• Title/Summary/Keyword: Chronic viral hepatitis

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A Case of Adverse effects during Interferon plus Ribavirin Treatments for Chronic Hepatitis C (Interferon과 Ribavirin 병용요법 시행중인 만성 C형간염 환자에서 발생한 부작용에 대한 침구치료 증례)

  • Kim, Sung-hwan;Hong, Sang-hoon;Park, Dong-il
    • Journal of Acupuncture Research
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    • v.20 no.1
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    • pp.244-253
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    • 2003
  • Objective : Interferon-alpha and Rivabirin are much used at the same time to treat Chronical C viral hepatitis. But interferon caused lots of unexpected side effects, Acupuncture Treatment for them will be an alternative plan. Methods : We first posed questions to a 4 year-old man who ha skin flare, fatigue, itching, insomnia, pronounced a diagnosis based on overall of symptoms and signs and then treated Acupuncture, Moxibustion and Electroacupuncture. We acupunctured a BL17, BL18, BL20 and removed it at once. We electroacupunctured at GV20, Yin tang(Ex-HN3) form 20 minutes, acupunctured at Bi yi(鼻翼, Extra-point), S36, P6. Pizhengge(脾定格) was acupunctured for 10 minutes. Results : The symptoms of fatigue, insomnia, itching are reduced after acupuncture treatments and they made a person keep interferon treatment on. Conclusions : We confirmed that acupuncture treatments make a patient of chronic C viral hepatitis reduce and improve side effects of interferon treatment. We should keep on studying the various and efficient method of acupuncture treatment to improve living quality and treatment efficiency of patients.

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Host Innate Immunity against Hepatitis E Virus and Viral Evasion Mechanisms

  • Kang, Sangmin;Myoung, Jinjong
    • Journal of Microbiology and Biotechnology
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    • v.27 no.10
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    • pp.1727-1735
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    • 2017
  • Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences, such as chronic hepatitis and liver damage, mortality of the latter of which reaches up to 20-30%. Type I interferon (IFN)-induced antiviral immunity is known to be the first-line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors, leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of IFN-stimulated genes, helping the cells cope with viral infection. Interestingly, some of the HEV-encoded genes seem to be involved in disrupting signaling cascades for antiviral immune responses, and thus crippling cytokine/chemokine production. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge, and in this review, we summarize known HEV evasion strategies and compare them with those of other hepatitis viruses.

A Clinical study of HBsAg and Anti-HBs in the serum of patients with various liver diseases (각종(各種) 간질환(肝疾患)에 있어서 혈청(血淸) HBsAg 및 Anti-HBs에 관한 임상적(臨床的) 고찰(考察))

  • Kim, Hak-San;Kim, Jong-Mann;Kim, Hwa-Sook;Kim, Yul-Ja;Lee, Hak-Choong;Lee, Chong-Suk
    • The Korean Journal of Nuclear Medicine
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    • v.15 no.2
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    • pp.59-66
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    • 1981
  • Serum HBsAg and Anti-HBs obtained by radioimmunoassay were studied in 109 cases of various liver diseases who visited or were admitted to National Medical Center from December, 1980 to July, 1981. The results were as follows; 1) HBsAg was detected in 67.0% of total 109 cases; 71.9% of 32 cases with acute viral hepatitis, 71.4% of 14 cases with chronic hepatitis, 65.2% of 46 cases with liver cirrhosis and 58.8% of 17 cases with hepatoma. 2) Anti-HBs was detected in 32.1% of total 109 cases; 37.0% of 46 cases with liver cirrhosis, 29.4% of 17 cases with hepatoma, 28.6% of 14 cases with chronic hepatitis, 28.1% of 32 cases with acute viral hepatitis. 3) HBsAg or Anti-HBs, the markers of Hepatitis B virus was detected in 89.0% of total 109 cases; 93.6% of 32 cases with acute viral hepatitis, 89.1% of 46 cases with liver cirrhosis, 85.7% of 14 cases with chronic hepatitis and 82.4% of 17 cases with hepatoma, which strongly suggested that the various liver diseases were associated with hepatitis B virus infection.

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Effect of Korean Red Ginseng in chronic liver disease

  • Park, Tae Young;Hong, Meegun;Sung, Hotaik;Kim, Sangyeol;Suk, Ki Tae
    • Journal of Ginseng Research
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    • v.41 no.4
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    • pp.450-455
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    • 2017
  • Chronic liver disease, one of the most common diseases, typically arises from nonalcoholic fatty liver disease, alcoholic liver disease, chronic viral hepatitis, or hepatocellular carcinoma. Therefore, there is a pressing need for improved treatment strategies. Korean Red Ginseng has been known to have positive effects on liver disease and liver function. In this paper, we summarize the current knowledge on the beneficial effects of Korean Red Ginseng on chronic liver disease, a condition encompassing nonalcoholic fatty liver disease, alcoholic liver disease, chronic viral hepatitis, and hepatocellular carcinoma, as supported by experimental evaluation and clinical investigation.

Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases

  • Khlaiphuengsin, Apichaya;Kiatbumrung, Rattanaporn;Payungporn, Sunchai;Pinjaroen, Nutcha;Tangkijvanich, Pisit
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.18
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    • pp.8377-8382
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    • 2016
  • Background: The aim of this study was to evaluate any association between a single nucleotide polymorphism (SNP) in the patatin-like phospholipase domain containing 3 (PNPLA3) (rs738409, C>G) and the development and prognosis in patients with hepatocellular carcinoma (HCC). Materials and Methods: Two hundred heathy controls and 388 HCC cases were included: 211 with HBV, 98 patients with HCV, 29 with alcoholic steatohepatitis (ASH) and 52 with non-alcoholic steatohepatitis (NASH). The SNP was determined by real-time PCR based on TaqMan assays. Results: The prevalence of rs738409 genotypes CC, CG and GG in controls was 91 (45.5%), 88 (44.0%), and 21 (10.5%), respectively, while the corresponding genotypes in all patients with HCC was 158 (40.7%), 178 (45.9%), and 52 (13.4%). The GG genotype had significantly higher distribution in patients with ASH/NASH-related HCC compared with controls (OR=2.34, 95% CI=1.16-4.71, P=0.018), and viral-related HCC cases (OR=2.15, 95% CI=1.13-4.08, P=0.020). However, the frequency of the GG genotype was similar between controls and patients with viral-related HCC. At initial diagnosis, HBV-related HCC were larger and at more advanced BCLC stage than the other HCC groups. There were no significant differences between the GG and non-GG groups regarding clinical characteristics, tumor stage and overall survival. Conclusions: These data suggest an influence of the PNPLA3 polymorphism on the occurrence of HCC in patients with ASH/NASH but not among those with chronic viral hepatitis. However, the polymorphism was not associated with the prognosis of HCC.

The rapid recovery of serum aminotransferase in a case of chronic active hepatitis type B treated with Sengangeonbi-tang (만성 활동성 B형 간염에서 생간건비탕(生肝健脾湯)으로 혈청 aminotransferase 수치가 저하된 1례)

  • Park, Jung-Mi;Jung, Woo-Sang
    • The Journal of Internal Korean Medicine
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    • v.21 no.2
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    • pp.337-339
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    • 2000
  • Indigestion is one of the most frequent symptom in chronic hepatitis. We treated a 20 year-old female patient of chronic active hepatitis type B with Sengangeonbi-tang. The patient complained indigestion and constipation. The serum aminotransferase were higher and viral marker showed hepatitis was in active phase. 1 week later, the symptom had been changed from severe to mild and aminotransferase decreased. We continued to prescribe the medicine 2 weeks more and could observe that the symptom disappeared and the aminotransferase fell down under normal value with no side effect. Sengangeonbi-tang showed desirable effect on indigestion and more rapid recovery of aminotransferase than previous reports about treating hepatitis.

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Hepatitis C Virus Nonstructural Protein 5A Interacts with Immunomodulatory Kinase IKKε to Negatively Regulate Innate Antiviral Immunity

  • Kang, Sang-Min;Park, Ji-Young;Han, Hee-Jeong;Song, Byeong-Min;Tark, Dongseob;Choi, Byeong-Sun;Hwang, Soon B.
    • Molecules and Cells
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    • v.45 no.10
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    • pp.702-717
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    • 2022
  • Hepatitis C virus (HCV) infection can lead to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. HCV employs diverse strategies to evade host antiviral innate immune responses to mediate a persistent infection. In the present study, we show that nonstructural protein 5A (NS5A) interacts with an NF-κB inhibitor immunomodulatory kinase, IKKε, and subsequently downregulates beta interferon (IFN-β) promoter activity. We further demonstrate that NS5A inhibits DDX3-mediated IKKε and interferon regulatory factor 3 (IRF3) phosphorylation. We also note that hyperphosphorylation of NS5A mediates protein interplay between NS5A and IKKε, thereby contributing to NS5A mediated modulation of IFN-β signaling. Lastly, NS5A inhibits IKKε-dependent p65 phosphorylation and NF-κB activation. Based on these findings, we propose NS5A as a novel regulator of IFN signaling events, specifically by inhibiting IKKε downstream signaling cascades through its interaction with IKKε. Taken together, these data suggest an additional mechanistic means by which HCV modulates host antiviral innate immune responses to promote persistent viral infection.

