Adult ; Aged ; Alcohol Drinking ; adverse effects ; epidemiology ; Alcoholism ; complications ; pathology ; China ; epidemiology ; Female ; Humans ; Liver Cirrhosis, Alcoholic ; epidemiology ; etiology ; Liver Diseases, Alcoholic ; complications ; epidemiology ; Male ; Middle Aged ; Risk Factors

No abstract available.
Aged ; Antigens, Tumor-Associated, Carbohydrate/blood ; Carcinoma, Hepatocellular/radiography ; Humans ; Liver Abscess/*complications/pathology/*radiography ; Liver Diseases, Alcoholic/*complications/*pathology ; Liver Neoplasms/radiography ; Magnetic Resonance Imaging ; Male ; Tomography, X-Ray Computed

Alcohol Drinking ; adverse effects ; Hepatitis, Viral, Human ; complications ; diagnostic imaging ; pathology ; Hepatocytes ; pathology ; Humans ; Liver ; diagnostic imaging ; pathology ; Liver Cirrhosis, Alcoholic ; diagnostic imaging ; etiology ; pathology ; Liver Diseases, Alcoholic ; diagnostic imaging ; etiology ; pathology ; Liver Neoplasms ; epidemiology ; etiology ; pathology ; Prognosis ; Radiography ; Risk Factors

We report on a 55-year-old man with alcoholic liver cirrhosis who presented with status epilepticus. Laboratory analysis showed markedly elevated blood ammonia. Brain magnetic resonance imaging (MRI) showed widespread cortical signal changes with restricted diffusion, involving both temporo-fronto-parietal cortex, while the perirolandic regions and occipital cortex were uniquely spared. A follow-up brain MRI demonstrated diffuse cortical atrophy with increased signals on T1-weighted images in both the basal ganglia and temporal lobe cortex, representing cortical laminar necrosis. We suggest that the brain lesions, in our case, represent a consequence of toxic effect of ammonia.
Ammonia/blood ; Atrophy/pathology ; Brain Diseases/blood/*diagnosis/*etiology ; Hepatic Encephalopathy/*complications ; Humans ; Liver Cirrhosis, Alcoholic/*complications ; Magnetic Resonance Imaging/*methods ; Male ; Middle Aged ; Necrosis/pathology ; Status Epilepticus/pathology

BACKGROUND/AIMS: The aim of this study was to describe the types and causes of liver disease in patients from a single community hospital in Korea between April 2005 and May 2010. METHODS: A cohort of patients who visited the liver clinic of the hospital during the aforementioned time period were consecutively enrolled (n=6,307). Consistent diagnostic criteria for each liver disease were set by a single, experienced hepatologist, and the diagnosis of all of the enrolled patients was confirmed by retrospective review of their medical records. RESULTS: Among the 6,307 patients, 528 (8.4%) were classified as acute hepatitis, 3,957 (62.7%) as chronic hepatitis, 767 (12.2%) as liver cirrhosis, 509 (8.1%) as primary liver cancer, and 546 (8.7%) as a benign liver mass or other diseases. The etiologies in the acute hepatitis group in decreasing order of prevalence were hepatitis A (44.3%), toxic hepatitis (32.4%), other hepatitis viruses (13.8%), and cryptogenic hepatitis (9.1%). In the chronic hepatitis group, 51.2% of cases were attributed to viral hepatitis, 33.3% to nonalcoholic fatty liver disease, and 13.0% to alcoholic liver disease (ALD). Of the cirrhoses, 73.4% were attributable to viral causes and 18.1% to alcohol. Of the hepatocellular carcinoma cases, 86.6% were attributed to viral hepatitis and 11.6% to ALD. Among the benign tumors, hemangioma comprised 52.2% and cystic liver disease comprised 33.7%. CONCLUSIONS: Knowledge of the current status of the type and cause of liver disease in Korea may be valuable as a basis for evaluating changing trends in liver disease in that country.
Acute Disease ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alcohol Drinking/adverse effects ; Carcinoma, Hepatocellular/epidemiology/etiology/pathology ; Chronic Disease ; Cohort Studies ; Fatty Liver/epidemiology ; Female ; Hepatitis/epidemiology ; Hepatitis, Viral, Human/complications/epidemiology ; Humans ; Liver Cirrhosis/epidemiology/etiology ; Liver Diseases/*diagnosis/epidemiology ; Liver Diseases, Alcoholic/complications/epidemiology ; Liver Neoplasms/epidemiology/etiology/pathology ; Male ; Middle Aged ; Prevalence ; Republic of Korea/epidemiology ; Retrospective Studies ; Young Adult

OBJECTIVETo investigate the effect of tea polyphenol (TP)'s on liver fibrosis in rats and its possible mechanism.

METHODRats were divided into 5 groups, 4 groups of which were stomach perfused with alcohol resulting in alcoholic liver fibrosis, and 3 groups of which were stomach perfused with TP simultaneously. Another group was normal control one. Histological change of rat liver was investigated and quantitative analysis was made in 24 weeks, and rat liver anti-oxidation index and serum endotoxin were determined at the same time.

RESULTLiver fibrosis in TP group was slight, and anti-oxidize index and endotoxin level were markedly improved in comparison with those of alcohol groups.

CONCLUSIONTea polyphenol can protect hepatocytes from fibrosis. Its mechanism is possibly due to cleaning up overfull lipid per-oxidation and reducing the level of endotoxin.

Animals ; Collagen ; metabolism ; Endotoxins ; blood ; Female ; Flavonoids ; isolation & purification ; pharmacology ; Glutathione ; blood ; Liver ; metabolism ; pathology ; Liver Cirrhosis ; blood ; etiology ; metabolism ; Liver Diseases, Alcoholic ; complications ; Male ; Malondialdehyde ; blood ; Phenols ; isolation & purification ; pharmacology ; Polyphenols ; Protective Agents ; isolation & purification ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood ; Tea ; chemistry

OBJECTIVETo investigate the effect of hypoxia on chronic alcoholic liver disease.

METHODSTwenty four male Sprague-Dawley rats were randomly into two groups. The alcohol group (n=12) was fed 56% (v/v) of ethanol once per day by gastric infusion at 8 g/kg body weight for 24 weeks. The control group (n=12) was gastrically infused with normal saline with the same dose. At the end of 24 weeks, a blood sample was collected for determination of hepatic enzymes and then the rat was killed. Liver specimens were obtained for immunohistochemical staining and frozen at -80 degrees C used for RT-PCR.

RESULTSSerum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity increased significantly compared to the control group. A significant elevation in the expression of HIF1-alpha in liver of alcohol group was found compared to the control group.

CONCLUSIONHypoxia inducible factor 1-alpha expression was activated by ethanol-induced injury. This information suggested that hypoxia was involved in mechanism of alcoholic liver disease.

Animals ; DNA-Binding Proteins ; biosynthesis ; genetics ; Hypoxia ; complications ; metabolism ; Hypoxia-Inducible Factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit ; Liver Diseases, Alcoholic ; complications ; metabolism ; pathology ; Male ; Nuclear Proteins ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Transcription Factors ; biosynthesis ; genetics