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Background. Ultrasonography is a noninvasive, inexpensive, and widely available diagnostic tool. In the last two decades, the development of ultrasound techniques and equipment has significantly increased the usage of intestine ultrasound (US) in the assessment of the gastrointestinal tract in patients with inflammatory bowel disease (IBD). Although current guidelines suggest routine utilization of US in patients with Crohn’s disease, data regarding US usage in ulcerative colitis are still scarce. We aimed to assess the reliability of intestinal ultrasonography in the assessment of disease activity and extension of patients with ulcerative colitis. Methods. Fifty-five patients with a histologically confirmed diagnosis of ulcerative colitis, treated at University Clinical Center of Serbia in the period from 2019 to 2022 were included in this retrospective observational study. The data were obtained from the patient’s medical records including history, laboratory, US, and endoscopy findings. US examined parameters were as following: bowel wall thickness (BWT), presence of fat wrapping, wall layer stratification, mesenteric hypertrophy, presence of enlarged mesenteric lymph nodes, and absence or presence of ascites. Results. Our results suggest that there is a strong correlation of BWT and colonoscopy findings regarding disease extension (r = 0.524, p = 0.01 , p < 0.05 ). Furthermore, our results have shown a statistically significant correlation of BWT with the Mayo endoscopic score (r = 0.434, p = 0.01 , p < 0.05 ), disease activity score (r = 0.369, p = 0.01 , p < 0.05 ), degree of ulcerative colitis burden of luminal inflammation (r = 0.366, p = 0.01 , p < 0.05 ), and Geboes index (r = 0.298, p = 0.027 , p < 0.05 ). Overall accuracy of US for disease extension and activity was statistically significant ( p < 0.05 ). Conclusions. Our results suggest that US is a moderately accurate method for the assessment of disease activity and localization in patients with UC.

The status of essential and toxic trace metals in the blood of Crohn’s disease (CD) patients is unexplained. This study aimed to provide the first elemental profiling of the most recognized essential elements (Mn, Cu, Zn, Se) and selected toxic trace elements (As, Cd, Pb, and U) in sera and cell lysate (CL) samples of CD patients (n = 84). The results were compared with sex- and age-matched samples from the control group (CG). CD sera contained significantly higher levels of Mn, As, Cd, Pb, and U than did CG sera. An identical pattern, with the added inclusion of Cu (also higher in CD patients than in the CG), was obtained for CL samples. However, the most important finding was hypermanganesemia, which indicates that Mn could act as a toxic trace metal in CD. As, Cd, and U were the most significant toxic elements that showed antagonistic effects on the extrusion of essential Mn and Cu. Circulatory system screening markers for CD are hereby proposed (Mn/Cu, Mn/As, and Mn/Pb ratios). These three metal ratios were strongly and significantly correlated with F-Calprotectin levels, and deserve consideration as new markers of CD. The target metals and metal ratios should be taken into consideration as novel initiating and/or modifying factors for CD.

Inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC) are complex diseases whose etiology is associated with genetic and environmental risk factors, among which are diet and gut microbiota. To date, IBD is an incurable disease and the main goal of its treatment is to reduce symptoms, prevent complications, and improve nutritional status and the quality of life. Patients with IBD usually suffer from nutritional deficiency with imbalances of specific micronutrient levels that contribute to the further deterioration of the disease. Therefore, along with medications usually used for IBD treatment, therapeutic strategies also include the supplementation of micronutrients such as vitamin D, folic acid, iron, and zinc. Micronutrient supplementation tailored according to individual needs could help patients to maintain overall health, avoid the triggering of symptoms, and support remission. The identification of individuals’ genotypes associated with the absorption, transport and metabolism of micronutrients can modify future clinical practice in IBD and enable individualized treatment. This review discusses the personalized approach with respect to genetics related to micronutrients commonly used in inflammatory bowel disease treatment.

Background: Jaundice is a common clinical finding in clinical practice of hepatologists and general practitioners. It occurs when serum bilirubin levels exceed 3 mg/dL. Summary: In this review, we summarize the pathophysiological mechanism of jaundice, clinical approach to the patient with jaundice, and laboratory and imaging techniques. Clinical presentation of jaundice manifests through yellow skin and sclera coloration. Evaluation of every patient includes detailed medical history and examination. In the laboratory, evaluation of enzymes of hepatic inflammation as well as cholestatic enzymes with serum bilirubin must be included. Additional laboratory analysis and imaging modalities are needed in order to differentiate jaundice etiology. Moreover, imaging is available and needed in further evaluation, and treatment is dependent on the underlying cause. Key Messages: In this review, we will outline the pathophysiological mechanism of jaundice, clinical approach to the patient with jaundice, and diagnostic and treatment approach to these patients.

A wide spectrum of extraintestinal manifestations (EIMs) can burden patients with inflammatory bowel disease (IBD). EIMs contribute fairly to morbidity and mortality rates in IBD patients. Moreover, EIMs in IBD patients are so frequent that some suggest that IBD should be approached as a systemic disorder. Anemia is very common in IBD patients. The two most common types of anemia in IBD, iron deficiency anemia and anemia of chronic disease, are extraintestinal complications. Autoimmune hemolytic anemia (AIHA) is a rare extraintestinal manifestation of IBD, more frequent in ulcerative colitis (UC) than in Crohn’s disease (CD). In this case-based review of the literature, we present a 36-year-old female patient diagnosed with Crohn’s disease (CD) and Coombs positive AIHA, complicated by pulmonary thromboembolism and successfully treated with anti-tumor necrosis factor (anti-TNF) therapy. The underlying pathophysiological mechanism of AIHA in IBD is unclear. Treatment options for AIHA in IBD patients before biologic therapy included corticosteroids alone or in combination with azathioprine (AZA), methotrexate, and surgical treatment (colectomy and/or splenectomy). Currently, biologic therapy is a promising therapeutic option, especially in corticosteroid refractory or corticosteroid-dependent IBD patients with AIHA.

Background: Anemia is present in almost 5% of adults worldwide and accompanies clinical findings in many diseases. Diseases of the gastrointestinal (GI) tract and liver are a common cause of anemia, so patients with anemia are often referred to a gastroenterologist. Summary: Anemia could be caused by various factors such as chronic bleeding, malabsorption, or chronic inflammation. In clinical practice, iron deficiency anemia and the combined forms of anemia due to different pathophysiological mechanisms are most common. Esophagogastroduodenoscopy, colonoscopy, and the small intestine examinations in specific situations play a crucial role in diagnosing anemia. In anemic, GI asymptomatic patients, there are recommendations for bidirectional endoscopy. Although GI malignancies are the most common cause of chronic bleeding, all conditions leading to blood loss, malabsorption, and chronic inflammation should be considered. From a gastroenterologist’s perspective, the clinical spectrum of anemia is vast because many different digestive tract diseases lead to bleeding. Key Messages: The gastroenterological approach in solving anemia’s problem requires an optimal strategy, consideration of the accompanying clinical signs, and the fastest possible diagnosis. Although patients with symptoms of anemia are often referred to gastroenterologists, the diagnostic approach requires further improvement in everyday clinical practice.

