This research is aiming to set higher standards in healthcare research in Bosnia and Herzegovina from the aspect of mathematical and information science methodology. The data on Hepatitis C virus treatment published in previous work was reinvestigated using the Bayesian network methodology. The results are still in the line with the results published worldwide, but this research provides an additional quality, through the conditional probabilities for treatment outcome. Further development of this model may result in an acceptable prediction model for HCV treatment outcome.

Budd-Chiari syndrome is a rare but life-threatening disorder characterized by obstruction of the hepatic venous outflow. Treatment depends on underlying cause, extent of the obstruction and functional capacity of the liver. When all other therapy options are unsuccessful, liver transplant should be considered. Portal vein thrombosis (PVT) is a frequent event in patients with cirrhosis which can be treated with anticoagulants, but there are limited data regarding safety and efficacy of this approach.

INTRODUCTION Hepatitis C virus infection (HCV) is an important cause of morbidity and mortality in patients with end-stage renal disease (ESRD). PATIENTS AND METHODS In this prospective, observational study, 205 patients, 37 (18%) of them with chronic HCV infection, were followed up for a one-year period at Department of Hemodialysis, Sarajevo Clinical Center, University of Sarajevo. The following parameters were analyzed: dialysis duration, sex, PCR RNA, HCV genotypes and biochemical parameters. Thirteen anti-HCV PCR RNA positive patients were treated with pegylated interferon alpha (Pegasys, Hoffman-La Roche). The goal of therapy was to reach sustained virologic response. The presence of anti-HCV antibodies in serum was detected by enzyme linked immunosorbent assay (ELISA). RESULTS Of 37 anti-HCV positive patients, there were 20 (54%) males and 17 (45.9%) females with the mean hemodialysis duration of 143.67 +/- 57.64 months and mean age of 54.45 +/- 8.93 years. Of 37 anti-HCV positive patients, 30 (81.08%) patients were HCV RNA PCR positive. Among HCV RNA PCR positive patients, two had up to twofold elevated ALT values, one had twofold elevated AST values, and one had sixfold elevated GGT values. Thirteen RNA PCR positive patients were treated with pegylated interferon alfa for 48 weeks. Only one patient had genotype 1 virus. Upon therapy completion, only three patients were negative by PCR RNA (genotype 1b, 23.07%) at six months and yearly follow ups remained PCR negative. CONCLUSION Sustained virologic response was achieved in three study patients. Monitoring guidelines for infection control, isolation of seropositive patients, and strict hygienic preventive measures can prevent HCV seroconversion in hemodialysis patients.

BACKGROUND Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the digestive tract. The majority of GISTs are located in the stomach. Only 3-5% of GISTs are located in the duodenum associated with an increased risk of gastrointestinal bleeding as primary manifestation. AIM The aim of our study was to present frequencies of GIST in patients who underwent endoscopic procedures at Gastroenterohepatology Department due to different reasons. We also investigated the most frequent localization of GIST tumors and pathohistologicall pattern of tissue samples. PATIENTS AND METHODS Twenty two patients examined at gastroenterology department were analyzed in the period from 2005 until 2012. All of the patients were endoscopically examined ( gastroscopy, colonoscopy, endoscopic ultrasound). A few patients were referred from surgery where GIST was diagnosed during surgical procedure. Macroscopically noticed changes were pathohistologically analyzed by immunohistochemical staining (Alpha-smooth muscle actin (SMA), CD34, CD117, Ki-67 antigen, cytokeratin i desmin). RESULTS No significant difference in gender distribution of patients with GIST-s was found. We also analyzed the appearance of GIST with respect to mean patient age and no statistically significant difference was found either. However, investigation of tumor localization related to gender of patients we found a difference in gender distribution of tumor localization. In female GIST-s are more often located in the stomach than in men, with a significance level of 0.05. Immunohistochemical analysis of biopsy samples showed that CD 117 is statistically significant more frequent in men than in woman. CONCLUSION Taking in account the small sample size in our investigation over a period of seven years, we are not able to give a definitive conclusion about GIST. Further studies and observations are necessary to give a definite conclusion.

