Hepatitis: Kim JY

Waasdorp CE, Kim JY. · U.S. Army, 121st Combat Support Hospital, Seoul, South Korea. · Wilderness Environ Med. · Pubmed #17896850 No free full text.

Abstract: Families are traveling with their children in increasing frequency. Travel to Asia offers children many opportunities to learn about new cultures and history. It also offers the potential for exposure to numerous infectious agents not commonly encountered in the United States. Families must begin to prepare for travel to Asia weeks before departure. Children should be up to date on routine vaccinations. Appropriate education should be given on arthropod avoidance and malaria prophylaxis. Additional education and possible prophylaxis should be completed for other infectious agents frequently encountered in Asia. With appropriate pretrip immunizations and prophylaxis, children can travel to Asia with minimal risk of acquiring infection. This article provides general advice to assist providers with pretravel preparation and education of families traveling with children to Asia.

Kim SH, Yoon HE, Kim YK, Kim JY, Choi BS, Choi YJ, Kim YO, Kim YS, Bang BK, Yang CW. · Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, South Korea. · Nephron Clin Pract. · Pubmed #18663324 No free full text.

Abstract: BACKGROUND/AIMS: The development of acute renal failure (ARF) is a very rare complication in patients with acute hepatitis A (AHA). METHODS: We retrospectively investigated the overall incidence, risk factors, and clinical outcomes of ARF associated with AHA. Diagnosis of AHA was made according to the typical hepatitis symptoms and positivity of immunoglobulin M anti-hepatitis A virus in 208 patients with AHA. RESULTS: ARF was noted in 12 (5.7%) patients, and dialysis was required in 8 (66%) patients. The median duration of hospitalization for patients with ARF was 18 days (range, 6-50 days). The development of ARF was observed in older patients (p = 0.004) and in patients with diabetes (p = 0.001), excessive alcohol consumption (p = 0.01), prolonged international normalized ratio (p = 0.019), and elevated aspartate aminotransferase concentration (p = 0.034). Multivariate analysis revealed that old age (odds ratio, OR, 1.2), elevated aspartate aminotransferase concentration (OR, 1.05), and diabetes (OR, 18.5) were independent risk factors for ARF (each p < 0.001). The prognosis of patients with ARF was good, and renal function recovered completely. CONCLUSION: ARF associated with AHA is not rare, and the possibility of AHA should be considered in patients with ARF with hepatic dysfunction.

Choi GH, Ju MK, Kim JY, Kang CM, Kim KS, Choi JS, Han KH, Park MS, Park YN, Lee WJ, Kim BR. · Department of Surgery, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul, Korea. · J Korean Med Sci. · Pubmed #18437023 links to  free full text

Abstract: We report on a case of hepatic splenosis. A 32-yr-old man underwent a splenectomy due to trauma at the age of 6. He had been diagnosed as being a chronic hepatitis B-virus carrier 16 yr prior to the surgery. The dynamic computer tomography (CT) performed due to elevated serum alpha-fetoprotein (128 ng/mL) demonstrated two hepatic nodules, which were located near the liver capsule. A nodule in Segment IVa had a slight enhancement during both the arterial and portal phases, and another nodule in Segment VI showed a slight enhancement only in the portal phases. Dynamic magnetic resonance imaging (MRI) of the mass in Segment VI showed enhanced development in the arterial phases and slight hyperintensivity to the liver parenchyma in the portal phases. These imaging findings suggested a hypervascular tumor in the liver, which could be either focal nodular hyperplasia, adenoma, or hepatocellular carcinoma (HCC). Even though these lesions were diagnosed as HCC, some of the findings were not compatible with typical HCC. On dynamic CT and MRI, all lesions showed a slight arterial enhancement and did not show early venous washout. All lesions were located near the liver capsule. These findings, along with a history of splenectomy, suggested a diagnosis of hepatic splenosis.