Background: Abdominal pain is a common symptom of gastroenterology examination. Chronic abdominal pain is present for >3 months. Summary: Gastroesophageal reflux disease (GERD) is one of the most common gastrointestinal diseases encountered by both gastroenterologists and general practitioners. GERD is usually a chronic disease presented with a set of symptoms including heartburn and/or regurgitation, and less commonly epigastric pain. Epigastric pain syndrome is characterized by the following symptoms: epigastric pain and/or burning. It does not necessarily occur after meal ingestion, may occur during fasting, and can be even improved by meal ingestion. Duodenal ulcers tend to cause abdominal pain that is localized in the epigastric region and commence several hours after eating, often at night. Hunger provokes pain in most of the cases and decreases after meal. Gastric ulcer pain occurs immediately after eating, and consuming food increases pain. Pain is localized in the epigastrium and can radiate to the back. Abdominal pain in irritable bowel syndrome is related to defecation. A typical symptom of chronic pancreatitis is pain that radiates to the back. In Crohn’s disease, inflammation causes pain. Key Messages: Pain can occur at different locations with diverse intensity and propagation and is often associated with other symptoms. For any gastroenterologist, abdominal pain is a big challenge.

Introduction. Hereditary hemorrhagic telangiectasia (HHT) is a rare autosomal dominant disorder with estimated prevalence of one in 5,000 to 10,000. The disease has age-related penetrance and the HHT signs and symptoms occur and worsen with age. A diagnosis of HHT is based on the Curacao`s criteria. Case report. We report a case series of 6 patients diagnosed with HHT, 5 with definite and one with probable diagnosis according to the Curacao criteria. In 5 patients, the recurrent epistaxis occurred in adolescence as the first presentation while one patient presented with melena. The diagnosis was delayed in 5 patients and the presence of HHT was diagnosed during or after the fifth decade. In 4 patients, the overt gastrointestinal bleeding occurred in the later course of the disease. The asymptomatic pulmonary circulation arteriovenous malformations were detected in 2 patients. The cerebral arteriovenous malformations were not detected. Conclusion. Hereditary hemorrhagic telangiectasia is a rare disorder affecting multiple organs. It should be considered in the adolescents with recurrent epistaxis and in the differential diagnosis of anemia with signs of the gastrointestinal bleeding in order to shorten the delay in the diagnosis and subsequently improve the outcome of the disease.

Introduction. Angiosarcomas are malignant tumors of vascular endothelium that may arise from different locations. Although primary hepatic angiosarcoma accounts for only 1.8% of primary liver tumors, it is the most common malignant mesenchymal tumor of the liver. We report a case of primary hepatic angiosarcoma with melena as an unusual initial manifestation of this extremely rare tumor. Case report. Forty-four-years old patient with melena was referred to our Clinic because melena was not resolved after repeated argon plasma coagulation of bleeding lesions during esophagogastroduodenoscopy in the regional hospital. Abdominal ultrasound and multislice computed tomography (MSCT) revealed enlarged liver, with focal lesion 6 cm in diameter localized in the left lobe with multiple satellite lesions in both liver lobes, enlarged spleen and extremely dilated and long umbilical vein. Double-balloon enteroscopy and video capsule endoscopy detected the multiple bleeding vascular lesions in the small bowel. Histopathological examination and immunohistochemistry of the small bowel lesions revealed malignant mesenchymal proliferation with vascular/endothelium differentiation of neoplastic cells. The patient was diagnosed with metastatic angiosarcoma probably of hepatic origin with metastasis in the small bowel, that caused melena, and in the lumbar spine, causing back pain. Conclusion. Rare causes of melena include bleeding from primary or metastatic hemangiosarcoma localized in the gastrointestinal tract, especially small bowel.

Background and aims Mucosal gene expression have not been fully enlightened in inflammatory bowel disease (IBD). Aim of this study was to define IL23A, IL17A, IL17F and TLR9 expression in different IBD phenotypes. Methods Evaluation of mRNA levels was performed in paired non-inflamed and inflamed mucosal biopsies of newly diagnosed 50 Crohn's disease (CD) and 54 ulcerative colitis (UC) patients by quantitative real-time PCR analysis. Results IL17A and IL17F expression levels were significantly increased in inflamed IBD mucosa. Inflamed CD ileal and UC mucosa showed increased IL23A, while only inflamed CD ileal samples showed increased TLR9 mRNA level. Correlation between analysed mRNAs levels and endoscopic and clinical disease activity were found in UC, but only with clinical activity in CD. Conclusion Both CD and UC presented expression of Th17-associated genes. Nevertheless, expression profiles between different disease forms varies which should be taken into account for future research and therapeutics strategies.

Background/Aim. In recent years, many studies have demonstrated a proximal shift in the distribution of adenomas and colorectal cancers. The aim of this study was to investigate whether there are differences in the incidence and anatomical distribution of adenomas and colorectal cancers spanning a 20 year time gap. Methods. We performed a retrospective observational study of colorectal adenomas and cancers diagnosed during total colonoscopy in a high volume tertiary care facility in two 1-year periods of time ? 1990 and 2010. Results. During the analyzed period, 4,048 colonoscopies were performed, 1,148 were performed in 1990 and 2,900 were done in 2010. The study included 466 patients with adenomas and 121 patients with colorectal cancers. Frequency of proximal adenoma changed from 16.5% to 32.7% (p < 0.001). By analyzing colonoscopies in 2010, an increase in the incidence of adenomas compared to 1990 was noticed. The number of adenomas sized 0?5 mm rose from 32.8% to 56.9% (p < 0.001). Frequency of colon carcinoma changed from 5.3% to 2.0% (p < 0.001). Incidence of cancers in the proximal colon rose from 21.3% to 48.4% (p = 0.002). A higher incidence of cancers in the proximal colon and a lower incidence of distal cancers were observed, while no difference was observed in the incidence of rectal cancers. Conclusion. Presence of proximal colon adenoma and cancer is higher, while the overall incidence of colon cancer is lower. This finding should be taken into account when planning the screening for colorectal cancer.

Background and Objectives. Determination of inflammatory bowel disease activity determines further therapeutic approach and follow-up. The aim of our study was to investigate correlation between patients’ reported symptoms and endoscopic and histological disease activity. Methods. A cross-sectional study was conducted in consecutive newly diagnosed patients with inflammatory bowel disease in a tertiary care referral center. The initial evaluation included patient-reported outcome for stool frequency subscore and rectal bleeding. Endoscopic activity was determined using the Mayo scoring system for ulcerative colitis and the Simple Endoscopic Score for Crohn’s disease. Histopathological activity was assessed using a validated numeric scoring system. Results. We included 159 patients (63 Crohn’s disease with colonic involvement and 96 with ulcerative colitis). We found significant correlation between the Mayo endoscopic subscoring system and histology activity in ulcerative colitis, while no correlation was found in patients with Crohn’s disease. Patient-reported outcome showed inverse correlation with endoscopic and histological activity in Crohn’s disease (rs=−0.67; rs=−0.72), while positive correlation was found in ulcerative colitis (rs=0.84; rs=0.75). Interpretation and Conclusions. Patient-reported outcome is a practical and noninvasive tool for assessment of disease activity in ulcerative colitis patients but not in Crohn’s disease.

