No abstract available.
Hepatitis C, Chronic* ; Hepatitis, Chronic*

No abstract available.
Blood Group Incompatibility* ; Bromelains*

Chronic hepatitis B (CHB) can progress to cirrhosis which is one of the important clinical consequences. Recently antiviral therapy is known to reduce hepatic inflammation and prevent progression to cirrhosis and/or decompensation/hepatocellular carcinoma (HCC). When to start and stop, how to minimize antiviral resistance are major issues to be solved in antiviral therapy. To prevent HBV viral resistance, potent antiviral therapy with high genetic barriers is recommended. However we are not free from national insurance coverage in clinical practice, and there are limitations in imbursement coverage in clinical practice. Recently, guidelines of imbursement has been amended with extended coverage that goes with KASL and other guidelines. Major changes include the extension of duration of drugs beyond 3 years and approval of antiviral therapy in cirrhotic/HCC patients even with mild elevation of AST/ALT. This article reviews recent advance in management of chronic hepatitis B focusing on changes of imbursement regulation.
Fibrosis ; Hepatitis B, Chronic ; Hepatitis, Chronic ; Humans ; Inflammation ; Insurance ; Insurance Coverage

No abstract available.
Antiviral Agents/*therapeutic use ; Drug Resistance, Viral/*genetics ; Hepatitis B virus/drug effects/*genetics ; Hepatitis B, Chronic/*drug therapy/virology ; Humans ; *Mutation

No abstract available.
Hepatitis A/prevention & control ; Hepatitis A Antibodies/*blood ; Hepatitis A Virus, Human/*immunology ; Humans ; Korea ; Seroepidemiologic Studies

No abstract available.
Otoacoustic Emissions, Spontaneous*

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors and has the third highest mortality rate among malignancies in South Korea. Despite the continuing efforts for the early detection of HCC, the mortality rate and prognosis have not been improved yet. Its clinical behavior is quite different from other cancers. High recurrence rate after curative treatment might be the reason for poor prognosis. Several methods including chemoprevention, blocking the development of HCC, have been under investigations. The vaccine for hepatitis, in the form of primary prevention, is considered to be the most effective one inhibiting the development of liver disease. Furthermore, keeping away from hepatotoxic agents is another way for preventing liver cell injuries. Secondary prevention is to stop the developement of HCC in chronic liver diseases. Since the level of DNA in hepatitis B virus (HBV) hepatitis patients is closely related with the development of HCC, it is helpful to lower the DNA level using anti-viral agents. In addition, IFN, one of the anti-viral agents, can inhibit HCV hepatitis from tumorigenesis. Cyclo-oxygenase (COX)-2 inhibitors are also alleged to have a function in interrupting the development of HCC. Tertiary prevention means the prevention of recurrence of HCC after successful treatment. Because of high recurrence rate, the prevention of recurrence should be one of the important factors affecting the prognosis of HCC. Up to now, COX inhibitors, retinoic acids, vitamin K2, glycyrrhizin epigallocatechin-3-gallate (EGCG), and ginseng had been reported to be effective for the chemoprevention of HCC. Further studies are required for an advancement in the prevention of HCC.
Antiviral Agents/therapeutic use ; Carcinoma, Hepatocellular/*prevention & control ; Cyclooxygenase Inhibitors/therapeutic use ; Hepatitis B Vaccines ; Humans ; Interferons/therapeutic use ; Liver Neoplasms/*prevention & control