Association of Gastroenterologists and Hepatologists of Bosnia and Herzegovina based on the experiences of domestic and foreign centers operating in the field of hepatology and accepted guidelines of the European and the U.S. Association for Liver Diseases adopted the consensus for the diagnosis and treatment of chronic viral hepatitis B and C. The guidelines are intended for specialists in gastroenterology and hepatology, and infectious diseases physicians working in primary health care and family medicine, but also other physicians who are confronted with this disease in their practice, with the aim of facilitating and shortening the diagnostic and treatment protocols of patients with chronic viral hepatitis B and C. This ensures faster, more efficient, more rational and cost-effective care of patients with hepatitis, with an emphasis on stopping the deterioration of liver disease to liver cirrhosis and eventually hepatocellular carcinoma. Key words: Chronic hepatitis B and

INTRODUCTION Infection with hepatitis C is often manifested by a mild clinical course, and in many patients it is revealed incidentally, during routine laboratory ests. Progression of the disease often takes 10-20 years with specified high risk of fibrosis and hepatocellular carcinoma. MATERIAL AND METHODS The group of subjects with chronic liver disease of viral C etiology was consisted of 50 patients of both sexes, 38 (75%) were male and 13 (25%) females, aged 20-65 years. Patients were selected according to genotype hepatitis C viral infection and subsequently treated according to two current therapeutic protocols. All patients had prior therapy and after completion of treatment using standard methods of laboratory tests were done the following: functional hepatic tests, serological analysis, nucleic acid detection of hepatitis C virus polymerase chain reaction (PCR), quantitatively and qualitatively with the genotyping of the virus C, which determines the length of therapy. In determining the stage of chronic liver disease, histopathological examination of liver tissue samples obtained by biopsy of the liver was done and we analyzed the fibrosis and architectural changes. RESULTS By analyzing the HCV RNA PCR values at the beginning and end of treatment we tested the effect of treatment on PCR with paired samples t-test logarithm values of the PCR and came to the conclusion that the values after treatment are significantly lower with threshold of significance of 0.01. The results showed that the value of PCR before and after therapy, or achieved a response at the end of therapy, which achieved 77% of patients. The values of ALT in the group of patients with CHC were significantly higher than the values in the group of patients after the therapy. AST values in the patients with CHC were significantly higher than the values in the group of patients after therapy. There was a moderate correlation between ALT values at baseline and ALT values upon completion of treatment (0.5061). There was no correlation between HCV RNA PCR and ALT and AST. CONCLUSION Upon completion of antiviral treatment response at the end of treatment achieved 77% of patients, regardless of the genotype of the virus. Also, regardless of the genotype of the virus antiviral therapy led to statistically significant reduction of AST and ALT, indicating a direct effect of combination therapy on virological and biochemical response with no significant link between these two studied parameters.

Introduction: Sideropenic anemia is a hypochromic, microcytic anemia caused by insufficient iron level in the body. This is the most common anemia. In a large percentage it is the symptom of gastrointestinal tract cancer. Anemia was defined by hemoglobin level <119 g/dl, hematocrit <0.356 for women or hemoglobin level <138 g/dL and hematocrit <0415 for men. Gastric cancer after lung cancer is the second most common malignant tumor in the world. Frequent localization is the antrum, and less frequently in the cardia and fundus. Definite factors in the development of gastric cancer are chronic atrophic gastritis, H. pylori, intestinal metaplasia, and epithelial dysplasia as a precancerous lesion. Strong link between sideropenic anemia and gastrointestinal tract cancers recommend that patients with sideropenic anemia without a clear indication underwent same gastroscopic and colonoscopy examination. The goals were to prove sideropenic anemia, diagnose and histologically confirm tumors, tumors location and correlates anemia with tumor anemia or show the dependence of anemia on tumor Results: The study included 100 subjects (50 from counseling center for hematology that came due to sideropenic anemia and 50 patients from the Clinic for Gastroenterology who had gastrointestinal tract cancer). Respondents had regular laboratory tests and endoscopic examinations, ultrasound of the abdomen, CT of the abdomen and tumor markers. In the group of patients from Counseling center for hematology with sideropenic anemia was found 11 cancerous processes, mostly in form of gastric and colon cancer. In the group of patients hospitalized at the Clinic for Gastroenterology most cancer process were localized in the stomach and colorectum. Conclusion: Tumors of the gastrointestinal tract are the most common cause of sideropenic anemia, due to which the patients often first contact Counseling center for hematology. Sideropenic anemia is more common in men as also the number of digestive tract cancers in men. Sideropenic anemia has a significant place in the diagnosis of gastrointestinal tract tumors. Sideropenic anemia is most common in men after 50 years of age. The most common tumors of the gastrointestinal tube were gastric and colon cancer.

