著者
Keiji Yokoyama Naoaki Tsuchiya Ryo Yamauchi Takashi Miyayama Yotaro Uchida Kumiko Shibata Hiromi Fukuda Kaoru Umeda Kazuhide Takata Takashi Tanaka Shinjiro Inomata Daisuke Morihara Yasuaki Takeyama Satoshi Shakado Shotaro Sakisaka Fumihito Hirai
出版者
The Japanese Society of Internal Medicine
雑誌
Internal Medicine (ISSN:09182918)
巻号頁・発行日
vol.59, no.17, pp.2089-2094, 2020-09-01 (Released:2020-09-01)
参考文献数
37
被引用文献数
7

Objective The relationship between gut microbiota and portal hypertension remains unclear. We investigated the characteristics of the gut microbiota in portal hypertension patients with esophago-gastric varices and liver cirrhosis. Methods Thirty-six patients (12 patients with portal hypertension, 12 healthy controls, and 12 non-cirrhosis patients) were enrolled in this university hospital study. Intestinal bacteria and statistical analyses were performed up to the genus level using the terminal restriction fragment length polymorphism method targeting 16S ribosomal RNA genes, with diversified regions characterizing each bacterium. Results Levels of Lactobacillales were significantly higher (p=0.045) and those of Clostridium cluster IV significantly lower (p=0.014) in patients with portal hypertension than in other patients. This Clostridium cluster contains many butanoic acid-producing strains, including Ruminococcace and Faecalibacterium prausnitzii. Clostridium cluster IX levels were also significantly lower (p=0.045) in portal hypertension patients than in other patients. There are many strains of Clostridium that produce propionic acid, and the effects on the host and the function of these bacterial species in the human intestine remain unknown. Regarding the Bifidobacterium genus, which is supposed to decrease as a result of cirrhosis, no significant decrease was observed in this study. Conclusion In the present study, we provided information on the characteristics of the gut microbiota of portal hypertension patients with esophago-gastric varices due to liver cirrhosis. In the future, we aim to develop probiotic treatments following further analyses that include the species level, such as the intestinal flora analysis method and next-generation sequencers.
著者
Akira Sato Michio Sata Kenji Ikeda Takashi Kumada Namiki Izumi Yasuhiro Asahina Yukio Osaki Kazuaki Chayama Shuichi Kaneko Akito Sakai Morikazu Onji Yoichi Hiasa Takumi Omura Itaru Ozeki Osamu Yokosuka Shuichiro Shiina Mariko Itsubo Shuhei Nishiguchi Katsuharu Hirano Tatsuya Ide Shotaro Sakisaka Takahiro Yamasaki Isao Hidaka Masatoshi Tanaka Soo Ryang Kim Takafumi Ichida
出版者
一般社団法人 日本内科学会
雑誌
Internal Medicine (ISSN:09182918)
巻号頁・発行日
vol.52, no.24, pp.2701-2706, 2013 (Released:2013-12-15)
参考文献数
32
被引用文献数
4 14

Objective We attempted to elucidate the clinical features of chronic hepatitis C patients who develop hepatocellular carcinoma (HCC) after achieving a sustained viral response (SVR) to interferon (IFN) therapy. Methods The clinical features of 130 patients at 19 hospitals who developed HCC after obtaining an SVR were retrospectively reviewed. Results Overall, 107 (82%) of the 130 patients were men, with 92 (71%) being ≥60 years of age and 76, 38 and 16 developing HCC within 5, 5-10 and 10-16.9 years after IFN therapy, respectively. Before receiving IFN therapy, 92 (71%) patients had cirrhosis and/or a low platelet count (<15×104 cells/μL). Lower albumin (<3.9 g/dL) and higher alpha fetoprotein (AFP) (≥10 ng/mL) levels were identified in a multivariate analysis to be independent variables of the development of HCC within five years after IFN therapy. Among 4,542 SVR patients, HCC occurred in 109 (2.4%) during a 5.5-year follow-up period, thus resulting in an occurrence rate of 4.6% for men and 0.6% for women. Conclusion SVR patients with lower albumin or higher AFP levels require careful assessments to prevent early HCC development after IFN therapy. HCC occurrence within >10 years of IFN therapy is not uncommon, and the risk factors remain uncertain, thus suggesting that all SVR patients should undergo long-term follow-up examinations for HCC development.