Kim KA, Lee JS, Jung ES, Kim JY, Bae WK, Kim NH, Moon YS. · Department of Internal Medicine, College of Medicine, Inje University, Ilsanpaik Hospital, Ilsan-Gu, Goyang, Korea. · Korean J Gastroenterol. · Pubmed #17132920 links to  free full text

Abstract: BACKGROUND/AIMS: Serum alpha-fetoprotein (AFP) is frequently used for the diagnosis of hepatocellular carcinoma (HCC). Most available data concerning AFP came from studies of patients with chronic hepatitis B or mixed etiologies. Studies concerning the diagnostic value of AFP for HCV-related liver cirrhosis (LC) are limited. We evaluated the factors influencing AFP elevation in the absence of HCC and analyzed the diagnostic value of serum AFP in HCC surveillance of HCV-related LC patients. METHODS: We enrolled 55 patients of HCV-related LC with HCC and 62 patients without HCC as a case-control study were analyzed. The sensitivity and specificity were calculated and the clinical and biochemical factors influencing serum AFP levels. RESULTS: The sensitivities and specificities of serum AFP for the detection of HCC in HCV-related LC were 72.7% and 59.7% for AFP>or=20 ng/mL, and 47.3% and 92.5% for AFP>or=100 ng/mL, respectively. Elevated serum AST was independently associated with elevated serum AFP level in HCV-related LC. In cases of AST<or=2 upper limit of normal (ULN), the specificity of AFP>or=100 ng/mL for the diagnosis of HCC was 100%. However, in case of AST>2 ULN, the specificity was 85.0% for AFP>or=100 ng/mL and 95.0% for AFP>or=200 ng/mL. CONCLUSIONS: Serum AST levels influence serum AFP level in HCV-related LC. In cases of AST<or=2 ULN, AFP greater than 100 ng/mL highly indicates HCC in HCV-related LC, but not in case of AST>2 ULN.

Park SG, Chung C, Kang H, Kim JY, Jung G. · School of Biological Sciences, Institute of Microbiology, Seoul National University, Seoul 151-742, Korea. · J Biol Chem. · Pubmed #16940298 links to  free full text

Abstract: Cyclin D1 is frequently overexpressed in hepatocellular carcinoma (HCC) exhibiting increased malignant phenotypes. It has also been known that the hepatitis Bx (HBx) protein is strongly associated with HCC development and progression. Although overexpression of both proteins is related to HCC, the relationship between the two has not been well studied. Here we show that HBx up-regulates cyclin D1 and that this process is mediated by the NF-kappaB2(p52)/BCL-3 complex. Our experiments indicate that HBx up-regulates BCL-3 in the mRNA level, which subsequently results in the up-regulation of the NF-kappaB2(p52)/BCL-3 complex in the nucleus. Moreover, impaired HBx-mediated BCL-3 up-regulation by small interfering RNA for BCL-3 reduced HBx-mediated cyclin D1 up-regulation. Down-regulation of the HBx protein level by p53 also reduced HBx-mediated cyclin D1 up-regulation. From these results, we conclude that the up-regulation of cyclin D1 by HBx is mediated by the up-regulation of NF-kappaB2(p52)/BCL-3 in the nucleus. This HBx-mediated-cyclin D1 up-regulation might play an important role in the HBx-mediated HCC development and progression.

Hyun JJ, Kim JY, Bak YT, Lee CH, Choi SY. · Department of Internal Medicine, Korea University Guro Hospital, Seoul, South Korea. · J Gastroenterol Hepatol. · Pubmed #16911700 No free full text.

This publication has no abstract.

Byun KS, Kwon OS, Kim JH, Yim HJ, Chang YJ, Kim JY, Yeon JE, Park JJ, Kim JS, Bak YT, Lee CH. · Department of Internal Medicine, Korea University College of Medicine, Seoul, South Korea. · J Gastroenterol Hepatol. · Pubmed #16336441 No free full text.