INTRODUCTION Viral Hepatitis C, formerly known as non A-non B hepatitis, as a separate clinical entity described in 1975 is most often reported in patients who received blood transfusions, and also called it post transfusion hepatitis. AIM OF THE STUDY Goal was to quantify the number of HCV RNA copies by PCR method, histologically determine the stage of fibrosis and degree of necroinflammatory activity in biopsies of liver parenchyma, and compare the histopathological changes with the number of the virus copies. MATERIAL AND METHODS The study was prospective and involved 50 patients suffering from chronic hepatitis C of viral etiology. All patients underwent liver biopsy and the specimens were patohistologically investigated to determine the stage of fibrosis score, and necroinflammatory activities. In every case was determined the concentration of AST, ALT, bilirubin, CBC, DR, and all underwent percutaneous ultrasonography and gastroscopy. We performed genotyping of viruses and virus quantification of HCV RNA-PCR. RESULTS The study showed that women were older than men. The stage of fibrosis and degree of necroinflammatory activities were higher in women than men, meaning that older people carry the virus longer, increasing the number of virus copies the disease lasted longer. According to the etiology of infection the patients who were infected by blood transfusions had a higher stage of fibrosis. Score of necroinflammatory activity was significantly dependent on variables AST with p = 0.02 and ALT with p = 0026. CONCLUSION Our research has shown that the stage of fibrosis was significantly dependent on alanine aminotransferases, duration of infection, number of virus copies and mode of infection. Patients who received blood transfusions, had the longest duration of infection, higher stage of fibrosis and degree necroinflammatory activity.

Objectives: To assess prospects of endoscopic ultrasonography in the diagnostic methods of gastric cancer in our study and to determine the impact of this technique on the later use of therapy. Material and methods: This is a retrospective study which was conducted on the patients with histopathologic diagnosis of gastric adenocarcinoma being sent to examination with endoscopic ultrasound. We compared the initial decision concerning the therapy being based on the conventional diagnostic techniques with the application of the final therapy, which is based on the results of endoscopic ultrasound. Results: The study included 92 patients in the period from 2005 to 2010. The diagnostic precision was 71% in stage T, while in stages T1, T2, T3 and T4 the diagnostic precision was 100, 42, 78, and 100%. The sensitivity and accuracy for differentiation of T1-2 from T3- 4 was 95 and 82%. We could not identify factors associated with obtaining a correct diagnosis in staging T. The diagnostic accuracy was 74% for N stage (N0: 55% Nx 81%). The presence of the free perigastric fluid was found in 5 cases while the presence of peritoneal carcinomatosis was subsequently confirmed in 2 cases. The result of endoscopic US has led to some changes in subsequent therapeutic management in 26 patients (28%). Conclusion: Endoscopic ultrasonography is a useful technique for loco-regional staging in gastric adenocarcinoma, which can have significant implications for the therapeutic treatment of these patients.

Background and Aims: Hepatic steatosis seems to be a risk factor for poor response to interferon and ribavirin therapy in patients with chronic hepatitis C. The aim of this study was to determine presence of hepatic steatosis in chronic hepatitis C and its influence on early virological response in patients treated with combined antiviral therapy (pegylated interferon and ribavirin). Methods: We studied 96 patients treated at Gastroenterohepatology Department, in the period of four years (2005-2009). There were 71 males and 25 females enrolled in this study. 72 patients had genotype 1, 5 patients had genotype 2, 17 patients had genotype 3 and 2 patients had genotype 4. Liver histology was evaluated in order to establish presence of inflammation, fibrosis and steatosis. HCV RNA levels in sera were measured by real time PCR. Early virological response (EVR) was defined as negative serum HCV RNA at week 12. In order to measure the effect influence of steatosis on early response to therapy, as well as genotype and response to therapy, we calculated relative risk and the corresponding p-value after 12 and 48 weeks. Results: The overall rate of EVR was 70%. The rate was significantly lower in the group with steatosis, regardless of the presence of micro or macrosteatosis, amounting to 60%. Serum cholesterol level was significantly higher in females than in males (7.4±0.7 vs. 5.1±0.3 mg/mL). The values of relative risks (and p-values) for effect of steatosis on the response are RRS12=8.4615 (2.87E-05), and RRS48=0.9844 (0.7399), while the values for the effect of genotype to therapy were RRG12=1.3378 (0.7543), and RRG48=3.5862 (0.2709). Conclusions: Our findings suggested that hepatic steatosis may have a strong influence on interferon therapy response in the sence that it is eight times more probable to not respond in the presence of steatosis. The presence of steatosis was highly associated with progressive disease and failure to achieve the EVR; therefore it can be a predictor of poor response to antiviral therapy.

