Background/Aims: Although anti-hepatitis C virus (HCV) assay is widely used to screen for HCV infection, it has a high false-positive (FP) rate in low-risk populations. We investigated the accuracy of anti-HCV signal-to-cutoff (S/CO) ratio to distinguish true-positive (TP) from FP HCV infection. Methods: We retrospectively analyzed 77,571 patients with anti-HCV results. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic accuracy of anti-HCV S/CO ratio in anti-HCV positive patients. Results: Overall, 1,126 patients tested anti-HCV positive; 34.7% of patients were FP based on HCV RNA and/or recombinant immunoblot assay (RIBA) results. The age and sex-adjusted anti-HCV prevalence was 1.22%. We identified significant differences in serum aspartate transaminase and alanine transaminase levels, anti-HCV S/CO ratio, and RIBA results between groups (viremia vs. non-viremia, TP vs. FP). Using ROC curves, the optimal cutoff values of anti-HCV S/CO ratio for HCV viremia and TP were 8 and 5, respectively. The area under the ROC curve, sensitivity, specificity, positive and negative predictive values were 0.970 (95% CI, 0.959–0.982, p < 0.001), 99.7%, 87.5%, 87.4%, and 99.7%, respectively, for predicting HCV viremia at an anti-HCV S/CO ratio of 8 and 0.987 (95% CI, 0.980–0.994, p < 0.001), 95.3%, 94.7%, 97.1%, and 91.4%, respectively, for TP HCV infection at an anti-HCV S/CO ratio of 5. No patients with HCV viremia had an anti-HCV S/CO ratio below 5. Conclusions The anti-HCV S/CO ratio is highly accurate for discriminating TP from FP HCV infection and should be considered when diagnosing HCV infections.

Background: Liver fibrosis is defined as the accumulation of the extracellular matrix and scar formation. The receptor for advanced glycation end products (RAGE) has been demonstrated to participate in fibrogenesis. S100B is a ligand of RAGE and exerts extracellular functions by inducing a series of signal transduction cascades. However, the involvement of S100B and RAGE in cholestasis-induced liver fibrosis remains unclear. In this study, we investigated S100B and RAGE expression during liver fibrosis in mice that underwent common bile duct ligation (BDL). Methods: BDL was performed in 10-week-old male C57BL/6J mice with sham control (n = 26) and BDL (n = 26) groups. Expression levels of S100B, RAGE and fibrotic markers in the livers from both groups at week 1 and 3 after BDL were examined by western blot and quantitative real-time reverse transcription polymerase chain reaction analysis. Liver fibrotic changes were examined by histological and ultrastructural analysis. Results: Histological staining with Sirius Red and the evaluation of the messenger RNA expression of fibrotic markers showed noticeable periportal fibrosis and bile duct proliferation. S100B was mainly present in bile duct epithelial cells, and its expression was upregulated in proportion to the ductular reaction during fibrogenesis by BDL. RAGE expression was also increased, and interestingly, triple immunofluorescence staining and transmission electron microscopy showed that both S100B and RAGE were expressed in proliferating bile duct epithelial cells and activated hepatic stellate cells (HSCs) of the BDL livers. In addition, in rat HSCs (HSC-T6), treatment with recombinant S100B protein significantly increased fibrotic markers in a dose-dependent manner, and RAGE small interfering RNA (siRNA) suppressed S100B-stimulated upregulation of fibrotic markers compared with cells treated with scramble siRNA and S100B. Conclusion These findings suggest that the increased expression of S100B and RAGE and the interaction between S100B and RAGE may play an important role in ductular reaction and liver fibrosis induced by BDL.