Background Crohn's disease (CD) is chronic inflammatory bowel disease with different phenotypic characteristics influencing disease prognosis and therapeutic strategies. The aim of this pilot study was to analyze selected inflammatory and apoptotic markers in non-inflamed and inflamed samples of ileal mucosa of non-stricturing/non-penetrating (NS/NP) and stricturing (S) CD mucosal phenotypes in order to characterize their distinct profiles. Methods From twenty CD patients (9 NS/NP, 11 S) paired non-inflamed and inflamed ileal biopsies were collected and used for analysis of cytokine (TNF and IL6) and apoptotic (Bcl2, Bax, Fas and FasL) genes' expression levels by real-time PCR, while NFκB transcriptional potency was assessed by electromobility gel shift assay. Results Our results demonstrated significant upregulation of TNF and IL6 in inflamed area of both NS/NP (p = 0.03, p = 0.01) and S phenotypes (p = 0.04, p = 0.04), respectively. However, TNF increase was more prominent in NS/NP compared to S inflamed mucosa (p = 0.02). Also, level of proapoptotic Bax was significantly higher in NS/NP compared to S inflamed mucosa (p = 0.01). Opposing transcription potency of NFκB has been detected between two phenotypes: being decreased in NS/NP (p = 0.07) and increased in S (p = 0.1) inflamed compared to non-inflamed mucosa, demonstrating trend towards statistical significance. Conclusions We found that two distinct CD phenotypes have specific molecular signatures. Obtained results could direct improvement of current and development of new therapeutic strategies based on more specific molecular stratification of CD patients.

Objective Meckel's diverticulum (MD) is the most common congenital anomaly of the gastrointestinal tract. Although a majority of patients remain asymptomatic, complications may occur in a subset of patients. MD is a rare cause of gastrointestinal bleeding (GIB) in adults. We aimed to clarify the possible role of capsule endoscopy (CE) in the identification of Meckel's diverticulum. Patients and methods From October 2004 to December 2010, 157 CEs were performed (83 male individuals, mean age 51±20 years; range 3-83 years) for obscure GIB. Before CE, all patients underwent nonconclusive upper and lower endoscopy at least two times and barium follow-through. Results CE identified the source of bleeding in 70/157 patients (44.6%). MD was diagnosed in 13/70 (18.6%) patients (11 male individuals, mean age 35±20 years, range, 3-69 years) after CE. Nine patients presented with obscure overt and four with obscure occult bleeding. The mean duration of obscure GIB history was 13 months (range 1-72 months). The mean hemoglobin concentration at the time of the procedure was 115±12 g/l. The findings of MD on CE were double lumen sign (13/13), visible blood (7/13), and diaphragm sign (6/13). All patients were operated upon, and MD histologically verified in 11. In two patients CE was false-positive and in two patients, false-negative. Capsule endoscopy had a positive predictive value of 84.6% for the diagnosis of MD. Conclusion MD should be considered in the differential diagnosis of obscure GIB in adults. CE is an effective and promising modality for diagnosing MD in patients with obscure GIB.

Hereditary polyposis syndromes in which APC gene germline mutations can lead to colorectal carcinogenesis are familial adenomatous polyposis (FAP), attenuated FAP (AFAP) and MUTYH-associated polyposis. All 3 syndromes increase the potential for the development of colorectal cancer. AFAP is diagnosed if less than 100 adenomas are detected in the colon at presentation. AFAP is inherited in an autosomal dominant manner. We present a case of a 22-year-old female with AFAP who was treated with endoscopic polypectomy and surveilled by annual colonoscopy. Guidelines for AFAP surveillance suggest annual colonoscopy with endoscopic polypectomy in asymptomatic individuals. Indications for immediate surgery include documented or suspected cancer or significant symptoms. Preferred surgical option in AFAP is colectomy and ileo-rectal anastomosis. Surveillance of the AFAP patients should include upper GI endoscopy and duodenoscopy with random biopsies of fundic gland polyps and endoscopic resection of detected adenomas. Annual thyroid ultrasound is indicated due to increased risk for thyroid cancer. In pediatric patients tested positive for germline mutation of APC gene screening for hepatoblastoma using alpha-fetoprotein and liver ultrasound should be performed.

Incidence of gastrointestinal bleeding in most populations is about 1 per 1,000 inhabitants. More than 65% of all bleeding episodes are associated with drug use. The most often involved are non-steroidal antiinflammatory drugs and low doses of acetyl-salicylic acid. The mortality within the first month after the bleeding episode is about 10-12%, and has not significantly changed in the last decade. Therefore, bleeding prevention is of major importance. Appropriate selection of patients, proper drug choice, application of lowest efficient doses of potentially ulcerogenic drugs, and use of drugs that inhibit gastric acid secretion remain cornerstone preventive measures of gastrointestinal bleeding.

OBJECTIVE Research on inflammatory bowel disease (IBD) has highlighted genes involved in the regulation of inflammatory responses as contributors to disease pathogenesis. This study aimed to evaluate the associations between IBD and variations in NOD2, TLR4, TNF-α, IL-6, IL-1β and IL-1RN genes, and to use the genetic data obtained in predictive modeling. METHODS A total of 167 IBD patients and 101 healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Using the genotype data attained as the input to various classification algorithms, IBD prediction models were designed. The area under the receiver operating characteristic curve (AUROC) was used to measure their performance. RESULTS Significant associations were found between Crohn's disease (CD) and minor NOD2 variants, as well as TLR4 299Gly, TNF-α G-308A, IL-6 G-174C and IL-1RN VNTR A2 variants, while ulcerative colitis (UC) was associated only with IL-1RN VNTR A2 variants. CD and UC showed highly significant difference in the allelic distribution of TNF-α G-308A, where the A allele was found to be related to CD, and the G allele to UC. A combined effect of patients' gender and TLR4 variants was observed among CD patients. When all analyzed genotype and gender data were used, prediction performance achieved a maximum AUROC of 0.690 for CD and 0.601 for UC dataset. CONCLUSION Variations in the genes involved in immune regulation are genetic factors of importance in IBD susceptibility that could potentially be used as predictors of disease development.

