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Hepatocyte steatosis increases the expression of adhesion molecules in endothelial cells

: potential implications for inflammation and plaque instability. Circulation. 2000; 101: 1372-8. 13. Mazzone GL, Rigato I, Ostrow JD, Bossi F, Bortoluzzi A, Sukowati CH, et al. Bilirubin inhibits the TNFalpharelated induction of three endothelial adhesion molecules. Biochem Biophys Res Commun. 2009; 386: 338-44. 14. Jin X, Yang YD, Chen K, Lv ZY, Zheng L, Liu YP, et al. HDMCP uncouples yeast mitochondrial respiration and alleviates steatosis in L02 and hepG2 cells by decreasing ATP and H2O2 levels: a novel mechanism for NAFLD. J Hepatol

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Distribution of hepatitis C virus genotypes, hepatic steatosis and their correlation with clinical and virological factors in Pakistan

. Hepatology. 1992; 16:293-9. 6. Kanai K, Kako M, Okamoto H. HCV genotypes in chronic hepatitis C virus and response to interferon. Lancet. 1992; 339:1543. 7. Shah H.A, Jafri W, Malik I, Prescott L, Simmonds P. Hepatitis C virus (HCV) genotypes and chronic liver disease in Pakistan. J Gastroenterol Hepatol. 1997; 12: 758-61. 8. Szanto P, Grigorescu M, Dumitru I, Serban A. Steatosis in hepatitis C virus infection. Response to anti-viral therapy. J Gastrointestin Liver Dis. 2006; 15:117-24 9. Marzouk D, Sass J

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ST2 Deficiency Ameliorates High Fat Diet-Induced Liver Steatosis In BALB/c Mice

GCKR and PNPLA3 confer susceptibility to nonalcoholic fatty liver disease in obese individuals. Am J Clin Nutr. 2014;99(4):869-74. 8. Postic C, Girard J. Contribution of de novo fatty acid synthesis to hepatic steatosis and insulin resistance: lessons from genetically engineered mice. J Clin Invest. 2008;118(3):829-38. 9. Ferre P, Foufelle F. Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP-1c. Diabetes, obesity & metabolism. 2010;12 Suppl 2:83-92. 10. Negrin KA, Roth Flach RJ, DiStefano MT, Matevossian A

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The Incidence Of Hepatic Steatosis Recently Found In Patients With Diabetes Mellitus Type 2 Newly Discovered

Abstract

The nonalcoholic hepatic steatos is represents one of the most frequent disorders in patients with diabetes mellitus type 2. The obesity and especially the abdominal adipose tissue distribution represent factors of higher risk for nonalcoholic hepatic steatosis. The echographic examination and FirboScan are very important in identification of this disorder. The study consisted in analysis of the clinical and paraclinical results in order to identify the SHNA (The nonalcoholic hepatic steatosis) incidence. It must be mentioned the fact that the absence of the abdominal obesity and increased transaminases do not exclude SHNA(The nonalcoholic hepatic steatosis).

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Adipokines, insulin resistance, hepatic steatosis, and necroinflammation in patients with chronic viral hepatitis

Ther. 2005; 22(Suppl 2):24-7. 4. Lonardo A, Adinolfi LE, Loria P, Carulli N, Ruggiero G, Day CP. Steatosis and hepatitis C virus: mechanisms and significance for hepatic and extrahepatic disease. Gastroenterology. 2004; 126:586-97. 5. Clouston AD, Jonsson JR, Powell EE. Steatosis as a cofactor in other liver diseases: hepatitis C virus, alcohol, hemochromatosis, and others. Clin Liver Dis. 2007; 11:173-89. 6. Yokoyama H, Hirose H, Ohgo H, Saito I. Inverse association between serum adiponectin level and transaminase

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A Comparative Analysis of Serum Lipids in Patients with Chronic Hepatitis C, Nonalcoholic Fatty Liver Disease and Healthy Controls

REFERENCES 1. Lonardo A, Adinolfi LE, Loria P et al. Steatosis and hepatitis C virus: Mechanisms and significance for hepatic and extrahepatic disease. – Gastroenterology 2004, 126, 586-597. 2. Loria P, Marchesini G, Nascimbeni F et al. Cardiovascular risk, lipidemic phenotype and steatosis. A comparative analysis of cirrhotic and non-cirrhotic liver disease due to varying etiology. – Atherosclerosis. 232, 2014, 1, 99-109. 3. Adinolfi LE, Rinaldi L, Guerrera B et al. NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and