Background: Liver fibrosis is defined as the accumulation of the extracellular matrix and scar formation. The receptor for advanced glycation end products (RAGE) has been demonstrated to participate in fibrogenesis. S100B is a ligand of RAGE and exerts extracellular functions by inducing a series of signal transduction cascades. However, the involvement of S100B and RAGE in cholestasis-induced liver fibrosis remains unclear. In this study, we investigated S100B and RAGE expression during liver fibrosis in mice that underwent common bile duct ligation (BDL). Methods: BDL was performed in 10-week-old male C57BL/6J mice with sham control (n = 26) and BDL (n = 26) groups. Expression levels of S100B, RAGE and fibrotic markers in the livers from both groups at week 1 and 3 after BDL were examined by western blot and quantitative real-time reverse transcription polymerase chain reaction analysis. Liver fibrotic changes were examined by histological and ultrastructural analysis. Results: Histological staining with Sirius Red and the evaluation of the messenger RNA expression of fibrotic markers showed noticeable periportal fibrosis and bile duct proliferation. S100B was mainly present in bile duct epithelial cells, and its expression was upregulated in proportion to the ductular reaction during fibrogenesis by BDL. RAGE expression was also increased, and interestingly, triple immunofluorescence staining and transmission electron microscopy showed that both S100B and RAGE were expressed in proliferating bile duct epithelial cells and activated hepatic stellate cells (HSCs) of the BDL livers. In addition, in rat HSCs (HSC-T6), treatment with recombinant S100B protein significantly increased fibrotic markers in a dose-dependent manner, and RAGE small interfering RNA (siRNA) suppressed S100B-stimulated upregulation of fibrotic markers compared with cells treated with scramble siRNA and S100B. Conclusion These findings suggest that the increased expression of S100B and RAGE and the interaction between S100B and RAGE may play an important role in ductular reaction and liver fibrosis induced by BDL.

BACKGROUND/AIMS: The association between Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose aspirin therapy as a risk factor for peptic ulcer bleeding (PUB) remains unclear. This study investigated the risk of PUB associated with H. pylori infection and NSAID or low-dose aspirin therapy in patients with PUD. MATERIALS AND METHODS: This case-control study investigated 340 patients with PUB between 2012 and 2016. The control group comprised age and sex-matched patients with endoscopically documented non-bleeding ulcers. Using logistic regression analysis, the adjusted odds ratio (AOR) was calculated for the risk of PUB. RESULTS: Of the patients investigated, 57.9% in the study group and 51.8% in the control group were diagnosed with H. pylori infection (P=0.106). Logistic regression analysis showed synergistic interaction between H. pylori infection and low-dose aspirin therapy. Multivariate analysis showed that low-dose aspirin (AOR 3.92, P < 0.001), NSAIDs (AOR 2.98, P=0.001), warfarin (AOR 14.57, P=0.011), gastric ulcer (compared with duodenal ulcer) (AOR 1.65, P=0.01), and smoking (AOR 1.97, P=0.004) increased the risk of PUB compared with the risk of PUD. CONCLUSIONS: Both NSAIDs and aspirin are independent risk factors for bleeding in patients with PUD. Additionally, low-dose aspirin therapy concomitant with H. pylori infection produced a synergistic effect. Therefore, H. pylori eradication may be crucial in aspirin users. Moreover, a proton pump inhibitor should be prescribed in patients with a history of bleeding ulcers who need long-term NSAID treatment.
Anti-Inflammatory Agents, Non-Steroidal ; Aspirin ; Case-Control Studies ; Helicobacter pylori ; Helicobacter ; Hemorrhage ; Humans ; Logistic Models ; Multivariate Analysis ; Odds Ratio ; Peptic Ulcer ; Proton Pumps ; Risk Factors ; Smoke ; Smoking ; Stomach Ulcer ; Ulcer ; Warfarin