The aim of the study was to evaluate associations between inflammatory bowel disease (IBD) presentation and variants in NOD2, TLR4, TNF-α, IL-6, IL-1β, and IL-RN genes in order to identify possible environmental factors that may affect IBD occurrence, investigate potential predictors for surgical treatment of IBD, and correlate the presence of granulomas in biopsy specimens with clinical characteristics of Crohn's disease (CD) patients.We genotyped 167 IBD patients using PCR-based methodology and tested for disease genotype-phenotype associations.In CD patients ileal localization of disease was more frequent in NOD2 variant carriers. Ileal CD was associated with IL-6 GC+CC genotypes, identifying C allele as a possible marker of increased risk for ileal CD. In CD patients a positive family history for IBD was related to earlier onset of disease, higher risk for CD-related surgery, and appendectomy. CD patients who are TLR4 299Gly carriers are at higher risk for surgery at onset of the disease compared with TLR4 299Asp variant carriers. The presence of granuloma in biopsy specimens was more frequent in patients in whom a diagnosis of CD was made during emergency surgery. Multivariate analysis showed that CD carriers of the 299Gly allele had a 4.6-fold higher risk for emergency surgery before CD diagnosis is established compared with noncarriers, suggesting an aggressive disease course. Granuloma in endoscopic biopsies is detected 5.4-fold more frequently in patients treated surgically at the time of diagnosis.Genetic variants together with epidemiological and clinical data of IBD patients could potentially be used as predictors of the disease course.

Introduction. Primary biliary cirrhosis (PBC) is an immunemediated chronic progressive inflammatory liver disease leading to destruction of small interlobular bile ducts. Sarcoidosis is a chronic disorder of unknown etiology characterized by non-caseous granulomas. Case report. We reported a 69-year-old female patient with abdominal pain, malaise, vertigo, headaches, hands tremor and partial loss of hearing. Initial laboratory findings revealed elevated liver function tests and cholesterol with positive antimytochondrial and antinuclear antibodies. Liver biopsy revealed granuloma typical for PBC and granulomatous lesions typical for sarcoidosis. Elevated serum angiotensin-converting enzyme and granulomatous lesion on the brain magnetic resonance imaging (MRI) were detected and the patient was diagnosed with overlap of PBC and liver sarcoidosis and neurosarcoidosis. The patient was treated with ursodeoxicholic acid (UDCA) and prednisolone. Six months later the patient was symptom-free with laboratory findings within normal range. Conclusion. In PBC patients it is important to consider coexisting granulomatous liver diseases if elevated liver function tests persist despite UDCA therapy.

Epidemiology is a study of disease variations by geography, population demographics and time. Temporal influences can manifest themselves as age effects, period effects, cohort effects, seasonal or monthly variations. The acquisition of Helicobacter pylori infection during early childhood and the ensuing risk for the future development of peptic ulcer or gastric cancer represents a typical example for a cohort effect in digestive diseases. The incidence and prevalence of uncomplicated peptic ulcer have decreased in recent years, largely because of the availability of treatment to eradicate H. pylori and the decreasing prevalence of H. pylori infection. Nowadays, gastric and duodenal ulcers tend to occur in older people, who were more likely to have been exposed to H. pylori in their childhood than recently born generations. The overall incidence of gastric cancers is declining; however, there has been a relative increase in the incidence of tumors of the esophagogastric junction and gastric cardia. Thus, by extrapolating the strong, stable and consistent mortality rate declines in recent decades, gastric cancer was projected to become increasingly less important as a cause of death in Europe in the next decades.

The purpose of this study was to determine the frequency of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and to investigate its role as a potential risk factor in patients with chronic pancreatitis and pancreatic cancer. Deletion polymorphism of the 287-bp fragment of intron 16 of the ACE gene results in higher levels of circulating enzyme and therefore may represent a risk factor for disease development. The study included 55 patients with chronic pancreatitis, 45 patients with pancreatic cancer and 128 healthy subjects. The presence of I and D variants in the ACE gene was analyzed by a polymerase chain reaction (PCR) method. Distribution of ACE ID genotypes was analyzed by means of logistic regression. When chronic pancreatitis and pancreatic cancer groups were compared in the univariate analysis, the following factors were identified as statistically significant predictors of pancreatic disease: age, gender, smoking, fat intake, ACE II genotype and ACE DD genotype. However, in the multivariate analysis, only age, gender and smoking were singled out as predictors for the occurrence of pancreatic disease. Our findings indicate that the ACE I/D polymorphism could play a role in the development of chronic pancreatitis and pancreatic cancer through interaction with other genetic and environmental factors.

Uvod: Ehinokokoza predstavlja znacajan zdravstveni problem u endemskim podrucjima, ali zbog migracije ljudi, ovo postaje briga citavog covecanstva. Ehinokokoza najcesce zahvata jetru. Na osnovu ultrasonografskog izgleda, ehinokokusne ciste su klasifikovane u pet tipova. Međutim, razlicite ciste imaju razlicit klinicki tok, sa razlicitim terapijskim implikacijama. Stoga je Svetska zdravstvena organizacija 2003, dala novu podelu uzimajuci u obzir i morfoloske i klinicke karakteristike ehinokokusnih cisti, sa preporukom da naucnici sirom sveta koriste ove podelu u cilju da se njihovi podaci mogu upoređivati. Cilj: Cilj ove deskriptivne studije je prezentacija rezultat pregleda pacijenata pregledanih zbog ehinokokoze jetre tokom jedne godine. Metod: Ova studija je ukljucila 52 pacijenta ispitivanih i lecenih zbog ehinokokusne ciste jetre u Klinici za digestivnu hirurgiju, Klinickog centra Srbije u Beogradu podvrgnutih ehosonografskom pregledu abdomena. Analizirani su podaci o polu i uzrastu pacijenata, njihovi simptomi (abdominalni bol, mucnina, povracanje, povisena telesna tempretaura) i prisustvo solitarnih ili multiplih cista jetre. Prikazani su podaci o segmentnoj lokalizaciji i tipu ehinokokusnih cista jetre. Rezultati: U studiju je ukljuceno 16 muskaraca i 36 žena prosecne starosti 53,15+/-17,51 godina (najmanje 17; najvise 78). Bol u trbuhu je imalo 69,2% pacijenata, mucninu 23,1%, povracanje 15,4% i povisenu telesnu temperaturu 3,8% pacijenata. Solitarna ehinokokoza jetre je nađena kod 69,2% pacijenata. Kod 19,2% pacijenata je identifikovana Gharbi I cista, kod 29,8% Gharbi II, Gharbi III kod 33,7%, Gharbi IV kod 15,4%, a Gharbi V tip ciste je identifikovana kod 1,9% pacijenata. Vecina cisti je identifikovano u IV, VII i III segmentu jetre (34,6%, 23,1% i 11,5%). Zakljucak: Ova deskriprivna studija je analizirala, pored demografskih karakteristika i tipa i ucestalosti tegoba, rezultate ehosonografskog ispitivanja i primenu standardizovane klasifikacije ehinokokusnih cisti jetre radi doprinosa znanju o karakteristikama ehinokokusnih cisti jetre u nasem podrucju. Ovo je, takodje, koristan prikaz dijagnostickih standarda za ovo oboljenje.

