Human fascioliasis is a zoonosis caused by Fasciola hepatica, and this is a trematode that infests cattle and sheep. Humans are accidental hosts in the life cycle of this parasite. People are infected by ingestion of the water or the raw aquatic vegetables that are contaminated with the metacercaria. This fluke's worldwide distribution occurs in areas where sheep, cattle and goats are raised, and there is a life-cycle niche for this fluke in lymnaeid snails. However, it is a rare disease in Korea. We experienced four human fascioliasis which were difficult to differentiate from hepatic malignancy in three patients, and this was misdiagnosed as common hepatic duct tumor in one patient. The patients manifested only vague abdominal symptoms. Intrahepatic fascioliasis showed multiple ill-defined hypoattenuating lesions and filling defects of the lesion lumens on radiologic study. A striking eosinophilia from the patients' blood was identified and a positive finding of a serum enzyme linked immunosorbent assay for the Fasciola hepatica was also noted in three of four patients. The therapeutic trial with triclabendazole and praziquantel was not successful.
Adult ; Bile Duct Neoplasms/*diagnosis ; *Bile Ducts, Intrahepatic ; Cholangiocarcinoma/*diagnosis ; Diagnostic Errors ; English Abstract ; Fascioliasis/*diagnosis ; Female ; Humans ; Liver Diseases, Parasitic/*diagnosis ; Middle Aged

Cholestasis in a patient with Hodgkin's disease is uncommon, and the causes of cholestasis are mainly direct tumor involvement of the liver, hepatotoxic effects of drugs, viral hepatitis, sepsis and opportunistic infections. Vanishing bile duct syndrome (VBDS) represents a very rare cause for cholestasis in this disease. We report here on a case of a 45-year-old man who developed VBDS during the complete remission stage of Hodgkin's lymphoma. There was no history of hepatitis or intravenous drug abuse, and the patient had negative results for hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. The serological studies for antinuclear antibodies, anti-mitochondrial antibodies and anti-smooth muscle antibodies were also negative. Liver biopsy disclosed the absence of interlobular bile ducts in 9 of 10 portal tracts without any active lymphocyte infiltration and there were no Reed-Sternberg cell in the liver. The patient's cholestasis was in remission and the serum bililrubin level was normalized after two months without treatment, but tumor recurrence was noted at multiple sites of the abdominal lymph nodes on follow-up abdomino-pelvic computed tomogram.
Adult ; Bile Duct Diseases/*complications/diagnosis ; *Bile Ducts, Intrahepatic ; Cholestasis/*complications ; English Abstract ; Hodgkin Disease/*complications ; Humans ; Male ; Remission, Spontaneous

BACKGROUND/AIMS: Transjugular Intrahepatic Portosystemic Shunt (TIPS) is commonly used in patients with variceal bleeding. However, this procedure is contraindicated in hepatocellular carcinoma patients with portal vein thrombosis. This study was done to evaluate the effect of TIPS in those patients with variceal bleeding. METHODS: Between 1997 and 2004, six hepatocellular carcinoma (HCC) patients with portal vein thrombosis were enrolled in this study due to their variceal bleeding. All the patients underwent TIPS placement to treat the variceal bleeding that had not responded to endoscopic treatment. Effective shunt creation was assessed by the decrease of the portal pressure gradient (less than 12 mmHg) or if good patency and flow were seen on a doppler examination. RESULTS: Shunts were successfully created in all the patients and the bleeding was immediately controlled in the active bleeding cases. The bleeding was caused by esophageal varices in one patient and, by gastric varices in five patients. The HCC types were diffuse or massive in five patients, and a single nodule was present in one patient. All the patients had portal vein thrombosis. Rebleeding was noted in two patients at 10 days and 3 months, respectively, due to the shunt occlusion. Hepatic encephalopathy was noted in two patients. The causes of death were hepatorenal syndrome after 2 weeks in one patient, bleeding due to portal hypertensive gastropathy after 3 weeks in another, and cancer progression after 4 months in third patient. CONCLUSIONS: For HCC patients with portal vein thrombosis, TIPS can be an effective treatment modality if uncontrolled variceal bleeding presents when using endoscopic hemostasis or pharmacologic therapy. However, further studies are needed.
Adult ; Carcinoma, Hepatocellular/*complications ; English Abstract ; Esophageal and Gastric Varices/complications/*therapy ; Gastrointestinal Hemorrhage/*therapy ; Humans ; Liver Neoplasms/*complications ; Male ; Middle Aged ; *Portal Vein ; *Portasystemic Shunt, Transjugular Intrahepatic ; Venous Thrombosis/*complications