Occult HBV infection (OBI) is defined as presence of HBV DNA in the liver tissue in patients with serologically undetectable HBsAg. There are differences in virologic and serological profiles of OBI. Majority of OBI are positive for anti-HBs and/or anti-HBc and minor portion are negative for all HBV markers. However, there are no HBV mutations in the surface and its regulatory regions. HBV infection persists by the presence of covalently closed circular DNA (cccDNA) within the infected hepatocytes, which serves as a reservoir for future infection. OBI increases the risk of HBV transmission through transfusion, hemodialysis, and organ transplantation. Therefore effective measures should be employed to screen OBI. Antiviral therapy is needed in HBsAg-negative transplant patients who are anti-HBc positive to prevent the recurrence of HBV infection. Since HBV replication is strongly suppressed by immune surveillance system in OBI patients, immunosuppression results in massive HBV replication. This leads to acute hepatitis and sometimes mortality when immune surveillance is recovered after stopping immunosuppressive drugs/anticancer chemotherapy. Therefore, narrow surveillance is required to recognize the viral reactivation and start antiviral agents during immunosuppressive therapy/anticancer chemotherapy in patients with OBI.
Blood Transfusion ; DNA, Viral/analysis ; Hepatitis B/*diagnosis/transmission ; Hepatitis B Core Antigens/immunology ; Hepatitis B virus/genetics/*physiology ; Humans ; Liver Transplantation ; Renal Dialysis ; Virus Activation

Although much advancement has been achieved in the treatment of chronic hepatitis B, antiviral resistance is still a challenging issue. Previous generation antiviral agents have already developed resistance in a number of patients, and it is still being used especially in resource limited countries. Once antiviral resistance occurs, it predisposes to subsequent resistance, resulting in multidrug resistance. Therefore, prevention of initial antiviral resistance is the most important strategy, and appropriate choice and modification of therapy would be the cornerstone in avoiding treatment failures. Until now, management of antiviral resistance has been evolving from sequential therapy to combination therapy. In the era of tenofovir, the paradigm shifts again, and we have to decide when to switch and when to combine on the basis of newly emerging clinical data. We expect future eradication of chronic hepatitis B virus infection by proper prevention and optimal management of antiviral resistance.
Adenine/analogs & derivatives/pharmacology/therapeutic use ; Antiviral Agents/pharmacology/*therapeutic use ; Drug Resistance, Viral/drug effects ; Drug Therapy, Combination ; Hepatitis B virus/genetics ; Hepatitis B, Chronic/*drug therapy/prevention & control ; Humans ; Mutation ; Nucleosides/*chemistry/pharmacology/therapeutic use ; Organophosphonates/pharmacology/therapeutic use ; Virus Replication/drug effects

PURPOSE: The 12-lead electrocardiogram has limitation for detection of lateral wall myocardial infarction (MI). Therefore, this study was conducted to compare the location of leads V5 and V6 with the left ventricle (LV) lateral wall using multidetector computed tomography (MDCT) and propose new additional leads for detection of lateral wall MI. METHODS: From 120 study subjects who underwent chest MDCT, we measured the angle (Θ) between the midsagittal plane and long axis of LV on the coronal imaging of MDCT. Using this, another angle (90-Θ) between the long axis of LV and leads V5 and V6 was calculated. After the location of the leads V5 and V6 was identified using axial and coronal images of MDCT, the positional relationship between leads V5 and V6 and the lateral wall was compared based on the thoracic spine. RESULTS: The Θ and 90-Θ was 52.2°±10.3°and 37.8°±10.3°, respectively. Leads V5 and V6 faced the LV lateral wall very obliquely. The score of leads V5 and V6 position based on the thoracic spine was 6.9±1.8 points as the level of lower part of 9th vertebral body. Meanwhile, the lateral wall of LV was 4.7±2.2 points as the lower part of the 8th vertebral body. Thus, leads V5 and V6 were located lower by the height of one thoracic vertebral body than the lateral wall of LV on coronal images (p < 0.001). CONCLUSION: Leads V5 and V6 are inappropriate for detection of the lateral wall MI. To diagnose that more efficiently, we propose the new additional leads, elevated V5 and elevated V6, located two or three intercostal spaces upward from leads V5 and V6.
Coronary Vessels ; Electrocardiography ; Heart Ventricles ; Multidetector Computed Tomography ; Myocardial Infarction ; Spine ; Thorax