Endoscopic ultrasound for differential diagnosis of duodenal lesions.

PURPOSE: Duodenal tumors are rare and require a different management from that of esophagogastric neoplasia. The present study retrospectively analyses the endoscopic ultrasound (EUS) features of duodenal tumors of both epithelial and subepithelial origin. MATERIALS AND METHODS: During a 12 year period, all duodenal tumors with histologic confirmation by surgery or biopsy were collected including endoscopic and endosonographic images. EUS images were analyzed for specific features (echogenicity, wall layer structure and relation, outer margins) to possibly distinguish epithelial (polyps and carcinoma versus lymphoma) and subepithelial (tumor type) tumors. RESULTS: 53/80 cases had histologic confirmation (mean age 53.1 ±â€Š11.4 years, m:f = 33:20), 31 were epithelial (13 adenomas, 12 carcinomas, 6 lymphomas) and 22 subepithelial (11 GISTs, 7 Brunneromas, 1 lipoma, 3 NETs). EUS did not recognize carcinomas in 2/13 adenomas. EUS features suggesting carcinoma were loss of wall layers and irregular margins. 5/6 lymphomas showed inhomogeneous thickening with layers partially recognizable. Tumor type of subepithelial lesions correlated with echogenicity: GIST tumors were mostly (62.5 %) hypocheoic with the 3 malignant cases being characterized by heterogeneous echopattern with irregular outer margins. Of the hyperechoic lesions, lipomas had a homogeneous whitish appearance, while NET and Brunneromas were less hyperechoic. In the latter, the endoscopic aspect was also helpful for differential diagnosis. Accuracy of combined endoscopic/EUS imaging for all duodenal lesions was 84.9 % (45/53). No procedural complications occurred among all patients that received EUS examinations. CONCLUSION: EUS contributes to the differential diagnosis of epithelial lesions known to be malignant; in subepithelial tumors, tissue confirmation is still required.

[Treatment of gastrointestinal hemorrhage manifestation induced by nonsteroidal anti-inflammatory agents]].

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 critearia would probably result in better outcome of patients with active upper gastrointestinal bleeding.

[Role of Helicobacter pylori infection and use of NSAIDs in the etiopathogenesis of upper gastrointestinal bleeding].

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 upto 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 localisation 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. Fortunatelly, 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.

[Myeloproliferative diseases as causative agents of portal and hepatic veins thrombosis].

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.

[Acute upper gastrointestinal nonvariceal bleeding--how to determine low risk patients for rebleeding and mortality after endoscopic sclerotherapy?].

INTRODUCTION: Successful endoscopic sclerotherapy 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 3 15 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 < or = 4 had low risk of rebleeding. We identified 59 pts (18.7% of all) with score for rebleeding < or = 4. Score values for mortality risk ranged from 3 to 8 and the values < 5 revealed negligible risk of death. In our group we found 290 pts (92.1% of all) with low mortality score values. CONCLUSION: Following the successful initial endoscopic sclerotherapy, these scores can help to identify pts with low risk of rebleeding and negligible risk of death, so they can be treated as outpatients.

[Endoscopic haemostasis of bleeding duodenal ulcer].

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 haemorrhage, 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 chi2 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.

[Non-surgical approach to bleeding gastric ulcer].

Bleeding gastric ulcers is a common reason for emergency upper endoscopy in Emergency Center of Clinical Center of Serbia. Randomized controlled trials have shown that endoscopic hemostasis is beneficial for patients with a bleeding peptic ulcer. Aim of this study was to analyze the frequency, etiological factors and localization of bleeding gastric ulcer. At the same time we were evaluated a degree of bleeding activity according to Forrest's classification and modality of performed endoscopic hemostasis. All patients who underwent upper gastrointestinal (UGI) endoscopy for bleeding gastric ulcer in Emergency Center (January 2001 - December 2005.) were identified from an endoscopy database and the clinical records were reviewed retrospectivel. A total of 3954 patients underwent UGI endoscopy for presumed acute UGI hemorrhage. More than thirty % of them (31.1)-1230 had an endoscopic diagnosis of bleeding gastric ulcer. We observed 1230 bleeding patients (60% male and 40% female) with a mean age of 64.3. The commonest localization of bleeding gastric ulcers was antrum (54 - 15%). Percentage of patients who received non-steroidal anti-inflammatory drugs (NSAIDs) and/or salicilates before bleeding was 54 6%. The main symptom was melaena, which was observed in 82, 44% of patients with bleeding gastric ulcer. According to Forrest's classification of bleeding activity, the most of patients had F IB and F III degree (23, 41% and 22, 76%). Injection endoscopic hemostasis was performed in 26.34% patients, which had active bleeding (F IA, F IB) Hemostasis was initially obtained in 96% of bleeding patients. Bleeding gastric ulcer is one of the commonest endoscopic diagnosis in Emergency Center of Clinical Center of Serbia. The most frequent etiology factor was no--steroid antinflammatory drugs and/or salicilates. Injection endoscopic hemostasis is a safe procedure with a low cost, and, if successful, substantially reduces the need for emergency surgery.

Anti-CagA and anti-VacA antibodies in Helicobacter pylori-infected patients with and without peptic ulcer disease in Serbia and Montenegro.

BACKGROUND: 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. METHODS: 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. RESULTS: 129 (74.6%) patients were H. pylori-positive, 27 (96.4%) with DU, 3 (100%) with GU and 99 (69.7%) with NUD (P < 0.01); 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 (P < 0.05). CONCLUSIONS: 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.