BACKGROUND/AIMS: Selecting patients with an urgent need for endoscopic hemostasis is difficult based only on simple parameters of presumed acute upper gastrointestinal bleeding. This study assessed easily applicable factors to predict cases in need of urgent endoscopic hemostasis due to acute upper gastrointestinal bleeding. METHODS: The consecutively included patients were divided into the endoscopic hemostasis and nonendoscopic hemostasis groups. We reviewed the enrolled patients’ medical records and analyzed various variables and parameters for acute upper gastrointestinal bleeding outcomes such as demographic factors, comorbidities, symptoms, signs, laboratory findings, rebleeding rate, and mortality to evaluate simple predictive factors for endoscopic treatment. RESULTS: A total of 613 patients were analyzed, including 329 patients in the endoscopic hemostasis and 284 patients in the non-endoscopic hemostasis groups. In the multivariate analysis, a bloody nasogastric lavage (adjusted odds ratio [AOR], 6.786; 95% confidence interval [CI], 3.990 to 11.543; p < 0.0001) and a hemoglobin level less than 8.6 g/dL (AOR, 1.768; 95% CI, 1.028 to 3.039; p = 0.039) were independent predictors for endoscopic hemostasis. Significant differences in the morbidity rates of endoscopic hemostasis were detected between the group with no predictive factors and the group with one or more predictive factors (OR, 2.677; 95% CI, 1.920 to 3.733; p < 0.0001). CONCLUSIONS A bloody nasogastric lavage and hemoglobin < 8.6 g/dL were independent predictors of endoscopic hemostasis in patients with acute upper gastrointestinal bleeding.

BACKGROUND/AIMS: Long-term use of nucleos(t)ide analogues (NA) may lead to genotypic and/or phenotypic resistance of the hepatitis B virus (HBV). We investigated the efficacy of tenofovir-based rescue therapy in chronic hepatitis B (CHB) patients with newly developed genotypic resistance to prior NAs or partial virologic response to sequential rescue therapies. METHODS: Fifty-four CHB patients were included retrospectively. The patients were treated with tenofovir alone or combined with lamivudine or entecavir. RESULTS: There were 26 forms of genotypic resistance at enrollment. The median amount of serum HBV-DNA was 18,438 IU/mL and 83% of samples were positive for hepatitis B e antigen (HBeAg). Serum HBV-DNA was undetectable in 50%, 61%, and 76% of the patients at 3, 6, and 12 months, respectively. In multivariate analysis, HBV-DNA < 20,000 IU/mL and negative HBeAg at baseline were independent predictors of negativity for serum HBV-DNA. Interestingly, the rtS202 mutation tended to be associated with an unfavorable response. Other clinical variables and viral resistance genotypes showed non-significant viral response. CONCLUSIONS: Lower serum HBV-DNA, negative HBeAg and lack of rtS202G mutations at baseline may predict a favorable response to tenofovir-based rescue therapies in CHB patients with newly developed genotypic resistance to prior NAs or a partial virologic response to sequential rescue therapies.
Drug Resistance ; Genotype ; Hepatitis B ; Hepatitis B e Antigens ; Hepatitis B virus ; Hepatitis B, Chronic* ; Hepatitis, Chronic* ; Humans ; Lamivudine ; Multivariate Analysis ; Retrospective Studies ; Tenofovir

Up-to-date imaging modalities such as three-dimensional dynamic contrast-enhanced CT (3D CT) and MRI may contribute to detection of hypervascular nodules in the liver. Nevertheless, distinguishing a malignancy such as hepatocellular carcinoma from benign hypervascular hyperplastic nodules (HHN) based on the radiological findings is sometimes difficult. Multiple incidental liver masses were detected via abdominal ultrasonography (US) in a 65-year-old male patient. He had no history of alcohol intake and no remarkable past medical history or relevant family history, and his physical examination results and laboratory findings were normal. 3D CT and MRI showed numerous enhanced nodules with hypervascularity during the arterial phase. After US guided liver biopsy, the pathological diagnosis was HHN. To date, several cases of HHN have been reported in patients with chronic alcoholic liver disease or cirrhosis. Herein, we report on a case of HHN in a patient with no history of alcoholic liver disease or cirrhosis.
Abdomen/diagnostic imaging ; Aged ; Alcoholism/pathology ; Chronic Disease ; Diagnosis, Differential ; Focal Nodular Hyperplasia/*diagnosis ; Humans ; Imaging, Three-Dimensional ; Liver/diagnostic imaging/*pathology ; Liver Diseases/pathology ; Magnetic Resonance Imaging ; Male ; Tomography, X-Ray Computed ; Ultrasonography