Abstract: BACKGROUND AND AIM: It is uncertain if a patient's lamivudine response after HBeAg loss is durable. In Korean chronic hepatitis B patients, the relapse rate is high after termination of lamivudine therapy for patients with HBeAg loss. We evaluated the factors related to relapse in chronic hepatitis B patients with HBeAg loss after lamivudine therapy. METHODS: A total of 132 chronic hepatitis B patients, who initially had HBeAg and did not have decompensated features, were analyzed in this study. These patients lost the HBeAg after lamivudine therapy and then their therapy was stopped. Post-treatment serum alanine aminotransferase (ALT), HBeAg, anti-HBe and hepatitis B virus (HBV) DNA were monitored until relapse. RESULTS: Seventy-five patients relapsed (cumulative relapse rate: 56% at 6 months). Upon univariate analysis, the factors of age, serum total bilirubin, presence of anti-HBe after HBeAg loss, and the duration of additional lamivudine therapy after HBeAg loss were associated with relapse. Upon multivariate analysis, older age, a higher serum total bilirubin and the shorter duration of additional lamivudine therapy were significant risk factors for relapse. Patterns of relapse were the re-elevation of ALT, re-emergence of HBV DNA (69 patients) and reappearance of HBeAg (55 patients). CONCLUSIONS: To prevent relapse in patients with chronic hepatitis B infection after lamivudine therapy, age and serum bilirubin level of patients as well as a prolonged duration of additional lamivudine therapy should be considered.

Oh SN, Rha SE, Byun JY, Kim JY, Song KY, Park CH. · Department of Radiology, Kangnam St. Mary's Hospital, College of Medicine, Catholic University of Korea, 505 Banpo-Dong, Seoul, 137-040, South Korea. · Abdom Imaging. · Pubmed #16132430 No free full text.

Abstract: Chilaiditi syndrome is a condition in which the colon or small intestine is interposed temporarily or permanently between the liver and the diaphragm. Usually, it is an asymptomatic and incidental radiographic finding, but it may be a potential source of abdominal problems, ranging from intermittent mild abdominal pain to acute intestinal obstruction. We report multidetector computed tomographic findings of a case of Chilaiditi syndrome presenting as small bowel obstruction due to hepatodiaphragmatic interposition of the ileal loop, which was entrapped by adhesive bands caused by Fitz-Hugh-Curtis syndrome.

Yang BM, Kim CH, Kim JY. · School of Public Health, Seoul National University, Seoul 110-799, South Korea. · J Clin Gastroenterol. · Pubmed #15602164 No free full text.

Abstract: GOALS: To estimate the direct medical costs of chronic hepatitis B (CHB) infection and its liver disease sequelae in South Korea. BACKGROUND: Korea is a hepatitis B-endemic area with 5.79% to 10.87% of males and 1.51% to 4.44% of females over 20 years of age carrying the virus. It is estimated that 25% of carriers will develop serious hepatitis B virus (HBV)-related complications. While vaccination programs have reduced the prevalence of hepatitis B in people younger than 20 years, significant CHB-related morbidity will continue to occur for the next 15 to 30 years until the benefits of the vaccination programs take effect. STUDY: Direct medical costs for six CHB-related disease states, including hepatocellular carcinoma and liver transplant, were estimated for the year 2001. METHODS: Four data sources were used to gather information: the National Health Insurance Corporation database, patients' medical charts, expert opinion, and patient survey data. RESULTS: In 2001, the total medical costs of six CHB-related diseases were 250 million Korean Won (KRW) (equivalent to U.S. 208.6 million dollars), based on an exchange rate of KRW 1200 = US 1 dollar. Annual treatment costs per patient ranged from KRW297,392 (US 248 dollars) for chronic hepatitis B to KRW 80.6 million (U.S. 67,156 dollars) for liver transplant. The cost of treatment rose continuously with liver disease progression. The main cost driver was inpatient hospitalizations (including surgical costs). CONCLUSION: CHB-related diseases are a significant cost burden to the South Korean healthcare system. In addition to the obvious clinical benefits, the prevention or delay of chronic hepatitis B liver disease progression in South Korea could result in substantial economic benefits to the whole society.

Brozovic S, Nagaishi T, Yoshida M, Betz S, Salas A, Chen D, Kaser A, Glickman J, Kuo T, Little A, Morrison J, Corazza N, Kim JY, Colgan SP, Young SG, Exley M, Blumberg RS. · Gastroenterology Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. · Nat Med. · Pubmed #15107843 No free full text.

