins and upper gastrointestinal endoscopic findings. CONCLUSIONS: p120 (CagA), p33, p30 (OMP), and p19 (OMP) seropositivity was more often present in patients with higher grades of the histological parameters of gastritis and seropositivity to protein p95 (VacA) with endoscopic presence of duodenal ulcer. Histological parameters of gastritis are more associated with bacterial virulence than endoscopic findings.

Helicobacter pylori eradication therapy success regarding different treatment period based on clarithromycin or metronidazole triple-therapy regimens.

BACKGROUND: The study compares the eradication success of standard first-line triple therapies of different durations (7, 10, and 14 days). MATERIALS AND METHODS: A total of 592 naive Helicobacter pylori-positive patients were randomized to receive pantoprazole, amoxicillin, and clarithromycin or metronidazole for 14 days (PACl14 or PAM14), 10 days (PACl10 or PAM10), or 7 days (PACl7 or PAM7). H. pylori eradication was assessed by histological, microbiological, and rapid urease examination. RESULTS: The intention-to-treat (ITT) and per-protocol (PP) analyses have shown no overall statistically significant differences between the eradication success of PACl and PAM treatment groups (ITT p = .308, PP p = .167). Longer treatment duration has yielded statistically significant increase in eradication success for clarithromycin (ITT p = .004; PP p = .004) and metronidazole (ITT p = .010; PP p = .034) based regimens. Namely, PACl10, PACl14, and PAM14 protocols resulted in eradication success exceeding 80% in ITT and 90% in PP analysis. Primary resistance to clarithromycin and metronidazole equals 8.2% and 32.9%, respectively. Prolonging the metronidazole-based treatment duration in patients with resistant strains resulted in statistically significant higher eradication success. CONCLUSIONS: For all antimicrobial combinations, 14 days protocols have led to a significant increase of H. pylori eradication success when compared to 10 and 7 days, respectively. Prolonging the treatment duration can overcome the negative effect of metronidazole resistance. Only PAM14, PACl10 protocols achieved ITT success > 80% and should be recommended as the first line eradication treatment in Croatia.

Influence of Helicobacter pylori infection persistence on bcl-2 expression in gastric mucosa inflammatory cells.

Chronic Helicobacter (H.) pylori infection is an etiological factor related to gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. The expression of bcl-2 protein significantly decreases as the grade of MALT lymphoma advances. The aim of this study was to evaluate bcl-2 expression in inflammatory cells in lamina propria in gastric biopsy samples collected from two groups of patients with chronic gastritis divided on the basis of the success or failure of H. pylori eradication. Sixty-five patients with chronic gastritis were divided into two groups of 45 and 20 patients according to their therapeutic response. The gastric mucosa samples were analyzed histologically in both groups of patients before and after standard therapy (for eradicated, after one therapeutic cycle; and for non-eradicated, after three therapeutic cycles) for H. pylori density, urease activity and bcl-2 expression. In the eradicated group of patients, H. pylori eradication was accompanied by significantly lower grades of bacterial colonization and lower urease activity in the corpus and antrum. Bcl-2 expression in inflammatory cells showed no statistically significant changes in either patient group at either location. There was no between-group difference in bcl-2 expression either. In conclusion, persistent long-lasting H. pylori infection is associated with higher grades of bacterial colonization and higher urease activity but not with bcl-2 expression in inflammatory cells.

Seroprevalence of Helicobacter pylori infection in dyspeptic patients.

The objective of the study was to assess the effect of age on the seroprevalence of Helicobacter (H.) pylori infection in dyspeptic patients. The results obtained in the patient group were compared with findings on the seroprevalence of H. pylori infection in 2051 blood donors. Serum samples were tested by the commercial ELISA and CFT assays according to manufacturer's instructions. The mean seroprevalence of H. pylori infection as determined by ELISA/CFT was 64.0%/51.7% in the group of blood donors and 92.3%/89.5% in the group of dyspeptic patients. Study results indicated a higher prevalence of H. pylori infection in dyspeptic patients as compared with blood donors in all age groups. In the patient S group, H. pylori seroprevalence was not age dependent.

Influence of H. pylori infection and eradication on p53, c-erbB-2 and Ki-67 in gastric mucosa.

BACKGROUND/AIMS: To evaluate the expression of antigens c-erbB-2, p53, and Ki-67 in gastric biopsy, bacteria density and urease activity in two groups of patients with chronic gastritis separated on the basis of the success or failure of H. pylori eradication. METHODOLOGY: Sixty-five patients with chronic gastritis were split in two groups (n=45/20) related to response to the therapy. The gastric mucosa samples (Sydney system) were analyzed histologically in both groups of patients before and after standard therapy (for eradicated, E group after one cycle; for non-eradicated, NE group after three cycles) for H. pylori infection, urease activity, c-erbB-2, p53 and Ki-67 expression. Sera samples taken before and after treatment were also analyzed for specific antibody against H. pylori. RESULTS: The eradication of H. pylori in patients of the E group was accompanied with significant lower colonization grades of bacteria, urease activity, proliferating rate, p53, and Ki-67 expression while c-erbB-2 expression was unchanged. In the NE group, all parameters were the same before and after therapy with exception of p53, which was slightly higher on both locations. Strong expression of c-erbB-2 in corpus of the NE group was determinate. Serum activity of specific antibodies against H. pylori was lower after the therapy in both groups of patients, but in the eradicated group this change was much stronger that in the non-eradicated. CONCLUSIONS: Long persisting infection is related with higher colonization grades of bacteria, urease activity, p53, c-erbB-2 and Ki-67 expression. Changes of those markers are connected with duration of infection and location where these changes were obtained.

