[Monitoring of patients with chronic hepatitis during and after therapy]. / Pracenje lijecenih i nelijecenih bolesnika s virusnim hepatitisom.

Different effective treatments, which are today available for chronic virus hepatitis C and B, reduce the rate of adverse outcomes but HCV and HBV infections are still one of the major health and public medical problems. Screening for HCV and HBV is performed only in high-risk groups with diagnostic tests with high sensitivity and specificity. In HCV antibody positive patients, serum HCV RNA has to be determined by quantitative assay and virus genotype identified. Liver fibrosis is determined by liver biopsy or widely accepted elastography and different serum fibrosis markers. In patients with HCV cirrhosis, HCC has to be detected by expert ultrasound performer or MSCT, MR, and liver transplantation performed according to indications. The current hepatitis B vaccination policy is universal neonatal vaccination. The risk population undergo screening for HBsAg, antiHBc and antiHBs antibodies. The HBsAg, HBeAg and antiHBe positive individuals undergo quantitative testing for HBsAg and HBV DNA. According to the stage of their liver disease, patients are treated with interferon or nucleos(t)ide analogues. The optimal treatment with oral antivirals are entecavir and tenofovir, but the duration of treatment with nucleos(t)ide analogues is generally life-long. In HBV cirrhosis and HBsAg inactive carriers, detection of HCC is essential, and liver transplantation is successfully performed in these patients.

[Liver transplantation in hepatitis B viral infection]. / Terapija hepatitisa B nakon transplantacije jetre.

Hepatitis B infection (HBV) causes liver cirrhosis and hepatocellular carcinoma that are indications for orthotopic liver transplantation (OLT). The outcome of OLT depends on the prevention of HBV reinfection and disease relapses. Out of 692 liver transplantations performed at Merkur University Hospital, 30 were done for HBV infection. These patients were treated with HBIG post OLT and lamivudine, entecavir, adefovir, tenofovir prior and post OLT. All patients became HBsAg and HBV DNA negative but four of them became HbsAg positive one year post OLT. The patients survived for 2 months to 7 years post OLT. With the introduction of HBIG immunoprophylaxis and new efficient antiviral treatment, the risk of relapse is only < 10%, and survival is the same as in other indications for OLT. Because of the high cost and long-term treatment, efforts have been made to prevent recurrent HBV disease by using the schedules according to pre- and post-transplant HBV viremia and introducing the new potent antiviral analogue nucleos(t)ides.

[Treatment of recurrent HCV infection after liver transplantation]. / Terapija HCV infekcije nakon transplantacije jetre.

Recurrent infection with HCV after liver transplantation (LT) is almost universal and is associated with substantial morbidity, mortality and graft loss. In contrast to immunocompetent individuals, HCV infection in immunosuppressed transplant recipients usually has an accelerated course. Acute hepatitis develops in approximately 75% of HCV recipients in the first six months following LT. Within the five years after LT, over 80% of HCV-infected liver transplant recipients develop histologic evidence of chronic allograft injury secondary to HCV, with up to 30% of cirrhosis. While the choice of calcineurin inhibitors has not clearly shown to affect the histologic HCV recurrence or the frequency of rejection in HCV-infected recipients, the cumulative exposure to corticosteroids is associated with increased mortality, higher levels of HCV viremia, and more severe histologic recurrence. Successful therapy has been shown to have a positive impact on both graft and patient survival. Combination therapy with interferon (pegylated and non-pegylated forms) plus ribavirin appears to provide maximum benefits. Drug therapy is usually administered for recurrent disease. No prophylactic therapy is available. Preemptive regimens offer no distinctive advantages over treatments for recurrent disease. Overall, treatment is poorly tolerated, with frequent need for dose reductions, especially due to cytopenias, and drug discontinuation in up to 50% of patients. Optimizing drug doses is important in maximizing sustained virologic response rates (SVR). The SVR achieved is between 33% and 42% in randomized studies treating patients with histologic recurrence. The potential factors that influence this low SVR rate are:1) genotype 1 virus; 2) high viral load; 3) prior nonresponding to therapy; 4) side effects of antiviral treatment; 5) use of growth factors; and 6) effect of immunosuppression. In post-transplant patients with recurrent HCV disease, combination peg alpha-2b or alpha-2a in standard dose and ribavirin (800-1200 mg either ab initio or as an increasing dose) regimen for 48 weeks was significantly better than no therapy but not than any other therapy.