Abstract: CD1d is a major histocompatibility complex (MHC) class I-related molecule that functions in glycolipid antigen presentation to distinct subsets of T cells that express natural killer receptors and an invariant T-cell receptor-alpha chain (invariant NKT cells). The acquisition of glycolipid antigens by CD1d occurs, in part, in endosomes through the function of resident lipid transfer proteins, namely saposins. Here we show that microsomal triglyceride transfer protein (MTP), a protein that resides in the endoplasmic reticulum of hepatocytes and intestinal epithelial cells (IECs) and is essential for lipidation of apolipoprotein B, associates with CD1d in hepatocytes. Hepatocytes from animals in which Mttp (the gene encoding MTP) has been conditionally deleted, and IECs in which Mttp gene products have been silenced, are unable to activate invariant NKT cells. Conditional deletion of the Mttp gene in hepatocytes is associated with a redistribution of CD1d expression, and Mttp-deleted mice are resistant to immunopathologies associated with invariant NKT cell-mediated hepatitis and colitis. These studies indicate that the CD1d-regulating function of MTP in the endoplasmic reticulum is complementary to that of the saposins in endosomes in vivo.

Kim LH, Shin HD, Park BL, Jung JH, Kim JY, Kim YJ, Lee HS. · Department of Genetic Epidemiology, SNP Genetics, Inc., 11th Floor, Maehun B/D, 13 Chongro 4 Ga, Chongro-Gu, Seoul, Korea. · Hum Mutat. · Pubmed #14961554 No free full text.

Abstract: Human nuclear factor of kappa light chain gene enhancer in B cells inhibitor, alpha (NFKBIA) inhibits the action of NF-kappaB by forming a heterodimer with NF-kappaB, and preventing its translocation to the nucleus. We have sequenced a human NFKBIA full gene including -1000bp promoter region to identify its gene polymorphisms as a potential candidate gene for host genetic study of Hepatocellular Carcinoma (HCC). Nine novel single nucleotide polymorphisms (SNPs) and one GAA deletion were identified; two in promoter region (c.-673A>T, c.-642C>T), two in exon 1 (c.78G>A (Leu26Leu), c.81C>T (Asp27Asp)), three in introns (c.284T>A, c.1952A>G and c.2444C>T) and three in 3'UTR (c.2710-2712delGAA, c.2758G>A and c.3053G>A). Among ten identified variants, six were selected for larger scale genotyping (n=1,750) for association study based on frequencies and location. Haplotypes, their frequencies and linkage disequilibrium coefficients (/D'/) between SNP pairs were estimated. Allele frequencies of each SNPs and haplotypes were compared between patients with HCC and patients without HCC among HbsAg positives by logistic regression. As a conclusion, we could not find any significant association of NFKBIA variants with development of HCC among chronic hepatitis B patients.

Kim YJ, Lee HS, Im JP, Min BH, Kim HD, Jeong JB, Yoon JH, Kim CY, Kim MS, Kim JY, Jung JH, Kim LH, Park BL, Shin HD. · Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Korea. · Exp Mol Med. · Pubmed #12858019 links to  free full text

Abstract: Transforming growth factor-beta1 (TGF-beta1) can act as both a tumor suppressor and a stimulator of tumor progression. We have examined the relationship between polymorphisms of the TGF-beta1 gene and the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B virus (HBV) infection. A total of 1,237 Korean subjects were prospectively enrolled; 1,046 patients with chronic HBV infection and 191 healthy controls with no evidence of recent or remote HBV infection. The patients were divided into two groups: those without (n = 809) and those with HCC (n = 237). Single nucleotide polymorphisms (SNPs) of TGF-beta1 were searched for and genotyped using the single base extension method. In Korean subjects, only two SNPs were found among the seven known polymorphisms of TGF-beta1, at position -509 and in codon 10. The risk of HCC was significantly lower in patients with the T/T or C/T genotypes than in those with the C/C genotypes at position -509 (P < 0.02), and also lower among those with the Pro/Pro or Leu/Pro genotypes than in those with the Leu/Leu genotypes in codon 10 (P < 0.007). Haplotype analysis revealed that the possession of [-509C > T; L10P] conferred a decreased likelihood of HCC (OR = 0.74; 95% CI, 0.59-0.93; P = 0.008). In conclusion, the presence of the TGF-beta1 -509C > T promoter or of the L10P polymorphism, and the combination of both [-509C > T; L10P] as a haplotype were strongly associated with a reduced risk of HCC in patients with chronic HBV infection.