BACKGROUND/AIMS: As the incidence rate of and mortality from pseudomembranous colitis (PMC) are increasing worldwide, it is important to study the simple predictive risk factors for PMC among patients with hospital-acquired diarrhea (HAD). This study focused on identifying the clinical risk factors that can easily predict PMC. METHODS: The presumed HAD patients were prospectively recruited at the Hallym University Kangdong Sacred Heart Hospital. RESULTS: Age of 70 and older (adjusted odds ratio [OR], 1.76; 95% confidence interval [CI], 1.12 to 0.75), use of proton pump inhibitors (adjusted OR, 4.07; 95% CI, 2.512 to 6.57), use of cephalosporins (adjusted OR, 2.99; 95% CI, 1.82 to 4.94), and underlying cancer (adjusted OR, 1.72; 95% CI, 1.04 to 2.82) were independent risk factors for PMC in the multivariate logistic regression analysis. The prevalence of PMC was very low in the patients with HAD who exhibited no risk factors. CONCLUSIONS: The risk factors for PMC in patients with HAD included cephalosporin use, proton pump inhibitor use, old age, and cancer. Considering the strongly negative predictive values of these risk factors, endoscopic evaluation can be delayed in patients with HAD without risk of developing PMC.
Adult ; Aged ; Aged, 80 and over ; *Clostridium difficile ; Cross Infection/complications/*epidemiology ; Diarrhea/complications/*epidemiology ; Enterocolitis, Pseudomembranous/complications/*epidemiology ; Female ; Humans ; Male ; Middle Aged ; Prevalence ; Prospective Studies ; Republic of Korea/epidemiology ; Risk Factors

Vertical transmission from mother to child, the main route of chronic hepatitis B virus (HBV) infection in the East Asia, is considered one of the most important predictors for the response to antiviral therapies as well as its complications such as cirrhosis and hepatocellular carcinoma. Therefore, it is critical in both etiologic and prognostic aspects to confirm whether or not chronic HBV infection is acquired vertically. This study investigated whether mother-to-child infection could be proved by the phylogenetic analyses of HBV pre-S/S genes ever since several decades have elapsed in mother-child pairs with presumed vertical transmission. The pre-S and S regions of HBVs were compared and analyzed phylogenetically in a total of 36 adults (18 mother-child pairs) with chronic HBV infection. All of the isolates of HBV were genotype C and serotype adr. The divergence between mothers and offsprings was 0 to 1.5%. Phylogenetic trees revealed that 17 of 18 pairs (94%) with presumed vertical transmission were grouped into the same cluster. Vertical transmission from mother to child could be strongly suggested even in adults with a history of several decades of HBV infection using the phylogenetic analyses of pre-S and S genes.
Adult ; Aged ; DNA, Viral/analysis ; Female ; Genotype ; Hepatitis B Surface Antigens/classification/*genetics ; Hepatitis B virus/classification/*genetics/metabolism ; Hepatitis B, Chronic/diagnosis/*virology ; Humans ; Infectious Disease Transmission, Vertical ; Male ; Middle Aged ; Mothers ; Phylogeny ; Polymerase Chain Reaction ; Sequence Analysis, DNA ; Serotyping ; Young Adult

Clostridial septicemia usually occurrs in patients with immunocompromised diseases such as diabetes and malignancy. Clostridial liver abscess is very rare but highly fatal. We experienced a case of Clostridial septicemia due to liver abscess in a 73-year-old man. He was presented with fever and chills. On admission, abdominal CT scan showed about 35 mm sized hypoattenuated lesion with multiple central air-bubbles. After the diagnosis of liver abscess, the patient underwent prompt empirical antimicrobial therapy and percutaneous drainage. In spite of early therapy, the patient had gone into shock and death.
Aged ; Clostridium/*isolation & purification ; Clostridium Infections/diagnosis/*microbiology ; Drainage ; Humans ; Liver/radiography ; Liver Abscess/complications/*diagnosis/microbiology ; Male ; Sepsis/complications/*diagnosis ; Tomography, X-Ray Computed