[Viralhepatitis. Croatian Consensus Statement 2013]. / Virusni hepatitis. Hrvatska konsenzus konferencija 2013.

Croatian Consensus Conferences on Viral Hepatitis took place in 2005 and 2009. Considering the numerous novel concepts on the epidemiology, diagnosis and management of viral hepatitis (chronic hepatitis C genotype 1 in particular) that have emerged in the past four years, a new Croatian Consensus Conference on Viral Hepatitis was held in Zagreb on February 28, 2013. The abridged text of the Croatian Consensus Conference on Viral Hepatitis 2013 presents the new concepts on the epidemiology of viral hepatitis, serologic and molecular diagnosis of viral hepatitis, determination of the IL-28 gene promoter polymorphism, fibrosis grading, algorithm for patient diagnostic follow up, treatment of chronic hepatitis C (genotypes 1-6) and hepatitis B, treatment of special populations (children, dialysis patients, transplanted patients, individuals with HIV/HCV co-infection), and therapy side effects.

[Needle tract seeding of hepatocellular carcinoma after liver transplantation]. / Presadba hepatocelularnog karcinoma uzduz bioptickog kanala igle nakon transplantacije jetre.

Ultrasound guided fine needle aspiration cytology (FNAC) and core needle biopsy (CNB) are effective methods for the diagnosis of focal hepatic lesions. In case of neoplastic lesions, however, this may be followed by the seeding of malignant cells along the needle tract. We report a case of subcutaneous needle tract seeding of hepatocellular carcinoma (HCC) 25 months after liver transplantation. A 57-year-old man with compensated hepatitis-B-related liver cirrhosis was diagnosed with HCC by CNB, and the lesion was resected. Ten months after the procedure, FNAC of a small hepatic lesion confirmed tumor recurrence. The patient was successfully transplanted and 25 months later, a subcutaneous tumor appeared on the abdominal wall over the previous site of puncture without further dissemination of the disease. Total resection of the lesion confirmed HCC. It remains undetermined whether the seeding appeared after FNAC or CNB. After 18-month follow-up the patient was uneventful. The objectives of this report are to present clinical aspects and outcome of HCC needle tract seeding in a transplanted patient, discussing the problems and pitfalls of diagnostic workup and management of HCC.

[Multifocal epithelioid hemangioendothelioma treated by liver transplantation--case report]. / Multifokalni epiteloidni hemangioendoteliom jetre lijecen ortotopnom transplantacijom jetre--prikaz bolesnika.

Multifocal epithelioid hemangioendothelioma of the liver is a rare primary tumor with a variable course of disease. A case is presented of a 27-year-old female patient with multiple hepatic lesions on ultrasonography, suspect of metastatic tumor of the liver. Serum tumor markers were not elevated, while clinical examination of the lungs, gastrointestinal and gynecologic systems did not confirm the presence of a primary tumor process. Metastatic tumor and primary hepatocellular tumor were ruled out by fine needle aspiration cytology. Along with a characteristic immunophenotype of the vascular cell endothelium (positive for CD31 and CD34), high proliferation demonstrated by the analysis of argyrophilic nucleolar organization regions (AgNOR) and DNA aneuploidy, cytomorphological pattern suggested the diagnosis of angiosarcoma. Histopathologic finding corresponded to epithelioid hemangioendothelioma. Ten years after orthotopic liver transplantation, the patient is free from disease relapse, with regular follow up testing. Hemangioendothelioma of the liver is characterized by multifocality, which excludes resection; thus, liver transplantation is the method of choice. Therefore, preoperative diagnostic workup is of utmost importance to differentiate it from other primary and metastatic tumors of the liver.