Park BL, Lee HS, Kim YJ, Kim JY, Jung JH, Kim LH, Shin HD. · Department of Genetic Epidemiology SNP Genetics, Inc., 11th Floor, Maehun B/D 13 Chongro 4 ga, Chongro-gu, Seoul 110-834, Korea. · Exp Mol Med. · Pubmed #12754410 links to  free full text

Abstract: Interleukin 6 (IL6) plays an essential role in the regulation of immune response to chronic disease. In this study, the three known single nucleotide polymorphisms (SNPs) in the IL6 promoter region were genotyped in a large chronic hepatitis B cohort to evaluate the effects of IL6 promoter variants. The single base extension method was used for this genotyping. Haplotypes were constructed by the three SNPs in IL6. Allele frequencies were compared for; i) patients with chronic hepatitis (CH) and chronic carriers vs. chronic hepatis patients with clinical evidence of liver cirrhosis (LC) (i.e., portal hypertension), ii) cirrhotic patients with hepatocellular carcinoma (HCC) vs. without HCC by logistic regression, and iii) with respect to the time intervals from the onset of infection to HCC. Results were analyzed by Cox relative hazard analysis on the assumption that all the patients were infected during early infancy. The frequencies of each SNP were 0.002 (IL6-597 G>A), 0.25 (IL6-572 C>G) and 0.002 (IL6-174 G>C), respectively, in the Korean population (n = 1,046). No significant associations were detected between IL6-572 C>G and chronic hepatitis B outcome in this study; i.e., LC occurrence on CH (OR = 0.16-1.27, P = 0.13- 0.71) and HCC occurrence on LC (OR = 1.04-1.23, P = 0.89-0.60) of heterozygotes and homozygotes for G allele in referent comparison to homozygotes for common allele (C/C genotype), and time interval to HCC (RH = 0.67-1.00; P = 0.14-0.99). In conclusion, there appeared to be no significant associations between IL6 promoter variants and disease outcome in chronic hepatitis B.

Kim JY, Kim KM, Nan JX, Zhao YZ, Park PH, Lee SJ, Sohn DH. · College of Pharmacy, Wonkwang University, Iksan, Jeonbuk 570-749, South Korea. · Pharmacol Toxicol. · Pubmed #12753423 No free full text.

Abstract: Hepatic stellate cells play central roles in hepatic fibrosis. The therapeutic goal in hepatic fibrosis is to halt or reverse fibrosis. Apoptosis is suggested to eliminate activated hepatic stellate cells in fibrosis. Salvia miltiorrhiza is a traditional medicine used to improve blood circulation and treat chronic hepatitis and hepatic fibrosis. We investigated the effect of tanshinone I, an ingredient of Salvia miltiorrhiza, on the apoptotic death of rat hepatic stellate cells transformed by simian virus 40 (T-HSC/Cl-6), which retains the features of activated stellate cells. Treatment of T-HSC/Cl-6 cells with tanshinone I resulted in the induction of typical DNA fragmentation and DNA ladder formation in a concentration- and time-dependent manner. The induction of apoptosis was confirmed by flow cytometric analysis. Treatment of T-HSC/Cl-6 cells with tanshinone I caused activation of caspase-3 and subsequent proteolytic cleavage of poly(ADP-ribose) polymerase. Tanshinone I induced mitochondrial membrane dipolarization and the release of cytochrome c from mitochondria into the cytosol. In conclusion, our results demonstrate that tanshinone I induces apoptosis of T-HSC/Cl-6 cells and that tanshinone I-induced apoptosis involves caspase activation through cytochrome c release and loss of mitochondrial membrane potential.

Shin HD, Park BL, Kim LH, Jung JH, Kim JY, Yoon JH, Kim YJ, Lee HS. · Department of Genetic Epidemiology, SNP Genetics, Inc., 11th Floor, MaeHun B/D, 13 Chongro 4 Ga, Chongro-Gu, Seoul 110-834, Korea. · Hum Mol Genet. · Pubmed #12668613 links to  free full text