The role of ferritin in fibrogenesis of liver parenchyma in patients with alcoholic liver disease has been investigated in previous studies. Ferritin was shown to be an indirect marker of ferum deposition in liver parenchyma in alcohol liver disease. The aim of the present study was to examine the role of nitric oxide (NO) in the pathogenesis of alcoholic liver disease as well as the influence of NO on iron (ferritin) metabolism in patients with alcoholic liver disease. Serum concentrations of NO and iron markers (iron, total iron binding capacity, ferritin) were measured in 30 male patients (aged 20-60 years) with alcoholic liver disease, as well as from a control group (30 male patients (aged 20-60 years) without liver disease). NO concentration was detected by measuring production of nitrates and nitrites using classical colorimetric Griess reactions. There was a statistically significant increase in serum NO concentration in patients with alcoholic liver disease compared to the control group (mean +/- SEM; 41,2 +/- 25,3 vs. 28,9 +/- 12,3 mmol/dm3, respectively; p<0,03). Similarly, serum iron levels (18,7 +/- 8,2 vs. 13,2 +/- 10,2 g/100 cm3, respectively; p<0,03) and serum total iron binding capacity (51,3 +/- 13,9 vs. 41,4 +/- 11,4 micromol/dm3, respectively; p<0,005) were also significantly higher in patients with alcoholic liver disease compared to control patients. The serum concentration of ferritin was 27% higher in patients with alcoholic liver disease than in the control group; however this was not statistically significant (283,2 +/- 291,0 vs. 222,9 +/- 252,0 g, respectively; p<0,4). There was no correlation between NO and ferritin in the investigated groups. These results suggest a possible role of NO and iron in the pathogenesis of alcoholic liver disease. NO and iron may be used as non-invasive predictors of liver damage. Also the role of iron in sera, and its deposition in liver parenchyma, could be used in clinical practice, especially in regards to assessing the fibrogenesis of liver parenchyma induced by ferritin.

Th e role of ferritin in fi brogenesis of liver parenchyma in patients with alcoholic liver disease has been investigated in previous studies. Ferritin was shown to be an indirect marker of ferum deposition in liver parenchyma in alcohol liver disease. Th e aim of the present study was to examine the role of nitric oxide (NO) in the pathogenesis of alcoholic liver disease as well as the infl uence of NO on iron (ferritin) metabolism in patients with alcoholic liver disease. Serum concentrations of NO and iron markers (iron, total iron binding capacity, ferritin) were measured in  male patients (aged – years) with alcoholic liver disease, as well as from a control group ( male patients (aged – years) without liver disease). NO concentration was detected by measuring production of nitrates and nitrites using classical colorimetric Griess reactions. Th ere was a statistically signifi cant increase in serum NO concentration in patients with alcoholic liver disease compared to the control group (mean ± SEM; , ± , vs. , ± , mmol/dm, respectively; p<,). Similarly, serum iron levels (, ± , vs. , ± , g/ cm, respectively; p<,) and serum total iron binding capacity (, ± , vs. , ± , μmol/dm, respectively; p<,) were also signifi cantly higher in patients with alcoholic liver disease compared to control patients. Th e serum concentration of ferritin was  higher in patients with alcoholic liver disease than in the control group; however this was not statistically signifi cant (, ± , vs. , ± , g, respectively; p<,). Th ere was no correlation between NO and ferritin in the investigated groups. Th ese results suggest a possible role of NO and iron in the pathogenesis of alcoholic liver disease. NO and iron may be used as non-invasive predictors of liver damage. Also the role of iron in sera, and its deposition in liver parenchyma, could be used in clinical practice, especially in regards to assessing the fi brogenesis of liver parenchyma induced by ferritin.