[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.

[Monitoring patients with chronic hepatitis during and after therapy]. / Pracenje lijecenih i nelijecenih bolesnika s virusnim hepatitisom.

Chronic viral hepatitis C and B are one of the major public health and medical problems. Both viruses cause life threatening liver diseases, i.e. cirrhosis, liver failure and hepatocellular carcinoma (HCC). Effective treatment for both hepatitis B and hepatitis C to reduce the rate of adverse outcomes is now available. There is no recommendation for mass screening for HBV and HCV in the general population but only in the high risk groups. There is wide availability of diagnostic tests for HCV and HBV infection with high sensitivity and specificity. Prior to therapy initiation, serum HCV RNA by quantitative assay and HCV genotype should be determined. Liver biopsy is performed to assess the disease severity, not always including genotype 3. Response to antiviral therapy should be assessed by AST, ALT and qualitative HCV RNA, and in patients with liver cirrhosis early detection of HCC by alpha fetoprotein, ultrasound, CT, or MR should be done every 6 months. Chronic HCV infection with cirrhosis and HCC is the leading indication for liver transplantation. The current hepatitis B vaccination policy is universal neonatal vaccination. HBsAg, HbBeAg and antiHBe positive patients should be qualitatively tested for HBV DNA and liver biopsy is performed according HBV DNA level. Patients are treated with interferon and nucleos(t)ide analogues. Treated patients should be tested for HBsAg, HBeAg and HBV DNA every 3 and 6 months. The optimal duration of therapy for oral drugs is not well established and life long treatment is generally recommended. Chronic HBV infection is the leading cause of HCC and its early detection is essential. Liver transplantation is successfully performed for HBV cirrhosis, liver failure and HCC. Patients with HBV/HDV, HBV/HCV or HIV/HBV/HCV co-infection should be treated accordingly. TTV, GBV-C and HEV hepatitis do not cause chronic liver diseases.

[Treatment of recurrent hepatitis C infection after liver transplantation]. / Terapija infekcije hepatitisom C nakon transplantacije jetre.

Recurrent infection with HCV after liver transplantation is almost universal and is associated with substantial morbidity, mortality and graft loss. In contrast to immunocompetent individuals, HCV infection in immunosuppressed transplant recipients usually has an accelerated course. Acute hepatitis develops in approximately 75% of HCV recipients in the first six months following orthotopic liver transplantation (OLT). By the fifth postoperative year, over 80% of HCV-infected liver transplant recipients will develop histologic evidence of chronic allograft injury secondary to hepatitis C, with up to 30% developing cirrhosis. While the choice of calcineurin inhibitor has not been clearly shown to affect histologic recurrence of hepatitis C or the frequency of rejection in HCV-infected recipients, cumulative exposure to corticosteroids is associated with increased mortality, higher levels of HCV viremia and more severe histologic recurrence. Unfortunately, treatment of chronic HCV in liver transplant recipients is suboptimal. Combination therapy with interferon (pegylated and nonpegylated forms) plus ribavirin appears to provide maximum benefits. Drug therapy is usually administered for recurrent disease. No prophylactic therapy is available. Preemptive regimens offer no distinctive advantages over treatments initiated for recurrent disease. Overall, treatment is poorly tolerated, with frequent need for dose reductions, especially for cytopenias, and drug discontinuation in up to 50% of patients. Optimizing drug doses is important in maximizing sustained virologic response rates. The achieved SVR is between 33% and 42% in randomized studies treating patients with histologic recurrence and 0% to 33% when used in a preemptive protocol. The potential factors that influence this low SVR rate are: 1) high percentage of patients with genotype 1 virus; 2) high viral load at the start of treatment; 3) high percentage of prior non-responders to therapy; 4) side effects that often make the use of standard doses and duration of treatment difficult; 5) the use or not of growth factors; and 6) the effect of immunosuppression. In post-transplant patients with recurrent HCV disease, combination Peg alfa-2b or alfa-2a in standard dose and ribavirin (800-1200 mg either ab initio or as an increasing dose) regimen for 48 weeks was significantly better than no therapy, but not than any other therapy.

