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Miwa Kawanaka,
Takahito Oka,
Noriyo Urata,
Tomonari Kimura,
Jun Nakamura,
Daisuke Goto,
Ryumei Yamato,
Ken Nishino, Mitsuhiko Suehiro,
Hirofumi Kawamoto,
Gotaro Yamada
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ABSTRACT: The present study investigated the clinical characteristics of non-alcoholic steatohepatitis (NASH) patients who progressed from stage 3, zone 3 bridging fibrosis (F3 stage NASH) to cirrhosis. Of 95 NASH patients with repeated liver biopsies during a period of 4.6 years, 6 patients progressed to cirrhosis. The initial liver biopsies of these 6 patients were diagnosed as F3 stage NASH. Simple clinical variables and non-invasive biological tests were evaluated in 33 cases of F3 stage NASH. Increases in body mass index and fluctuations in transaminase levels, as well as the evaluation of homeostatic model assessment-insulin resistance, ferritin, and hyaluronic acid in F3 stage NASH patients may prove useful in identifying individuals at risk of progression to cirrhosis.
Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 01/2012; 109(12):2042-2048.
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ABSTRACT: The natural history of alcoholic cirrhosis, especially in Asian countries, has not been completely understood thus far.
We retrospectively compared the outcomes of compensated cirrhosis between Japanese alcoholic and hepatitis C virus (HCV)-infected patients.
A total of 227 patients (75 alcoholic and 152 HCV-infected patients) with compensated cirrhosis were enrolled. The median follow-up period was 4.9 years. The cumulative rates of hepatocellular carcinoma (HCC) development were significantly lower in the alcoholic patients than in the HCV-infected patients (6.8% vs 50.3% at 10 years, P = 0.0003), while the cumulative rates of hepatic decompensation (37.4% vs 51.7% at 10 years) and survival (53.8% vs 47.4% at 10 years) did not significantly differ between the two groups (Kaplan-Meir analysis). The main causes of death were hepatic failure and non-hepatic diseases in the alcoholic patients and HCC and hepatic failure in the HCV-infected patients. Multivariate analyses using the Cox proportional hazard model revealed that the risk of HCC was lower in alcoholic cirrhosis than in HCV-related cirrhosis (hazard ratio (HR), 0.46), while the risk of hepatic decompensation and mortality was the same. Predictors of decreased survival were non-abstinence (HR, 2.53) in the alcoholic patients and low serum albumin level (1.58) in the HCV-infected patients.
Survival of patients with alcoholic cirrhosis was similar to that of patients with HCV-related cirrhosis. The risk of HCC development was lower in alcoholic cirrhosis than in HCV-related cirrhosis. Abstinence from alcohol was important for improving the survival of patients with alcoholic cirrhosis.
Journal of Gastroenterology and Hepatology 05/2009; 24(7):1276-83. · 2.87 Impact Factor
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ABSTRACT: Although both primary biliary cirrhosis (PBC) and idiopathic thrombocytopenic purpura (ITP) are autoimmune diseases, the association of the 2 diseases is rare. Here, we report a case of ITP that developed during the follow-up of PBC in a 74-year-old man. The patient had been diagnosed with PBC 12 years previously, and had received treatment with ursodeoxycholic acid. The platelet count decreased from approximately 60 x 10(9)/L to 8 x 10(9)/L, and the association of decompensated liver cirrhosis (PBC) with ITP was diagnosed. Steroid and immune gamma globulin therapy were successful in increasing the platelet count. Interestingly, human leukocyte antigen genotyping detected the alleles DQB1*0601 and DRB1*0803, which are related to both PBC and ITP in Japanese patients. This case suggests common immunogenetic factors might be involved in the development of PBC and ITP.
World Journal of Gastroenterology 05/2008; 14(15):2451-3. · 2.47 Impact Factor
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ABSTRACT: Hepatitis B virus (HBV) is an important factor in the development of hepatocellular carcinoma (HCC). We studied the influence of HBV viral load on HCC occurrence in HBV related liver cirrhosis (LC).
Ninety-one LC patients were followed up over a period of 7 years. Twenty three patients received Interferon (IFN) therapy.
In 7 years, 23 patients developed HCC. Of them twenty-two (95.6%) were of genotype C. HBV DNA was found to be the only significant variable associated with HCC occurrence on both univariate (P = 0.029) and multivariate analysis (odds ratio 2.33; P < 0.033). The cumulative survival at 5 years was 83% and the annual rate of hepatitis B surface antigen clearance was 0.9 %. All of 17 HCC patients observed over a period of 5 years or more belonged to the continuously high HBV DNA group (annual average >3.7 log copies/ml) and all but one belonged to the continuously high alanine aminotransferase group (annual average >40 IU/l).
Patients with genotype C and a continuously high HBV DNA for 5 years or more are at a high-risk group for HCC development. Maintaining continuously low HBV DNA for 3 years or more with anti-viral therapy, may be useful in preventing or delaying HCC occurrence.
Liver international: official journal of the International Association for the Study of the Liver 04/2005; 25(2):220-5. · 3.82 Impact Factor
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Miwa Kawanaka,
Sabina Mahmood,
Gouichi Niiyama,
Akiyoshi Izumi,
Ayumi Kamei,
Hideji Ikeda, Mitsuhiko Suehiro,
Kazumi Togawa,
Takayo Sasagawa,
Misako Okita,
Hajime Nakamura,
Junji Yodoi,
Gotaro Yamada
Hepatology Research 06/2004; 29(1):39-41. · 2.20 Impact Factor
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Sabina Mahmood,
Miwa Kawanaka,
Ayumi Kamei,
Akiyoshi Izumi,
Keiichi Nakata,
Gouichi Niiyama,
Hideji Ikeda,
Shinichi Hanano, Mitsuhiko Suehiro,
Kazumi Togawa,
Gotaro Yamada
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ABSTRACT: Oxidative stress (OS) plays a major role in chronic hepatitis C. Various OS markers have been found to be elevated in hepatitis C virus (HCV)-related liver disease. This study detected the presence of OS in serum and liver biopsy specimens of HCV patients. Reactive oxygen molecules (ROM) in sera of 54 HCV patients were compared with 23 controls. OS markers 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxy-2-nonenal, malondialdehyde, and thioredoxin were measured in liver biopsy specimens of 18 HCV patients with fibrosis staging F1 (six); F2 (two), F3 (four), and F4 (six). The interferon (IFN) response and hepatocellular carcinoma (HCC) occurrence in the presence of OS markers were also evaluated. The level of ROM in HCV patients was 318 +/- 56.7 Carr compared with 248 +/- 40.8 Carr in controls (p=0.032). Multivariate analysis found age (p=0.0236) to be the only independent variable associated with increase in ROM in sera. In liver biopsy specimens, OS markers were found mainly around the area of piecemeal necrosis or the periportal area. The presence of OS markers seemed to increase with fibrosis staging, although not significantly. The OS DNA damage marker 8-OHdG was detected in the nucleus of hepatocytes. Thirteen patients received IFN therapy. During the 4-year follow-up period, HCC developed in four nonresponders to IFN and in one untreated patient. OS markers were stained in both HCC cells and non-HCC cells in HCC patients. OS markers were found in serum and liver specimens of HCV-associated liver disease and in HCC tissue. Detection of OS markers may be important for monitoring disease progression in HCV patients. Antioxidant therapy in combination with antiviral therapy may minimize liver damage and aid in the prevention and subsequent development of HCC.
Antioxidants and Redox Signaling 03/2004; 6(1):19-24. · 8.46 Impact Factor