Introduction: Available literature states that the incidence of colorectal adenomas and cancer is more common in men, however, lately has been observed increasing number of patients among women. Aim: to analyze the frequency and clinical characteristics of colorectal adenomas and cancer in women. Materials and Methods: We performed a retrospective study in which data of 695 patients with colorectal adenomas and carcinomas have been analyzed from a total of 10,659 patients who underwent colonoscopy. Results: Colonoscopy and colorectal neoplasms were more frequently diagnosed in man (71.88%/67.4%) than women (28.12%/32.65%), so the results must be interpreted with caution. Conclusion: The increase in the number of women who suffer from colorectal adenoma and carcinoma can be explained by balancing lifestyle and increasing the number of women who are examined, given up the initial resistance that women had to colonoscopy, which is a potentially painful and embarrassing.

We aimed to determine differences in gastroduodenal damage related to the presence of Helicobacter pylori (Hp) in patients starting long-term NSAID therapy. Seventy-one candidates for chronic NSAIDs therapy (33 Hp negative and 38 Hp positive) entered the study and underwent upper GI endoscopy before, and 8 and 16 weeks after, continuous NSAID therapy. Lanza score increased in both Hp positive and negative patients in the course of NSAID therapy (P

Introduction: The risk of upper gastrointestinal tract bleeding in the patients taking NSAID estimates 1% per year. Bleeding stops spontaneously in approximately 80% of all cases. Persistent and repeated bleeding (expecialy during the initial hospitalization ) still represent the serious clinical problem . In this group of patients, mortality rate is between 6-10 % , which in the USA counts 10- 20000 patients per year. Aim of the Study: The purpose of this review is to update the current knowledge of the use of different therapeutic strategies in patients with NSAID induced upper gastrointestinal bleeding. Results: Proton pump inhibitors (PPI) therapy is effective as a prevention of NSAID induced acidopeptic lesions, and also represents the first and best therapeutic option for the treatment of complications, such as upper gastrointestinal bleeding. In the last three decades use of early flexibile (diagnostic and therapeutic) endoscopy, agressive acidosupression (PPIs), and surgical treatment in restrictive indications, resulted in decreasing of the mortality rates from 25-35 % to 6-10%. When PPIs and flexible endoscopy are not sufficient in the control of upper gastrointestinal bleeding, use of systemic hemostatic drugs could be taken into consideration. Conclusion: Multidisciplinary approach, precise diagnostic and therapeutic criteria would probably result in better outcome of patients with active upper gastrointestinal bleeding.

Introduction: Successful endoscopic sclero-therapy is effective in securing hemostasis for bleeding lesions and remains the first line and only needed therapy for most of the patients (pts), but bleeding reoccurs in 10% to 30% pts, and 4% to 14% of the pts die after acute nonvariceal upper gastrointestinal bleeding (UGIB). The need for hospitalization and its duration for all the bleeding pts is still a controversial question. AIM: To create the simple scoring system able to determine low risk pts for rebleeding and mortality by establishing the relative importance of risk factors for rebleeding and mortality after successful endoscopic sclerotherapy of acute nonvariceal UGIB. Patients and methods: Prospective study included 315 pts who where admitted to hospital because of acute nonvariceal UGIB. All of them underwent gastroscopy with successful sclerotherapy within 12 hours after the admission. We investigated the episode of rebleeding and death during the initial hospitalization, and analyzed the following parameters: age, gender, drug intake, shock, bleeding stigmata, location of bleeding lesion and comorbidity. Results: Rebleeding occurred in 53 pts (16.8%) and was determined by shock, bleeding stigmata and comorbidity. Eleven pts (3.5%) died and shock, rebleeding and comorbidity were all independent, statistically significant predictors of pts? mortality. The numerical scores for determination of pts with different risk levels for rebleeding and mortality have been developed using the significant predictors of rebleeding and death. The score values for rebleeding ranged from 3 to 9 and pts with values

Helicobacter pylori (H. pylori) plays a role in the pathogenesis of gastric cancer. The outcome of the infection depends on environmental factors and bacterial and host characteristics. Gastric carcinogenesis is a multistep process that is reversible in the early phase of mucosal damage, but the exact point of no return has not been identified. Therefore, two main therapeutic strategies could reduce gastric cancer incidence: (1) eradication of the already present infection; and (2) immunization (prior to or during the course of the infection). The success of a gastric cancer prevention strategy depends on timing because the prevention strategy must be introduced before the point of no return in gastric carcinogenesis. Although the exact point of no return has not been identified, infection should be eradicated before severe atrophy of the gastric mucosa develops. Eradication therapy rates remain suboptimal due to increasing H. pylori resistance to antibiotics and patient noncompliance. Vaccination against H. pylori would reduce the cost of eradication therapies and lower gastric cancer incidence. A vaccine against H. pylori is still a research challenge. An effective vaccine should have an adequate route of delivery, appropriate bacterial antigens and effective and safe adjuvants. Future research should focus on the development of rescue eradication therapy protocols until an efficacious vaccine against the bacterium becomes available.

Research on inflammatory bowel disease (IBD) has highlighted genes involved in the regulation of inflammatory responses as contributors to disease pathogenesis. This study aimed to evaluate the associations between IBD and variations in NOD2, TLR4, TNF-α, IL-6, IL-1β and IL-1RN genes, and to use the genetic data obtained in predictive modeling.A total of 167 IBD patients and 101 healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Using the genotype data attained as the input to various classification algorithms, IBD prediction models were designed. The area under the receiver operating characteristic curve (AUROC) was used to measure their performance.Significant associations were found between Crohn's disease (CD) and minor NOD2 variants, as well as TLR4 299Gly, TNF-α G-308A, IL-6 G-174C and IL-1RN VNTR A2 variants, while ulcerative colitis (UC) was associated only with IL-1RN VNTR A2 variants. CD and UC showed highly significant difference in the allelic distribution of TNF-α G-308A, where the A allele was found to be related to CD, and the G allele to UC. A combined effect of patients' gender and TLR4 variants was observed among CD patients. When all analyzed genotype and gender data were used, prediction performance achieved a maximum AUROC of 0.690 for CD and 0.601 for UC dataset.Variations in the genes involved in immune regulation are genetic factors of importance in IBD susceptibility that could potentially be used as predictors of disease development.