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Clinical and Pathological Findings on Intoxication by Yellow Phosphorus After Ingesting Firework Cracker: A Rare Case of Autopsy

Abstract

Yellow phosphorus is a toxic substance used in the production of firework cracker, fireworks, ammunition and agricultural dung. When ingested, it shows its effects mainly in the liver, the kidneys, and the brain. A four-year-old girl had died as a result of acute hepatic failure caused by ingesting a firework cracker. The case showed high levels of hepatic enzymes, along with non-specific signs such as nausea, vomiting and diarrhea. Autopsy revealed diffuse microvesicular steatosis in the liver and disseminated degeneration in the proximal tubules of the kidneys. In cases with concomitant hepatorenal failure and cardiovascular collapse, death is inevitable. However, when only hepatic failure develops, hepatic transplantation may be lifesaving. Although intoxication from ingesting yellow phosphorus has a very high rate of mortality, forensic cases are extremely rare in the literature.

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Histopathology of Hepatic Sinusoidal Obstruction Syndrome After Neoadjuvant Oxaliplatin-Based Chemotherapy

Abstract

Sinusoidal obstruction syndrome („blue liver syndrome“) has been frequently associated with oxaliplatin-based neoadjuvant chemotherapy in patients with colorectal liver metastasis. Hepatotoxic vascular lesions in the nontumourous liver parenchyma result in hypoperfusion and tissue hypoxia leading to lower tumour response to oncologic treatment and to increase the risk of liver metastasectomies. Furthermore, hepatic parenchyma injuries could be aggravated by hepatic resection itself. Contrary to standard surgical techniques, radiofrequency assisted liver resection significantly reduce harmful intraoperative blood loss and perfusion-reperfusion effects. We compared histological alterations in 59 specimens of bloodless radiofrequency-assisted liver recetions made for colorectal metastases to those in 38 specimens of standard liver resections. In general, the main histologic alterations in both examined groups related to oxaliplatin include SOS lesions (69.35%), fibrosis (50.95%) and steatosis (38%). After scoring of histopathological parameters based on modified criteria according to Rubbia-Brandt et al., they were statistically insignificant between both groups for portal and/or porto-portal fibrosis (59.3% vs 47.4%, respectively) and moderate/severe macrovacuolar steatosis (10.2% vs 26.3%). Similar distribution between groups was shown for surgical hepatitis with „borderline“ statistical significance (23,7% vs 42,1%, p= 0.05). However, there were significant differencies in vascular lesions, particularly for hemorrhagic centrilobular necrosis (10,2% vs 31,5%, p= 0.01) and peliosis (15,2% vs 36,8%, p= 0.04), but were not significant for sinusoidal dilatation and congestion as well as surgical necrosis. Highgrade vascular lesions such as hemorrhagic centrilobular necrosis and peliosis are less frequent in cases of radiofrequency-assisted liver recetions and might be associated with better clinical outcome in these patients.

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Can examination of tissue stained with Oil red O be postponed up to three months?

References [1] Levene AP, Kudo H, Thursz MR, Anstee QM, Goldin RD. Is Oil Red-O Staining and Digital Image Analysis the Gold Standard for Quantifying Steatosis in the Liver? Hepatology. 2010;51(5):1859-. [2] Thomsen JL, Hansen TP. Lipids in the proximal tubules of the kidney in diabetic coma. The American journal of forensic medicine and pathology. 2000;21(4):416-8. [3] Parai JL, Kodikara S, Milroy CM, Pollanen MS. Alcoholism and the Armanni-Ebstein lesion. Forensic science, medicine, and pathology. 2012

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Severe hepatocytolisis syndrome - a challenge in medical therapy of Cushing’s disease

. 3,31-38. 4. Rockall, A. G., Sohaib, S. A., Evans, D., Kaltsas, G., Isidori, A. M., Monson, J. P., Besser, G.M., Grossman, A.B. & Reznek, R. H. (2003). Hepatic steatosis in Cushing’s syndrome: a radiological assessment using computed tomography. Eur J Endocrinol. 149(6), 543-548. 5. Biller, B. M., Grossman, A. B., Stewart, P. M., Melmed, S., Bertagna, X., Bertherat, J., Buchfelder, M.,Colao, A.,Hermus, A. R.,Hofland, L.J., Klibanski, A., Lacroix, A., Lindsay, J.R., Newell-Price, J., Nieman, L.K., Petersenn, S., Sonino, N., Stalla, G

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