[Viral hepatitis. Croatian consensus conference--2009]. / Virusni hepatitis. Hrvatska konsenzus konferencija 2009.

Summarized text of Croatian Consensus Conference on Viral Hepatitis of 2009 comprises the following chapters: 1) Epidemiology, 2) Clinical Picture, 3) Diagnostic Procedure, 4) Aims of Treatment of Viral Hepatitis, 5) Terminology, 6) Medicaments (6.1. Interferon, 6.2. Analogues of Nucleozides and Nucleotides), 7) Hepatitis B (7.1. Serologic and Molecular HBV Diagnostics, 7.2. Terminology, 7.3.Whom to Treat? 7.4. Therapy), 8) Hepatitis C (8.1. Serologic and Molecular HCV Diagnostics, 8.2. Terminology, 8.3. Whom to Treat? 8.4. Therapy). Clinical, laboratory and histologic assessment of patients with chronic viral hepatitis (algorythm of pretherapeutic treatment; histologic evaluation) and notions related to therapy of viral hepatitis (category of the patient and category of the response to treatment) are presented in related tables.

[Monitoring patients with chronic hepatitis during and after therapy]. / Pracenje lijecenih i nelijecenih bolesnika s virusnim hepatitisom.

Hepatitis C is a major public health problem. General screening is not advisable and should be limited to risk groups. The gold standard for the assessment of disease severity is liver biopsy. AST and ALT do not correlate with histology. Serum HCV RNA by qualitative assay and HCV genotype should be determined prior to therapy. Response to antiviral therapy should be assessed by testing AST, ALT and qualitative HCV RNA. Repeat liver biopsy is not necessary. The incidence of HCC related to HCV infection is rising. Early detection by a cost effective screening program is essential. In patients with liver cirrhosis caused by hepatitis C, alpha fetoprotein and liver sonography should be done every 6 months. Upper GI endoscopy is recommended every 1-4 years in cirrhotic patients. Over 350 000 000 people are infected with HBV worldwide, and chronic HBV infection is the leading cause of liver cancer and tenth leading cause of death. HBs Ag, HBeAg and HBV DNA positive patients should be monitored for 6 months before treatment. Patients treated with antiviral therapy should be tested for HBAg, HBeAg and HBV DNA at the end of treatment and every 6 months thereafter to assess virologic response. Monitoring of serum HBV DNA is done by PCR. Patients treated with lamivudine should be tested for YMDD mutation. Ultrasound and AFP monitoring are recommended for detection of HCC, but results are not always reliable. Approximately 40% -70% of HIV infected patients have coinfection with HCV, HBV and HDV. HIV/HCV coinfected patients have an increased risk of progressive liver disease and should be treated accordingly.

[Viral hepatitis: Croatian consensus statement]. / Virusni hepatitis: Hrvatska konsenzus konferencija.

There has been a dramatic improvement in diagnostic procedures and therapy of viral hepatitis in the last 20 years. Improvements in therapy caused an increase in actual cost, however, with significant long-term savings through a decreased cost of treatment of advanced liver disease including liver transplantation. The Croatian National Board for Viral Hepatitis has decided to initiate the organization of consensus conference on viral hepatitis enabling the leading experts in the country to give the best possible recommendations for the diagnosis, prophylaxis and therapy in our circumstances. The Consensus Conference took place in Zagreb in June 2004, with update in March 2005, organized by the Croatian National Board for Viral Hepatitis, Reference Centers of the Ministry of Health for Chronic Liver Diseases, Infectious Diseases and AIDS, Croatian Society of Gastroenterology--Hepatology Section, Croatian Society for Nephrology, Dialysis and Transplantation, and Croatian Institute for Health Insurance. Invited experts provided written reports on the respective subjects that appear in this issue and their recommendations resulting in this consensus statement.