The expression of two Helicobacter pylori proteins, CagA and VacA, is associated with more severe pathogenesis and clinical outcomes of the infection. However, this association varies among geographical regions and ethnic groups. We therefore evaluated CagA and VacA seroprevalence in H. pylori-positive dyspeptic patients in Serbia and Montenegro.In 173 consecutive dyspeptic patients referred to endoscopy (67M, mean age 49 +/- 15, 76 smokers), immunoblot assay was used to detect serum antibodies against CagA and VacA. Presence of H. pylori infection was assessed using a rapid urease test (RUT), routine histology and serology (anti-IgG ELISA). Duodenal ulcer (DU) was diagnosed in 28, gastric ulcer (GU) in 3 and non-ulcer dyspepsia (NUD) in the remaining 142 patients.129 (74.6%) patients were H. pylori-positive, 27 (96.4%) with DU, 3 (100%) with GU and 99 (69.7%) with NUD (P0.01); 121 (93.8%) patients carried anti-CagA antibodies and there was no difference between the DU and NUD groups. VacA antibodies were detected in sera of 50 (38.75%) and were more prevalent in patients with DU compared to the NUD group (P0.05).In Serbia and Montenegro there is high seroprevalence of CagA-positive H. pylori strains in dyspeptic patients with and without peptic ulcer, while VacA-positive strains are more closely related to peptic ulcer disease.

Helicobacter pylori (H. pylori) colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, t gastric ulcer in 13%, while gastric adenocarcinoma develops in 1% of all infected individuals. Pathogenesis of H. pylori infection is related to the virulence factors of the bacterium, environmental (dietary habits, hygiene, stress) and host factors (age, sex, blood type). Colonization of the gastric mucosa is related to the motility of the bacterium, presence of lipopolysacharide (LPS) and various bacterial enzymes. Gastric mucosal injury is the result of H. pylori LPS, vacuolization cytotoxin (vacA), cytotoxin associated protein (cagA), heat shock proteins and factors responsible for neutrophil chemotaxis and activity. H. pylori colonizes the gastric mucosa and zones of ectopic gastric epithelium. H. pylori infection is transmitted via oral-oral, fecal-oral and iatrogenic way (during endoscopy). Higher prevalence of the infection is associated with lower socioeconomic level, lack of drinking water, and living in a community. Acute H. pylori gastritis is superficial pangastritis progressing into the chronic phase after 7-10 days. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection. Clearly defined factors that influence the outcome of H. pylori infection include bacterial strain, distribution of gastritis, acid secretion and gastric mucosal atrophy.

Clinical relevance of infection with different Helicobacter pylori strains was reviewed in this paper. Helicobacter pylori (H. pylori) infection plays a role in pathogenesis of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and MALT lymphoma. Extragastric manifestations of H. pylori infection most probably include acne rosacea and chronic urticaria, while the importance of H. pylori infection for pathogenesis of growth retardation in children, iron deficiency anemia, coronary heart disease, stroke and idiopathic thrombocytopenic purpura remains vague. The expression of two H. pylori proteins, cytotoxin associated protein (cag A) and vacuolization cytotoxin (vac A) is considered to be related with pathogenicity of the bacterium. It is clear that presence of cag A+ strains is important for development of peptic ulcer; nevertheless, it is also protective against esophageal reflux disease. On the other hand, cag A+ strains are common in gastric adenocarcinoma and MALT lymphoma patients, but it seems that certain subtypes of vac A cytotoxin are more important risk factors. Infection with cag A+ strains is more common in patients with acne rosacea, stroke and coronary heart disease.

Background: Secretory leukocyte protease inhibitor (SLPI) represents a multifunctional protein of the gastric mucosa exerting anti-microbial and anti-inflammatory effects. Recently, a local down-regulation of antral SLPI expression in Helicobacter pylori (Hp)-infected healthy volunteers was demonstrated. Aim: To analyze mucosal SLPI expression in patients with various gastroduodenal disorders. Methods: The prospective study included 90 patients with following gastroduodenal disorders diagnosed: gastric cancer (GC, n = 22), duodenal ulcer (DU, n = 17), Hp-positive dyspeptic patients (NUD, n = 31) and Hp-negative NUD (n = 20). During esophagogastroduodenoscopy, biopsies were taken each from antrum, corpus and tumor. SLPI expression was analyzed by quantitative RT-PCR and ELISA. Results: Antral SLPI levels were reduced in all Hp-infected patients (NUD, DU, GC) by about 75% (1,494–1,826 pg/50 µg protein) compared to Hp-negative NUD (6,563 pg/50 µg protein, p < 0.001, ANOVA). Tumor tissue had twofold higher SLPI levels than surrounding tumor-free gastric mucosa (3,900 vs. 1,826 pg/50 µg protein, p = 0.013), but revealed reduced SLPI levels compared to Hp-negative NUD patients (p = 0.067). No differences were found between SLPI expression of intestinal and diffuse GC. SLPI transcript levels were unchanged throughout all groups and locations implying that transcriptional regulation of SLPI is not involved. Conclusion: Local down-regulation of SLPI in antral mucosa is a general phenomenon of Hp-related diseases.

Background/aims As well as causing chronic gastritis, Helicobacter pylori predisposes patients to peptic ulcer disease and gastric cancer, and induces gastric functional disorders. The aim of our study was to investigate the effects of H. pylori eradication therapy on the morphological and functional recovery of gastric antral and corpus D cells in patients with chronic gastritis during 6 months of follow-up. Patients and methods Forty consecutive, dyspeptic patients referred for endoscopy (31 with H. pylori infection and nine controls; mean age 49 years; 17 men, 23 women) entered the study. All patients had histological signs of gastritis but no signs of peptic ulcer or gastric cancer. Antrum (n = 8) and corpus (n = 6) biopsy specimens were collected for routine histology, radioimmunoassay tissue somatostatin levels, immunohistochemistry and electron microscopy, prior to and 6 months after therapy. Basal plasma somatostatin levels were determined prior to eradication, plus 6 weeks and 6 months after therapy. Eradication therapy consisted of amoxicillin, metronidazole and omeprazole. Results Basal somatostatin plasma values in antral and corpus tissue were lower in infected patients than in the H. pylori-negative controls at the beginning of the study. A significant increase occurred after successful eradication therapy, together with an increase in the number of D cells in both regions. Changes in the D-cell ultrastructure in antral and corpus mucosa after eradication therapy suggest an increase in somatostatin synthesis and secretion. Conclusions The structural and functional restoration of D cells following eradication therapy indicates possible recovery of the diseased mucosa.

Metabolic syndrome (MS), that has received increased attention in the past few years, consists of multiple, interrelated risk factors of metabolic origin that appear to directly promote the development of atherosclerotic cardiovascular disease (ASCVD). Most important of these underlying risk factors are abdominal obesity and insulin resistance. Other associated conditions include physical inactivity, aging, hormonal imbalance, and genetic or ethnic predisposition 1.