The place and role of serologic methods in detecting Helicobacter pylori infection.

The aim of the study was to determine the place and role of serologic methods in detecting Helicobacter pylori (H. pylori) infection, on the basis of estimated enzyme-linked immunosorbent assay (ELISA) and complement fixation test (CFT) sensitivity and specificity. A total of 549 patients were included in the study. ELISA and CFT as serologic methods were compared with invasive methods (rapid urease test--CLO test, culture, histology). The sensitivity of serologic methods was above 90%, and their specificity was around 80%. Study results confirmed the value, reliability and usefulness of serologic methods in the detection of H. pylori infection.

[Is the only good Helicobacter a dead Helicobacter?]. / Je li jedino mrtav Helicobacter--dobar Helicobacter?

The discovery of Helicobacter pylori (H. pylori) has revolutionised the pathophysiological and clinical approach to gastric and duodenal ulcer. Since the first paper identifying H. pylori was published only 19-20 years ago, it has been found out that this bacterium causes probably the commonest human infection. Like other revolutions in history, the original directions of the H. pylori story have changed in response to conflicting ideologies, observation, and practices. It is known that once H. pylori is acquired, colonisation continues for life unless the organism is eliminated by antimicrobial treatment or by the usually late-in-life development of the atrophic gastritis. If any recent achievement in the world of medicine is to be called revolutionary, then it is the discovery of the role of this spiral bacterium in the etiopathogenesis of gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinomas and gastric mucosa-associated lymphoid type (MALT) B-cell lymphomas. Essentially everyone who carries the organism in the gastric mucous layer has evidence of tissue reaction (termed chronic active gastritis), but most colonised persons remain asymptomatic for life. In the absence of treatment, the presence of H. pylori can be determined with a high degree of confidence by endoscopy (with culture, histologic examination, or urease testing of gastric biopsy specimens), by serologic testing, or by urea breath tests. After successful treatment, specific antibody levels decrease so slowly that serologic testing cannot be used to document success for at least 6 months. In most patients, elimination of H. pylori changes the natural history of peptic ulcer disease and of gastric MALT lymphomas. It is now recommended that these patients have to be treated to eliminate H. pylori because the benefits seem to substantially outweigh the risks and costs. Currently, enthusiasts, drug companies, and the lay press are putting pressure on physicians to eliminate H. pylori from all patients, symptomatic or not, in whom it is detected. There is little evidence that this is appropriate, and management will continue to change as new knowledge emerges and socioeconomic environments change in ways that are relevant to H. pylori and clinical medicine.

[Endoscopic methods of treatment of precancerous lesions of the colon]. / Endoskopske metode lijecenja prekanceroznih lezija kolona.

The endoscopic method--colonoscope, has become the tool of choice for diagnosing many colonic disorders, including the acute and chronic inflammatory bowel disease, lower gastrointestinal bleeding, benign and malignant tumors, and various others abnormalities appearing on the radiographs. The colonoscope is also useful and become the main confirmation method in screening for and monitoring colonic cancer. In the same time, colonoscopy offers numerous therapeutic options. The colonic polyps, well-known colonic precancerous lesions, with incidence ranges from 7 to 50%, can be removed completely during the colonoscopy, with a snare or biopsy forceps (polypectomy). Early cancers limited to the mucosal layer (intraepithelial cancer or carcinoma in situ) can be treated endoscopically too (mucosectomy), as well as various gastrointestinal bleeding (with sclerotherapy, electrocoagulation, APC, laser-fotocoagulation), inflammatory and postsurgical strictures (endoscopic dilation), and foreign bodies in the rectum and sigma (endoscopic extraction).

[Helicobacter pylori--introduction and review of research]. / Helicobacter pylori--uvod i pregled istrazivanja.

The discovery of Helicobacter pylori has revolutionized the pathophysiological and clinical approach to gastric and duodenal ulcer. Since the first paper identifying H. pylori was published only 17 years ago, it has been found out that this bacterium causes probably the commonest human infection. Numerous papers published so far have confirmed causal relationship between H. pylori infection and gastritis, duodenal ulcer, gastric ulcer and gastric cancer. If any recent achievement in the world of medicine is to be called revolutionary, then it is the discovery of the role of a spiral bacterium in the etiopathogenesis of gastritis, gastric ulcer, duodenal ulcer and gastric cancer. The discovery of the role of Helicobacter pylori has entirely changed our views and approach to the treatment of patients with stomach disorders. Not only do these discoveries change our actions, but above all our way of thinking. Almost routine diagnostics and treatment of gastritis, gastric ulcer or cancer has been replaced by studies in epidemiology, isolation and eradication of a single bacterium.

[Epidemiology of Helicobacter pylori infection]. / Epidemiologija infekcije Helicobacterom pylori.

About 50% of adults in the developed and 80-90% in the developing countries are estimated to be infected by Helicobacter pylori. Being 68% nationally, this rate is higher in the northern continental parts of Croatia, which also have higher gastric cancer rates. Low socio-economic status, poor living conditions in childhood (the age when Helicobacter pylori is typically acquired), and exposure to the stomach content of an infected person are risk factors for Helicobacter pylori. Most of the infected are symptomless, with 10 to 20% subsequently developing the disease, and this mainly from peptic ulcer, asymptomatic chronic gastritis and chronic dyspepsia. Less than 5/10,000 become affected with adenocarcinoma, MALT lymphoma or primary non-Hodgkin's gastric lymphoma. Helicobacter pylori is under intensive study for possible association with other diseases. As transmission route of the infection is still unclear, any mechanism allowing the bacteria entry into a non-infected individual's stomach is probably a possibility. In addition to improved socio-economic status, eradication or vaccination may be contributors to the reduction in the number of the infected.