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Review Emerging need for vaccination against hepatitis A virus in patients with chronic liver disease in Korea. free! 2007
Song HJ, Kim TH, Song JH, Oh HJ, Ryu KH, Yeom HJ, Kim SE, Jung HK, Shim KN, Jung SA, Yoo K, Moon IH, Chung KW. · Department of Internal Medicine, Ewha Medical Research Institute, Ewha Womans University College of Medicine, Seoul, Korea. · J Korean Med Sci. · Pubmed #17449927 links to free full text
Abstract: Vaccination against hepatitis A virus (HAV) is recommended for patients with chronic liver disease (CLD), but this has been deemed unnecessary in Korea since the immunity against HAV was almost universal in adults. However, this practice has never been reevaluated with respect to the changing incidence of adult acute hepatitis A. We retrospectively reviewed the medical records of 278 patients with acute hepatitis A diagnosed from January 1995 to November 2005 and prospectively tested 419 consecutive CLD patients from July to December 2005 for the presence of IgG anti-HAV. The number of patients with acute hepatitis A has markedly increased recently, and the proportion of adult patients older than 30 yr has been growing from 15.2% during 1995-1999, to 28.4% during 2000-2005 (p=0.019). Among 419 CLD patients, the seroprevalences of IgG anti-HAV were 23.1% for those between 26 and 30 yr, 64% between 31 and 35 yr, and 85.0% between 36 and 40 yr. These data demonstrate that immunity against HAV is no more universal in adult and substantial proportion of adult CLD patients are now at risk of HAV infection in Korea. Therefore, further study on seeking proper strategy of active immunization against HAV is warranted in these populations.
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Clinical Conference Individualization of interferon therapy using serum hepatitis B virus DNA to reduce viral relapse in patients with chronic hepatitis B: a randomized controlled trial. 2003
Chung YH, Song BC, Lee GC, Shin JW, Ryu SH, Jung SA, Yoo K, Lee HC, Lee YS, Suh DJ. · Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Centre, Seoul, Korea. · Eur J Gastroenterol Hepatol. · Pubmed #12702905 No free full text.
Abstract: OBJECTIVE: In patients with chronic hepatitis B, viral relapse following interferon (IFN) therapy may be the result of a treatment duration that is too short to prevent hepatitis B virus (HBV) from replicating later. To reduce viral relapse in patients with chronic hepatitis B who responded to IFN, we individualized the duration of therapy according to serum HBV-DNA levels. METHOD: Treatment duration was prolonged to maintain negative serum HBV-DNA levels for the next 6 months in 30 patients who became HBV-DNA-negative following IFN therapy (group A). Another 35 patients were treated for only 6 months (group B). All patients had HBV-DNA as well as hepatitis B surface antigen (HBsAg) in their sera for more than 6 months and were proven histologically to have chronic hepatitis. Interferon alfa (IFN-alpha) was administered subcutaneously at a dose of 5 MU/m2 three times a week. RESULTS: There were no differences in age, gender, hepatitis B e antigen (HBeAg) positivity, serum alanine aminotransferase (ALT) levels, or serum HBV-DNA levels between the two groups. The mean duration of IFN therapy in group A was 7.2 months. At the end of treatment, serum HBV-DNA was negative in 16 patients in group A and in 18 patients in group B. The loss of serum HBV-DNA was maintained to the end of follow-up in 13 patients in group A but in only eight patients in group B. Similarly, serum ALT levels were normal in 14 patients in group A but in only nine patients in group B at the end of follow-up. CONCLUSION: Individualization of the duration of treatment to maintain serum HBV-DNA negativity for at least 6 months may reduce the viral relapse rate following IFN therapy.
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Article Plasma isocitrate dehydrogenase as a marker of centrilobular hepatic necrosis in patients with hyperthyroidism. 2001
Chung YH, Jung SA, Song BC, Chang WY, Kim JA, Song IH, Kim JW, Choi WB, Shong YK, Lee YS, Suh DJ. · Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea. · J Clin Gastroenterol. · Pubmed #11468437 No free full text.
Abstract: Isocitrate dehydrogenase (ICDH) may be useful for differentiating centrilobular from periportal necrosis in rats with liver injury. In this study, we assessed the usefulness of ICDH as a marker of centrilobular necrosis in patients with hyperthyroidism. Isocitrate dehydrogenase and alanine aminotransferase (ALT) activities were measured in the plasma of 56 patients with hyperthyroidism, 16 patients with chronic viral hepatitis (CVH), and 17 controls. Isocitrate dehydrogenase levels were higher in patients with hyperthyroidism than in those with CVH or in the controls (p < 0.01 and p < 0.001, respectively), even though ALT levels were higher in patients with CVH than in patients with hyperthyroidism (p < 0.01). Isocitrate dehydrogenase/ALT ratios were also higher in patients with hyperthyroidism than in those with CVH (p < 0.0001). Isocitrate dehydrogenase correlated to ALT levels in patients with hyperthyroidism or CVH (p < 0.05). In a patient with hyperthyroidism, ICDH levels decreased progressively to normal, and the ALT level and thyroid function were normalized. Thus, the plasma ICDH or ICDH/ALT ratio might be useful for differentiating centrilobular from periportal necrosis and for monitoring the degree of hepatic necrosis in patients with hyperthyroidism.
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Article Experimental model of hepatic fibrosis following repeated periportal necrosis induced by allylalcohol. 2000
Jung SA, Chung YH, Park NH, Lee SS, Kim JA, Yang SH, Song IH, Lee YS, Suh DJ, Moon IH. · Dept. of Internal Medicine, Asan Medical Center, Ewha Womans University College of Medicine, Seoul, Korea. · Scand J Gastroenterol. · Pubmed #11063159 No free full text.
Abstract: BACKGROUND/AIMS: In most patients with chronic viral hepatitis the predominant lobular location of hepatic necrosis and fibrosis is the periportal zone. We established a new simple model of hepatic fibrosis in rats by repetitive periportal necrosis with allylalcohol. METHODS: Of 40 male adult rats, 30 were injected with 0.62 mmol/kg of allylalcohol intraperitoneally twice a week, the remaining 10 with normal saline as controls. Ten rats were killed at each of 4, 8, and 16 weeks later. The extent of fibrosis was evaluated according to the portal-portal extent. Transforming growth factor (TGF) beta1 mRNA in liver tissues was detected by reverse transcriptase polymerase chain reaction, and its levels were determined by the endpoint titers of serial two-fold dilutions of cDNA. RESULTS: After 4 weeks, periportal fibrosis was produced in only 6 out of 10 rats, and was mild in extent. However, after 8 weeks, 8 out of 9 survivors showed moderate to severe fibrosis, which corresponded to a score of 7 or more. The extent of fibrosis correlated significantly with the amount of collagen and TGFbeta1 mRNA expression in liver tissues. The collagen content and expression of TGFbeta1 mRNA were also upregulated significantly in liver tissues with a fibrosis score of 7 or more. CONCLUSIONS: Hepatic fibrosis can be sufficiently induced by repetitive intraperitoneal injection of 0.62 mmol/kg of allylalcohol twice a week for 8 weeks. This simple model of hepatic fibrosis, in which TGFbeta1 is overexpressed at the transcriptional level, may be useful in the study of patients who have predominantly periportal necrosis and fibrosis.
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