Abstract: Interleukin 10 (IL10) is a powerful Th-2 cell cytokine produced by lymphoid cells that exerts its functions by inhibiting macrophage/monocyte and T-cell lymphocyte replication and secretion of inflammatory cytokines (IL1, TNFA, TGFB, IL6, IL8 and IL12). Genetic association analysis of a well-characterized HBV cohort revealed that one of IL10 haplotypes, IL10-ht2, was strongly associated with hepatocellular carcinoma (HCC) occurrence in gene dose-dependent manner. The frequency of susceptible IL10-ht2 was much higher in HCC patients and significantly increased in order of susceptibility to HBV progression from chronic hepatitis to liver cirrhosis and HCC among hepatitis B patients. In addition, survival analysis clearly showed that the onset age of HCC was also accelerated among chronic hepatitis B patients who were carrying IL10-ht2. Increased IL10 production mediated by IL10-ht2 suggests that up-regulated IL10 accelerates progression of chronic HBV infection, especially to HCC development.

Shin HR, Kim JY, Kim JI, Lee DH, Yoo KY, Lee DS, Franceschi S. · Division of Cancer Control and Epidemiology, National Cancer Center Research Institute, 809 Madu-dong, Ilsan-Gu, Koyang, Kyonggi, 411-764 South Korea. · Br J Cancer. · Pubmed #12177801 links to  free full text

Abstract: A cross-sectional study evaluated the prevalence of and the risk factors for hepatitis C and B viruses among 700 adults above the age of 40 years in a rural area of South Korea. Seropositivity for hepatitis C virus antibody (11.0%, 95% confidence interval: 8.7-13.6) was higher than that for hepatitis B surface antigen (4.4%, 95% confidence interval: 3.0-6.2). Anti-hepatitis C virus seropositivity was associated with a history of repeated acupuncture (odds ratio=2.1, 95% confidence interval: 1.1-4.0), and blood transfusion (odds ratio=5.5, 95% confidence interval: 1.6-19.3) before 1992 when hepatitis C virus screening in blood donors became mandatory. Hepatitis C virus 2a was the most prevalent genotype, followed by 1b. Hepatitis C virus risk attributable to acupuncture was 38% (9% for men and 55% for women). Safer acupuncture practice has become a priority for hepatitis C virus prevention in South Korea.

Chun YK, Kim JY, Woo HJ, Oh SM, Kang I, Ha J, Kim SS. · Department of Molecular Biology, School of Medicine, Kyung Hee University, Seoul 130-701, Korea. · Hepatology. · Pubmed #11050069 No free full text.

Abstract: Hepatitis B virus (HBV) core promoter mutants have been proposed to contribute to severe liver damage by increasing viral loads, but this has not yet been clearly shown. To examine the effects of core promoter mutants on viral load and liver damage, we first developed a polymerase chain reaction (PCR)-based semiquantitative HBV DNA detection method with a high sensitivity (able to detect as low as 10(3) molecules/mL). Then we cloned 12 predominant core promoter mutants from 41 chronic hepatitis B patients. The in vitro promoter and replication activities of these mutants were similar to those of wild-type virus. However, viral load was highly variable, and this was dependent on individual patients rather than mutant type. In addition, there was no mutant type that showed any unique correlation with alanine transaminase (ALT) levels. Viral load was not significantly correlated with ALT level in both cross-sectional and longitudinal studies. Quantitation of HBV levels also revealed no clear correlation between hepatitis B e antigen (HBeAg) status and viral load. Taken together, these results indicated that the replication activity of core promoter mutants has little effect on viral load, and that viral load does not correlate with the severity of liver damage or with HBeAg status.

Cho JY, Yeon JD, Kim JY, Yoo ES, Yu YH, Park MH. · Department of Immunology, Windeyer Institute of Medical Sciences, University College London Medical School, United Kingdom. · Biol Pharm Bull. · Pubmed #11041260 No free full text.

Abstract: The hepatoprotecive effects of recombinant human epidermal growth factor (hEGF) on chemically and immunologically induced experimental liver injury models were examined. The hEGF clearly decreased serum transaminase levels in D-galactosamine (D-GalN) and D-GalN/lipopolysaccharide (LPS)-induced liver injury models under sub-lethal conditions. However, it has not significantly changed either serum or in vitro tumor necrosis factor (TNF)-alpha production or in vitro nitric oxide (NO) production, suggesting that the hepatoprotection by EGF is not mediated by inhibiting these pathological mediators produced in D-GalN and D-GalN/LPS-induced liver injury.