BACKGROUND/AIMS: The liver function tests (LFTs), such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltranspeptidase (gamma-GT), have been widely used as screening tests but their low positive predictive value can cause many false positive results. To evaluate the clinical usefulness of these tests, we analyzed the serial LFT results for factory workers, and we compared the risk factors for the groups that were divided according to the serial LFT results. METHODS: From June 2001 to October 2001, 1223 consecutive healthy workers in a single factory were enrolled in our study; a questionnaire, LFT and liver ultrasonography were done for all the subjects. The previous LFT results were collected from the Annual health examination survey. According to the abnormalities on the serial LFT, the participants were classified into three groups (abnormal-in-both, alternating or, normal-in-both) and the risk factors were compared among these groups using multiple logistic regression analysis. RESULTS: The prevalence of LFT abnormality on a single test was 16.8%, but on the serial LFT, only 5% of the study participants showed consistent abnormality. The risk factors for the abnormal-in-both group, compared with the alternating group, were liver ultrasonography abnormality such as a fatty liver (odds ratio, 2.2; P=0.026) and a heavy alcohol intake (more than 210 g/week) (odds ratio, 7.2; P=0.064). HBsAg was not a significant risk factor for any of the three groups. CONCLUSIONS: In factory workers having serial LFT abnormalities, alcoholic liver disease could be the principal cause of abnormal LFT. Even if the HBsAg were positive in patients with abnormal LFT, there is the possibility of another causes for LFT abnormalities such as alcoholic liver disease and non-alcoholic steatosis or steatohepatitis.
Adult ; English Abstract ; Female ; Humans ; Korea ; Liver/*enzymology ; Liver Diseases/*diagnosis ; *Liver Function Tests ; Male ; Middle Aged ; Occupational Health Services ; Risk Factors

BACKGROUND/AIMS: Nonalcoholic steatohepatitis (NASH) is chronic liver disease that can potentially progress to end stage liver disease. Oxidative stress to the vulnerable fatty liver has been reported as a key mechanism in development of NASH. Several antioxidant pathways have been identified, but reports that involved quantitative analysis of each antioxidant systems are rare, and these reports have shown various results. So, we investigated antioxidant status and the degree of oxidative stress by measuring several antioxidant enzymes, the total antioxidant status (TAS), and the metabolites of superoxide in NASH patients. METHODS: Nineteen NASH patients who were confirmed by liver biopsy and fifteen controls were involved in this study. The levels of body mass index (BMI), AST, ALT, superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, TAS, hydrogen peroxide (H2O2), and malondialdehyde (MDA) were compared between both groups. The relationship between the histologic severity and the levels of each antioxidants were analyzed in the NASH group. RESULTS: The activities of SOD and catalase were lower in the NASH group. The concentrations of TAS and H2O2 were higher in NASH group. The level of GPx and MDA showed no significant differences between both groups. There were no significant relationships between the above variables and the pathological severity. CONCLUSIONS: The disturbed metabolism of superoxide due to the decreased activities of SOD and catalase seem to be important in the pathogenesis of NASH. Further investigations about the nonenzymatic secondary antioxidant mechanism are necessary because the TAS was higher for the NASH group. The lack of difference between both groups for the concentration of MDA indicates that mechanisms other than lipid peroxidation also may be important in the pathogenesis of NASH.
Adult ; Antioxidants/*metabolism ; English Abstract ; Fatty Liver/*metabolism/pathology ; Female ; Humans ; Liver/pathology ; Male ; Oxidative Stress