[Clinical aspects and therapy of toxic hepatitis]. / Klinicka slika i terapija toksicnih hepatitisa.

The different types of hepatotoxicity can be induced by drugs. Approximately 2%-5% of patients require hospitalization for jaundice. Drug-induced hepatic lesions are responsible for 10% of hepatitis cases in adults. Most hepatotoxic drug reactions are idiosyncratic and classified either as immunologic (hipersensitivity) or metabolic. In contrast to intrinsic hepatotoxins, these reactions are not dose-dependent nor predictable. The enzyme system responsible for drug biotransformation in liver is cytochrome P450, a large multigene family of enzymes with 300 members. Clinical presentation in patients who develop drug hepatotoxicity can be asymptomatic with mild biochemical abnormalities, resembling acute hepatitis or chronic autoimmune hepatitis, veno-occlusive disease and cirrhosis. Withdrawal of the drug usually leads to reversal of the lesion. A spectrum of drug induced hepatotoxicity, diagnosis and treatment is reviewed.

[Morphology of gastritis and Helicobacter pylori infection]. / Morfoloska slika gastritisa i infekcije Helicobacterom pylori.

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.

[Non-ulcer dyspepsia and Helicobacter pylori infection]. / Neulkusna dispepsija i infekcija Helicobacterom pylori.

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.

[The urea breath test]. / Izdisajni test ureje.

Helicobacter pylori is infective cause of peptic ulcer and a risk factor for gastric carcinoma. The discovery of the bacterial ed to importance of finding a new reliable and inexpensive diagnostic method for detection of infection before and after eradication therapy. Urea breath test is isotope based test. It has become the most specific and sensitive method in detection of Helicobacter pylori infection, therefore many other isotope based tests become popular in diagnostic of gastrointestinal diseases. Because of its simplicity and no need in using endoscopy in the procedure it is very popular in primary diagnosis and in controlling eradication. It is successfully used in diagnostics of Helicobacter pylori and bacteria eradication success testing, where it is one of most reliable diagnostic methods.

[The rapid urease test]. / Brzi ureazni test.

Today there are many methods in diagnostics of Helicobacter pylori infection. They are divided in two major groups based on using of endoscopy (invasive and non-invasive methods). Helicobacter pylori bacteria are specific because of having very big amounts of urease enzyme that divides urea on NH3 and CO2 which enables environment suitable for survival. Rapid ureas test is based on detecting of the enzyme activity. Because of its simplicity and high sensitivity and specificity it belongs to methods that are used in every day practice in endoscopic laboratories.

[Extra-gastrointestinal tract diseases and Helicobacter pylori infection]. / Bolesti izvan zeluca i probavnog sustava i infekcija Helicobacterom pylori.

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.

[Gastric ulcer and Helicobacter pylori infection]. / Zelucani ulkus i infekcija Helicobacterom pylori.

Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID) are considered to be the two major risk factors implicated in the development of gastric ulcer. Helicobacter pylori infection related chronic gastritis is known to be the underlying condition which may lead to gastric ulcer. Development of gastric ulcer as the consequence of underlying chronic gastritis is caused by many factors. Treating Helicobacter pylori infection entails the healing of gastric ulcer, it concomitantly prevents recurrences and complications of gastric ulcer, primarily bleeding, and changes the natural course of gastric ulcer disease. Continuation of antisecretory maintenance treatment beyond ulcus healing and eradication of Helicobacter pylori infection is only indicated in risk groups. Patients with gastric ulcer caused by NSAID use are managed with antisecretory therapy.