Hepatitis C Viral Infection in Children: Updated Review

  • El-Guindi, Mohamed A.
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.19 no.2
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    • pp.83-95
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    • 2016
  • Hepatitis C virus (HCV) infection is a major medical challenge affecting around 200 million people worldwide. The main site of HCV replication is the hepatocytes of the liver. HCV is a positive enveloped RNA virus from the flaviviridae family. Six major HCV genotypes are implicated in the human infection. In developed countries the children are infected mainly through vertical transmission during deliveries, while in developing countries it is still due to horizontal transmission from adults. Minimal nonspecific and brief symptoms are initially found in approximately 15% of children. Acute and chronic HCV infection is diagnosed through the recognition of HCV RNA. The main objective for treatment of chronic HCV is to convert detected HCV viremia to below the detection limit. Children with chronic HCV infection are usually asymptomatic and rarely develop severe liver damage. Therefore, the benefits from current therapies, pegylated-Interferon plus ribavirin, must be weighed against their adverse effects. This combined treatment offers a 50-90% chance of clearing HCV infection according to several studies and on different HCV genotype. Recent direct acting antiviral (DAA) drugs which are well established for adults have not yet been approved for children and young adults below 18 years. The most important field for the prevention of HCV infection in children would be the prevention of perinatal and parenteral transmission. There are areas of focus for new lines of research in pediatric HCV-related disease that can be addressed in the near future.

A Case of Interstitial Pneumonitis and Pancytopenia Following the Combination Therapy of Pegylated Interferon and Ribavirin (페그-인터페론과 리바비린 병합치료 중 발생한 간질성 폐렴 및 범혈구 감소증 1예)

  • Suh, Ji-Hyun;Hahn, Sung-Hwahn;Lee, Ji-Eun;Han, Jin-Hyung;Kim, Kyung-Mook;Kim, Doh-Hyung;Kim, Yon-Seop;Park, Jae-Suk;Jee, Young-Koo
    • Tuberculosis and Respiratory Diseases
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    • v.70 no.1
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    • pp.69-73
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    • 2011
  • The combination therapy of pegylated interferon and ribavirin is the mainstay of treatment for chronic hepatitis C patients. Anti-viral therapy is commonly associated with side effects such as headache, fever, myalgia, and arthralgia. However, anti-viral therapy can continue because these side effects are mostly mild and can be improved with supportive management. Anti-viral therapy should be stopped promptly if serious side effects, such as interstitial pneumonitis or hemolytic anemia occur, although those serious side effects are rare. There were a few case reports of interferon-related interstitial pneumonitis worldwide. In Korea, one atypical case report of interstitial pneumonitis has been reported, which followed the combination therapy of interferon-alpha and ribavirin in a patient with chronic hepatitis C. We present a case of interstitial pneumonitis and pancytopenia following the combination therapy of pegylated interferon and ribavirin in a patient with chronic hepatitis C.

Hepatitis C Virus Nonstructural 5A Protein Interacts with Telomere Length Regulation Protein: Implications for Telomere Shortening in Patients Infected with HCV

  • Lim, Yun-Sook;Nguyen, Men T.N.;Pham, Thuy X.;Huynh, Trang T.X.;Park, Eun-Mee;Choi, Dong Hwa;Kang, Sang Min;Tark, Dongseob;Hwang, Soon B.
    • Molecules and Cells
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    • v.45 no.3
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    • pp.148-157
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    • 2022
  • Hepatitis C virus (HCV) is a major cause of chronic liver disease and is highly dependent on cellular proteins for viral propagation. Using protein microarray analysis, we identified 90 cellular proteins as HCV nonstructural 5A (NS5A) interacting partners, and selected telomere length regulation protein (TEN1) for further study. TEN1 forms a heterotrimeric complex with CTC and STN1, which is essential for telomere protection and maintenance. Telomere length decreases in patients with active HCV, chronic liver disease, and hepatocellular carcinoma. However, the molecular mechanism of telomere length shortening in HCV-associated disease is largely unknown. In the present study, protein interactions between NS5A and TEN1 were confirmed by immunoprecipitation assays. Silencing of TEN1 reduced both viral RNA and protein expression levels of HCV, while ectopic expression of the siRNA-resistant TEN1 recovered the viral protein level, suggesting that TEN1 was specifically required for HCV propagation. Importantly, we found that TEN1 is re-localized from the nucleus to the cytoplasm in HCV-infected cells. These data suggest that HCV exploits TEN1 to promote viral propagation and that telomere protection is compromised in HCV-infected cells. Overall, our findings provide mechanistic insight into the telomere shortening in HCV-infected cells.