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A. Husic-Selimovic, S. Gornjakovic, M. Schuchmann, Z. Vukobrat-Bijedic

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.

S. Sahovic, Z. Vukobrat-Bijedic, V. Sahović

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.

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.

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.

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