[Stubborn nausea and not ease vomiting as a manifestation of glycoside toxicity in a patient with duodenal ulcer and gastric erosions in the background of Ebstein's anomaly].

In this article is presented the case of development of glycoside intoxication at patient of 26 years old, who has congenital heart disease (Ebstein's anomaly). He also has duodenal ulcer and gastric erosions, associated with Helicobacter Pylori, that were diagnosed for the first time. The clinical observation reflects the necessity of differential diagnostics between glycoside intoxication and manifestation of duodenal ulcer.

[Taurine in the treatment of non-alcoholic fatty liver disease].

Non-alcoholic fatty liver disease (NAFLD) has several phases of flow: from simple steatosis, steatohepatitis, and ending with fibrosis and cirrhosis. NAFLD characterized by elevated liver enzymes in blood serum, the morphological changes in biopsies of the liver often associated with metabolic disorders. Metabolic syndrome represents a complex of many linked to pathobiochemical and pathophysiological factors levels influencing the extremely high risk of developing coronary heart disease (CHD), diabetes mellitus type 2 and other diseases associated with atherosclerosis. NAFLD proceeds favorably without significant morphological changes in most of the patients. In connection with this treatment is given only to patients with high risk of progression of this disease or the presence of marked changes in biochemical liver tests. Therefore, prevention and treatment of these conditions should be conducted before the complications and lead to improvement of the liver.

[Cholesterosis of the gall bladder and atherogenic dyslipidemia: etiology, pathogenesis, clinical symptoms, diagnosis and treatment].

AIM: To detect specific morphological signs of hepatic lesion in patients with cholesterosis of the gall bladder and atherogenic dyslipidemia in the presence of steatohepatitis. MATERIAL AND METHODS: Atherogenic dyslipidemia was detected in 150 patients with steatohepatitis. Ultrasound investigation diagnosed cholesterosis of the gall bladder in 51.3% patients. The protocol included the following examinations: analysis of the disease history, physical examination, laboratory, device and morphological tests. Thirty patients received therapy with ursodesoxycholic acid medicine for 3 months. RESULTS: Basic clinical symptoms of gall bladder cholesterosis (GBC) and its risk factors are defined. The biochemical blood test registered elevated levels of transaminase, alkaline phosphatase and bilirubin. All the patients had an atherogenic type of dyslipidemia. According to USI, a focal-reticular form of GBC prevailed. Histologic examination of the liver detected the following alterations: fat infiltration, portal and intralobular infiltration, hydropic dystrophy, binuclear hepatocytes, lobular hepatitis, fibrosis of the portal tracts, periductular fibrosis, ductual proliferation, ductual epithelium detachment. Histologically, the walls of the gall bladder contain foam cells in the mucous and submucous layer. The same changes were seen in the wall of the hepatic artery as well as cholesterol polyps, epithelial destruction. Ursosan treatment resulted in a significant lowering of total cholesterol. CONCLUSION: GBC seems to be a chain of successive conditions: lipid disbolism at the level of hepatocyte, development of steatosis, steatohepatitis, fibrosis, involvement of all anatomo-morphological structures of the liver including the biliary tract, GBC.