The aim of the study was to define the distribution of p53, bcl-2 and Ki-67 proteins in the inflammatory-regenerative and dysplastic lesions of the colon mucosa. The relationship between the presentation of p53, bcl-2 and Ki-67 proteins and the intensity of the inflammatory-regenerative and dysplastic lesions in the colon flat mucosa was investigated as well. Biopsy specimens from 270 patients were examined: 74 were classified as inflammatory-regenerative and 196 as dysplastic lesions (108 mild, 58 moderate, and 30 severe dysplasia). The expression of all three proteins was assessed on the basis of location, quantity, and intensity of immunostaining, by counting antigen positive cells, in comparison with normal mucosa and adenocarcinoma. p53 protein appears only in sporadic cases (6.6%) of severe dysplasia. Bcl-2 expression appears significantly (p<0.005) more often in cases of mild dysplasia (61.1%) compared to inflammatory-regenerative mucosa (14.8%). In cases of mild dysplasia, bcl-2 positive cells were spreading from the lower third to the middle third of the crypts. Bcl-2 expression was maintained through the stadiums of moderate and severe dysplasia (75.8%), where antigen positive cells were found all along the crypts. A significant increase (p<0.005) in the expression of nuclear protein Ki-67 was noticed in the stadiums of moderate (labelling index =26.3) compared to mild dysplasia (labelling index=16.7), and severe (labelling index=36.7) compared to moderate dysplasia, where the zone of cellular proliferation was widen along the whole crypt length. In the process of the development of epithelial dysplasia in the flat mucosa of colon a degree of the gene p53 alteration is low and appears only in sporadic cases of severe dysplasia. Mutation of the bcl-2 gene is involved in the genesis of the lesion but not in its progression to carcinoma. Increased expression of Ki-67 protein speaks in favour of an increased cellular proliferation which, together with the above mentioned mechanisms, is involved in the process of occurrence and progression of epithelial dysplasia in the flat mucosa of colon.

The aim of the study was to verify the presence of mutated tumor suppresser gene p53 in intestinal mucosa with histologically confirmed premalignant lesions and gastric carcinoma, and assess its prognostic value. The paper presents prospective study that included 50 patients with gastric adeno-carcinoma of intestinal type that were treated at Gastroenterohepatology Clinic, and 50 patients with histologically confirmed chronic atrophic H. pylori positive gastritis. In the mucosa biopsy samples, we analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes. We typed intestinal metaplasia immunohistochemically and confirmed the presence of p53 onco-protein in antigen positive gastric carcinoma cells, and evaluated its prognostic value. Our results suggest that H. pylori acts as an initiator of inflammatory processes in gastric mucosa, which are followed by emergence of precancerous lesions. p53 is expressed late in carcinogenesis (14%) and as such, may be considered as an indicator of transformation of premalignant into malignant lesion.

The aim of our study was to determine the genotypes of viral hepatitis C. We examined 54 patients with chronic hepatitis C who were treated at Gastroenterohepatology Department University of Sarajevo. We also monitored effects of therapeutical results in same group of patients. Polymerasa chain reaction (PCR) was used to quantified the number of HCV-RNA copies in 1 ml of blood. Genotype of virus was determined as well. We created therapeutical protocols based on genotype and quantity of virus that contained pegilated interferon alpha2a(40) kD and ribavirin. The result of our investigation presented that the highest number of patients, 25 had genotype 1a; 13 patients had genotype lb; 11 patients had genotype 3; 4 patients had genotype 4 and 1 patients with genotype 2a. At the end of therapy, 42 patients were HCV-RNA PCR negative; 7 female and 35 male. Four women with genotype 1a, responded on therapy; two with genotype 1b and one with genotype 3. Within the male group of patients (35 patients), 16 patients had a genotype 1a, 3 patients had a genotype 1b, 11 patients had a genotype 3, 4 patients had genotype 4 and one patient had genotype 2a. Patients who did not respond on therapy or were HCV-RNA-PCR positive at the end of therapy were genotype 1a and 1b. According to result of our investigation, genotype 1 is the most frequent among our patients, and the most severe damages in liver parenchyma are associated with genotype 1a and 1b. Genotype 1b also had less respond on therapy.