Background/aims: Portal hypertension and development of esophageal varices is one of the major complications of liver cirrhosis. The aim of our study was to evaluate the possibility of the presence of esophageal varices and their size using biochemical and ultrasonography parameters in patients with alcoholic liver cirrhosis. Material and Methods: We included in our study 86 patients (74 males, mean age 55 +/- 7) with alcoholic liver cirrhosis. The control group consisted of 102 patients with cirrhosis of other etiologies. All patients underwent a complete biochemical work up, upper digestive endoscopy and ultrasonography examination. The right liver lobe diameter/albumin and platelet count/spleen diameter ratios were calculated. The correlation of the calculated ratios with the presence and degree of esophageal varices in patients with liver cirrhosis was also determined. Results: The mean value of right liver lobe diameter-albumin ratio was 6.15 +/- 1.77, and statistically significantly differed from values determined in the control group (4.97 +/- 1.68). The mean platelet count-spleen diameter ratio was 972.5 +/- 599.0 in alcoholic liver cirrhosis and 1055.9 +/- 821.3 in controls (p>0.05). In patients with alcoholic liver cirrhosis, none of the analyzed noninvasive markers was shown to be a good predictor of the presence and size of esophageal varices. Conclusions: Despite the important role of noninvasive markers in providing information pertinent to determination of esophageal varices in patients with liver cirrhosis, these markers have limited relevance in patients with alcoholic cirrhosis.

Introduction. Mastocytosis is a clonal neoplastic disorder of the mast cells. The clinical signs and symptoms of mastocytosis are heterogeneous ranging from indolent disease with a longterm survival to a highly aggressive neoplasm with survival of about 6 months. Systemic mastocytosis (SM) is characterized by mastocyte infiltration of one or more organs, with or without skin involvment. Case Outline. The presented patient presents a highly challenging diagnostic and therapeutic case. A 46-year-old man was referred to our Centre due to the 7-year-long history of hepatosplenomegaly and mild thrombocytopenia. Ultrasound examination showed hepatosplenomegaly (liver 170 mm; spleen 200 mm), platelet count was 90C109/L, serum tryptase level was elevated and bone marrow biopsy showed infiltration with mast cells (CD117, CD25 and mast cell tryptase positive). Our patient was diagnosed with aggressive systemic mastocytosis (SM) according to WHO Classification (2008), although the clinical course of the disease was indolent, without complications for more than 7 years. Because of the ‘intermediate’ course, this patient was referred to as smouldering or intermediate SM and was not treated with cytostatics. Conclusion. Utilizing the established criteria, indolent SM can be discriminated from the aggressive subvariants of SM in most cases. However, a small group of patients, like our case belongs to the „grey zone“. Therapeutic approach to these patients is individual and prognosis is uncertain.

Primary biliary cirrhosis (PBC) is a chronic, progressive liver disease with elevated serum lipids. It remains unclear if hyperlipidemia increases the risk for atherosclerosis in PBC patients. Metabolic syndrome (MS) promotes the development of atherosclerotic cardiovascular disease due to abdominal obesity and insulin resistance. The aim of this study was to assess incidence and parameters of MS, as well as subcutaneous and visceral fat using noninvasive ultrasonographic measurement in patients with PBC in our population. We included 55 patients with PBC and 44 age- and sex-matched healthy controls (CG-control group). Anthropometric measurements (weight, height, and waist circumference), age, sex, and body mass index were recorded for patients and controls. Laboratory tests for assessing MS and liver function tests were analyzed. We used ultrasonography to determine subcutaneous and visceral fat diameter and area (SF, VF and SA, VA, respectively), as well as perirenal fat diameter (PF). Patients with PBC had significantly higher levels of cholesterol and liver function tests. There were no statistically significant difference in serum insulin and HOMA levels, as well as incidence of MS was diagnosed in 30.9 % (17/55) PBC patients and 43.2 % (19/44) controls. We registered lower amount of VF (PBC:10.92 +/- 3.63 mm, CG:16.84 +/- 5.51 mm, lt 0.001), VA (PBC:403.64 +/- 166.97 mm(2), CG:720.57 +/- 272.50 mm(2), lt 0.001), and PF (PBC:7.03 +/- 1.82 mm, CG 10.49 +/- 2.70 mm, lt 0.001) in patients with PBC. MS is not more frequent in patients with PBC compared with healthy volunteers in our population. Lower amount of VF could be related to lower risk for cardiovascular events in PBC patients.

Background/Aim. Primary biliary cirrhosis (PBC) is a progressive, chronic liver disease with elevated serum lipids, but it is unclear whether hyperlipidemia in PBC patients is associated with atherosclerosis. Metabolic syndrome promotes development of atherosclerotic cardiovascular disease related to abdominal type obesity and insulin resistance. The aim of our study was to assess abdominal adiposity in patients with PBC. Methods. The study included 40 patients with PBC and 50 healthy controls. Age, sex and anthropometric measurements (weight, height, body mass index and waist circumference) were registered for all patients and controls. We used ultrasonography to measure subcutaneous (SF) and visceral fat (VF) diameter, subcutaneous area (SA) and visceral area (VA), as well as perirenal fat diameter (PF). Results. Values of SF, VF and PF thicknesses in PBC patients were 19.23 ± 5.85 mm, 10.92 ± 3.63 mm, and 7.03 ± 1.82 mm, respectively. In controls these measurements were 22.73 ± 6.70 mm, 16.84 ± 5.51 mm and 10.50 ± 2.70 mm respectively. In PBC patients SA and VA were calculated to 983.64 ± 322.68 mm2 and 403.64 ± 166.97 mm2 and in controls 1124.89 ± 366.01 mm2 and 720.57 ± 272.50 mm2 respectrively. Significant difference was found for VF, VA and RF values. Conclusions. Considering that the amount of visceral fat plays an important role in development of metabolic syndrome and cardiovascular diseases, we concluded that the lower amount of visceral fat in PBC patients could be related to lower incidence of cardiovascular events, despite hyperlipidemia.

Introduction It is now well established that Helicobacter pylori eradication can significantly modify the natural history of peptic ulcer disease. The aim of this study was to assess the frequency of duodenal ulcer among patients endoscopically examined for dyspeptic symptoms and analyse the disease time trend during two ten-year long distinctive retrospective periods (1987-2006). Material and methods Data were obtained through retrospective analysis of outpatients upper endoscopy reports. Full reports were available for 58 515 patients which were analysed for selected clinicopathological features in two clearly defined time periods. The first one, starting from 1987 to 1996 in which Helicobacter pylori infection was not assessed and treated accordingly and the second period from 1997 to 2006 during which the presence of Helicobacter pylori infection in certain diseases was routinely assessed and then treated with PPI based triple therapy. Results Syptoms of dyspepsia appeared to be approximately the same as the indication for endoscopy in both periods (65.1%:63.3%). The frequency of duodenal ulcer disease significantly decreased in the second period of analysis (t=14761; p