BACKGROUND/AIMS: Adefovir dipivoxil is effective in patients with lamivudine-resistant hepatitis B virus (HBV). However, little is known about its role in Korean patients with decompensated liver cirrhosis. We retrospectively evaluated the efficacy and safety of adefovir dipivoxil in patients with decompensated liver cirrhosis with lamivudine resistance, and we compared this to the patients having compensated liver disease. METHODS: The patients with lamivudine-resistant chronic liver disease were enrolled and they received adefovir dipivoxil 10 mg daily. The clinical course and the biochemical and virological response of the decompensated cirrhosis group were compared with those of the patients with compensated liver disease group. RESULTS: One-hundred and one patients (the decompensated cirrhosis group, n=53; the compensated liver disease group, n=48) were evaluated. During the following up, 13 patients in the decompensated group and 4 patients in the compensated group dropped out of the treatment (P=0.011). After adefovir treatment, the proportion of patients with serum HBV DNA below 0.5 pg/mL in the decompensated group was less than that in the compensated group (50.9% vs. 83.3%, P=0.001), but the rates of normalized ALT, HBeAg loss and HBeAg seroconversion did not differ. The change of the Child-Pugh score in the decompensated group was 9.1 +/- 1.8 to 6.9 +/- 1.6 (P<0.001). The biochemical response in decompensated group was slower than that in the compensated group. Renal toxicity was not observed in either group. CONCLUSIONS: These results suggest that adefovir dipivoxil would be an effective and safe treatment for patients with decompensated liver cirrhosis with lamivudine resistance, but its effect might be limited and slower for decompensated cirrhosis.
Adenine/*analogs & derivatives/therapeutic use ; Adult ; Aged ; Antiviral Agents/*therapeutic use ; *Drug Resistance, Viral ; English Abstract ; Female ; Hepatitis B/complications/*drug therapy ; Humans ; Lamivudine/*therapeutic use ; Liver Cirrhosis/*virology ; Male ; Middle Aged ; Phosphonic Acids/*therapeutic use

BACKGROUND/AIMS: Immunogenetic factors may play a role in determining the susceptibility of an individual to viral infection. CCR5 promoter polymorphisms are known to be associated with HIV infection. However, there has been no report on the association between CCR5 promoter polymorphism and HBV infection. Therefore, we investigated the relationship between the CCR5 promoter polymorphism and HBV infection. METHODS: A total of 377 patients were classified into two groups according to their HBV infection status: (1)he spontaneous clearance group (SC); HBsAg (-), anti-HBc (+), anti-HBs (+) (2)he chronic HBsAg (+) carrier group (CC); HBsAg (+), anti-HBc (+), anti-HBs (-). CCR5 polymorphisms were detected by employing matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS)- based SNP scoring assay, termed Restriction Fragment Mass Polymorphism (RFMP), which exploits the differences in molecular masses between the common allele and rare allele bases of interest. RESULTS: We found that the genotype frequencies of CCR5 A59029G significantly differed between the SC group (n=138) and CC group (n=239) (P<0.05). The CCR5 59029A allelic genotype was associated with an increased risks of chronic infection rather than spontaneous clearance (P=0.002), and the presence of the CCR5 59029G allele was significantly associated with the spontaneous clearance of HBV (P=0.001). Strong linkage disequilibrium between the CCR5-59029 and the CCR5-59353 polymorphic variants was identified. None of the 377 subjects had the CCR5-32 bp deletion mutation. CONCLUSIONS: The CCR5 promoter polymorphisms at position 59029 might play a role in the clearance of HBV infection. This primary experimental evidence needs further studies to clarify the clinical usefulness of CCR5 promoter polymorphisms as a target for the screening or treatment of HBV infection.
Adult ; English Abstract ; Female ; Genetic Predisposition to Disease ; Genotype ; Hepatitis B/*genetics ; Hepatitis B virus/genetics ; Humans ; Male ; Middle Aged ; *Polymorphism, Genetic ; Promoter Regions (Genetics)/*genetics ; Receptors, CCR5/*genetics

Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease. The reported incidence is 1-6%. The most common thromboembolic complications are deep venous thrombosis of legs and pulmonary thromboembolism. Cerebral thrombosis, portal vein thrombosis, retinal venous thrombosis and arterial thrombosis were also reported. We experienced a case of ulcerative colitis complicated with pulmonary thromboembolism. The patient was a 70-year-old woman who was diagnosed as ulcerative colitis on colonoscopy. We used prednisolone and sulfasalazine for the treatment of ulcerative colitis. Twenty five days later, she complained of abrupt dyspnea and chest pain. Chest CT and ventilation-perfusion scan revealed a thromboembolism in both lung. After the treatment of heparin & warfarin therapy, follow-up chest CT showed much regressed pulmonary thromboembolism. We report a 70-year-old woman with ulcerative colitis complicated with pulmonary thromboembolism and treated with heparin & warfarin therapy successfully.
Aged ; Colitis, Ulcerative/*complications ; English Abstract ; Female ; Humans ; Pulmonary Embolism/*complications

BACKGROUND/AIMS: As a preliminary study to test the possibility of oral transmission of hepatitis C virus (HCV), many investigations in order to detect the extrahepatic localization of HCV have been performed. In this study, we examined the presence of HCV viral proteins in gastric mucosa. METHODS: Immunohistochemical staining to NS3 protein were done to detect the HCV virus in gastric mucosa. The results were compared with NS5a protein staining to confirm the NS3 protein staining. RESULTS: Total of 164 patient were included. 58 patients with anti-HCV (+) were designated to case group and 70 with anti-HCV (-) to control group. 36 were excluded in this study due to concomittent illness. Anti-HCV (+) group showed 50.0% (29/58) of positivity to NS3 protein staining and anti-HCV (-) group showed 12.6% (9/70) of positivity (p<0.001). Immunohistochemical staining to NS5a protein were done to validate the result of NS3 (+) staining in the anti-HCV (+) group (n=58). NS5a (+) staining were observed in 58.6% (34/58). The results of NS5a staining were consistent with that of NS3 in 70.7%. The reliability coefficients by Chronbach's Alpha for NS3 and NS5a stain test was 0.59. CONCLUSIONS: HCV can exist in gastric mucosal cell as an extrahepatic presence. In the future, this study may provide some fundamental data for the research of possible oral transmission route of HCV.
Aged ; English Abstract ; Female ; Gastric Mucosa/*virology ; Hepacivirus/*isolation & purification ; Hepatitis C Antigens/*analysis ; Humans ; Male ; Middle Aged

BACKGROUND/AIMS: X-linked inhibitor of apoptosis (XIAP) is the most potent member of the IAP family that exerts antiapoptotic effects. Recently, XIAP-associated factor 1 (XAF1) and two mitochondrial proteins, Smac/DIABLO and HtrA2, have been identified to negatively regulate the caspase-inhibiting activity of XIAP. We explored the candidacy of XAF1, Smac/DIABLO and HtrA2 as a tumor suppressor in colonic carcinogenesis. METHODS: Expression and mutation status of the genes in 10 colorectal carcinoma cell lines and 40 primary tumors were examined by quantitative PCR analysis. RESULTS: XAF1 transcript was not expressed or present at extremely low levels in 60% (6/10) of cancer cell lines whereas Smac/DIABLO and HtrA2 are normally expressed in all cell lines examined. Tumor-specific loss or reduction of XAF1 was also found in 35% (14/40) of matched tissue sets obtained from the same patients. XAF1 transcript was reactivated in all the low expressor cell lines by treatment with the demethylating agent 5-aza-2'-deoxycytidine. Moreover, bisulfite DNA sequencing analysis for 34 CpG sites in the promoter region revealed a strong association between hypermethylation and gene silencing. Restoration of XAF1 expression resulted in enhanced apoptotic response to etoposide and 5-flurouracil, whereas knockdown of XAF1 expression by siRNA transfection significantly inhibited chemotherapeutic drug-induced apoptosis. CONCLUSIONS: XAF1 undergoes epigenetic gene silencing in a considerable proportion of human colon cancers by aberrant promoter hypermethylation, suggesting that XAF1 inactivation might be implicated in colonic tumorigenesis.
Cell Line, Tumor ; Colonic Neoplasms/*genetics ; *DNA Methylation ; English Abstract ; Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Mitochondrial Proteins/genetics ; Neoplasm Proteins/*genetics ; Promoter Regions (Genetics) ; Serine Endopeptidases/genetics