Introduction: Non-steroid antiinflammatory drugs (NSAIDs) and Helicobacter pylori (Hp) infection are two most important independent risk factors involved in the etiopathogenesis of gastroduodenal mucosal injury with a clear and critical role in both uncomplicated and complicated peptic ulcer disease. It is estimated that up to 90% of all peptic ulcers result from the effect of one or both of these factors. AIM: To determine the frequency of NSAIDs use and Hp infection in patients with acute upper gastrointestinal bleeding. Patients and methods: Study evaluated data from 500 patients in whom esophagogastroduodenoscopy was performed following presentation in emergency unit with acute upper gastrointestinal bleeding. Anamnestic data was collected together with detailed information on previous salicilates and/or NSAIDs use. Hp status was determined and anatomic localization of bleeding lesion was also registered. Results: Acute upper GIT bleading was caused solely by NSAIDs in 55 (11%), by aspirin in 66 (13.2%), while combined NSAID/aspirin therapy was identified in 19 (3.8%) of patients. In total NSAID and/or aspirin use were diagnosed in 139 (27.8%). while in 122 (24.4%) only Hp infection was diagnosed. Both risk factors were identified in 144 (28.8%) patients (Hp+NSAIDs in 12.2%, Hp+aspirin in 10.8% and Hp+aspirin+NSAIDs in 5.8%) . In 19.8% of the cases (14% of males and 27% of females) neither NSAID/aspirin use nor presence of Hp infection was noted. Out of 500 patients enrolled, 63% were mails. In females, bleeding lesion was most frequently localized in gastric mucosa, while males had equal chance of bleeding from either gastric or duodenal mucosa. Fortunately, only 5 to 7% of patients were bleeding from both gastric and duodenal lesion. Conclusion : Prevention of acute upper gastrointestinal bleeding can be achieved trough strict and limited use of aspirin and NSAIDs, eradication of Hp infection and use of gastroprotective therapy in well-defined risk patients that need chronic NSAIDs and/or aspirin therapy. In all patients starting long-term NSAID and/or aspirin therapy and all patients already on long-term aspirin therapy test and treat strategy for Hp infection should be used. On the other hand, only in high risk patients (more than 65 years, history of peptic ulcer disease, concomitant corticosteroid, aspirin, clopidogrel or warfarin therapy) already on chronic NSAID therapy long-term PPI therapy should be prescribed after testing and treating of Hp infection.

Introduction: Acute upper gastrointestinal bleeding is the commonest emergency managed by gastroenterologists. It manifests like: haematemesis, melaena or haemochezia. Diagnostic endoscopy accurately defining the cause of hemorrhage, while therapeutic endoscopy improves prognosis in patients who present with severe bleeding. Endoscopic therapies can be classified as those based on injection, application of heat, or mechanical clips. Patients and methods: This investigation was conducted in Department of endoscopic haemostasis, Clinic for gastroenterology and hepatology, CCS, using retrospective analysis of patients with acute upper gastrointestinal bleeding during the last five years. The aim of this study was to establish the number of upper gastrointestinal bleeding in our hospital during the last five years, and distribution of income according to type, difficulty, cause factors and risk factors of gastrointestinal bleeding and method of haemostasis. Results: In Department of endoscopic haemostasis 3954 patients with upper gastrointestinal bleeding were endoscoped, and 33,4% of them had bleeding duodenal ulcer. Male patients were statistically significant more present than female patients in group with duodenal ulcer ( 71,8%: 28,2%). 79.7% patients with duodenal ulcer had only haematemesis, while 14,4% patients had haematemesis and melaena. 59,1% patients with bleeding duodenal ulcer consumed salicylates and/or non-steroidal anti-inflammatory drugs ( NSAIDS) ( statistical significant differences ?2 test; p=0.007). Only endoscopic injection was used: in 36.8% of patients used injection of adrenaline solutions, while in 5,9% of patients used injection of adrenaline and absolute alcohol solutions. Conclusion: Using of therapeutic endoscopy improves better prognosis in patients who present with severe acute upper gastrointestinal bleeding. Endoscopist?s experience is an important independent prognostic factor for acute upper gastrointestinal bleeding.

Thrombosis of portal and hepatic veins is one of the most severe complications and most important causes of death of patients with chronic myeloproliferative diseases. Based on results of the past studies, myeloproliferative diseases were the causes of hepatic veins thrombosis in 30% and portal vein thrombosis in 20% of patients. The study presented 4 patients with myeloproliferative diseases complicated by thrombosis of splanchnic veins, aiming at the illustration of issue complexity in diagnostics and therapy. Two patients with portal vein thrombosis and recurring hemorrhage from esophageal varicosity were described. The first case was planned for shunting, while another case sustained bleeding on what account his anticoagulant therapy was discontinued, but it caused mesenterial thrombosis resulting in lethal outcome. Another two patients had hepatic veins thrombosis. Due to frequent, life-threatening bleeding from the esophageal and gastric varices, a patient with chronic Budd-Chiari syndrome and lineal vein thrombosis underwent mesocaval shunting. An immediate postoperative period was manifested by multiple thrombosis and hemorrhages that ended in his death. A patient with the acute Budd-Chiari syndrome was administered myelosuppressants and anticoagulants on time so reperfusion was restored. In myeloproliferative diseases, thrombosis of portal and hepatic veins gives rise to excessive portal hypertension with profuse hemorrhage from the esophageal and gastric varicosity which is difficult to manage because of complex coagulation disorders.

To investigate the expression of different cytokeratins (CKs) in gastric epithelium of adult patients with chronic gastritis infected with Helicobacter pylori (H pylori) cagA+ strains.The expression of CK 7, 8, 18, 19 and 20 was studied immunohistochemically in antral gastric biopsies of 84 patients. All the CKs were immunostained in cagA+H pylori gastritis (57 cases), non-H pylori gastritis (17 cases) and normal gastric mucosa (10 cases).In cagA+ H pylori gastritis, CK8 was expressed comparably to the normal antral mucosa from surface epithelium to deep glands. Distribution of CK18 and CK 19 was unchanged, i.e. transmucosal, but intensity of the expression was different in foveolar region in comparison to normal gastric mucosa. Cytokeratin 18 immunoreactivity was significantly higher in the foveolar epithelium of H pylori-positive gastritis compared to both H pylori-negative gastritis and controls. On the contrary, decrease in CK19 immunoreactivity occurred in foveolar epithelium of H pylori-positive gastritis. In both normal and inflamed antral mucosa without H pylori infection, CK20 was expressed strongly/moderately and homogeneously in surface epithelium and upper foveolar region, but in H pylori -induced gastritis significant decrease of expression in foveolar region was noted. Generally, in both normal antral mucosa and H pylori-negative gastritis, expression of CK7 was not observed, while in about half cagA+ H pylori-infected patients, moderate focal CK7 immunoreactivity of the neck and coiled gland areas was registered, especially in areas with more severe inflammatory infiltrate.Alterations in expression of CK 7, 18, 19 and 20 together with normal expression of CK8 occur in antral mucosa of H pylori-associated chronic gastritis in adult patients infected with cagA+ strains. Alterations in different cytokeratins expression might contribute to weakening of epithelial tight junctions observed in H pylori-infected gastric mucosa.