研究者詳細 - 寺井　崇二

論文 - 寺井　崇二

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アテゾリズマブ+ベバシズマブ併用療法の非奏効例におけるLate line移行時期についての検討

横尾健, 酒井規裕, 渡邉雄介, 荒生祥尚, 木村成宏, 阿部寛幸, 薛徹, 上村博輝, 坂牧僚, 上村顕也, 土屋淳紀, 寺井崇二

肝臓 63 ( Suppl.2 ) A582 - A582 2022年9月

慢性肝疾患におけるTGFβ3の発現と肝予備能との関連性についての検討

阿部寛幸, 酒井規裕, 渡邉雄介, 荒生祥尚, 木村成宏, 上村博輝, 坂牧僚, 横尾健, 上村顕也, 土屋淳紀, 寺井崇二

肝臓 63 ( Suppl.2 ) A597 - A597 2022年9月

大腸菌の外膜小胞は肝硬変での更なる炎症・線維化増悪に寄与する

夏井一輝, 土屋淳紀, 寺井崇二

肝臓 63 ( Suppl.2 ) A593 - A593 2022年9月

ウイルス駆除時代における,院内非専門医での効果的なC型肝炎患者の拾い上げ

荒生祥尚, 酒井規裕, 寺井崇二

肝臓 63 ( Suppl.2 ) A557 - A557 2022年9月

アテゾリズマブ+ベバシズマブ併用療法の非奏効例におけるLate line移行時期についての検討

横尾健, 酒井規裕, 渡邉雄介, 荒生祥尚, 木村成宏, 阿部寛幸, 薛徹, 上村博輝, 坂牧僚, 上村顕也, 土屋淳紀, 寺井崇二

肝臓 63 ( Suppl.2 ) A582 - A582 2022年9月

慢性肝疾患におけるTGFβ3の発現と肝予備能との関連性についての検討

阿部寛幸, 酒井規裕, 渡邉雄介, 荒生祥尚, 木村成宏, 上村博輝, 坂牧僚, 横尾健, 上村顕也, 土屋淳紀, 寺井崇二

肝臓 63 ( Suppl.2 ) A597 - A597 2022年9月

Synthesized HMGB1 peptide prevents the progression of inflammation, steatosis, fibrosis, and tumor occurrence in a non-alcoholic steatohepatitis mouse model. 国際誌

Yui Ishii, Atsunori Tsuchiya, Kazuki Natsui, Youhei Koseki, Nobutaka Takeda, Kei Tomiyoshi, Fusako Yamazaki, Yuki Yoshida, Takashi Shimbo, Katsuto Tamai, Shuji Terai

Hepatology research : the official journal of the Japan Society of Hepatology 2022年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

AIM: Non-alcoholic steatohepatitis (NASH) with fibrosis eventually leads to cirrhosis and hepatocellular carcinoma. Thus, the development of therapies other than dietary restriction and exercise, particularly those that suppress steatosis and fibrosis of the liver and have a long-term beneficial effect, is necessary. We aimed to evaluate the therapeutic effects of the HMGB1 peptide synthesized from box A using the melanocortin-4 receptor-deficient (Mc4r-KO) NASH model mouse. METHODS: We performed short- and long-term administration of this peptide and evaluated the effects on steatosis, fibrosis, and carcinogenesis using Mc4r-KO mice. We also analyzed the direct effect of this peptide on macrophages and hepatic stellate cells in vitro and performed lipidomics and metabolomics techniques to evaluate the effect. RESULTS: Although this peptide did not show direct effects on macrophages and hepatic stellate cells in vitro, in the short-term administration model, we could confirm the reduction of liver damage, steatosis, and fibrosis progression. The results of lipidomics and metabolomics suggested that the peptide might ameliorate NASH by promoting lipolysis via the activation of fatty acid β-oxidation and improving insulin resistance. In the long-term administration model, this peptide prevented progression to cirrhosis but retained the steatosis state, that is, the peptide prevents the progression to "burnt-out NASH." This peptide inhibited carcinogenesis by about one-third. CONCLUSION: This HMGB1 peptide can reduce liver damage, improve fibrosis and steatosis, and inhibit carcinogenesis, suggesting that the peptide would be a new treatment candidate for NASH and can contribute to the long-term prognosis for patients with NASH.

DOI： 10.1111/hepr.13825

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Effects of a selective PPARα modulator, sodium-glucose cotransporter 2 inhibitor, and statin on the myocardial morphology of medaka nonalcoholic fatty liver disease model. 国際誌

Marina Ohkoshi-Yamada, Kenya Kamimura, Atsushi Kimura, Yuto Tanaka, Itsuo Nagayama, Shunta Yakubo, Hiroyuki Abe, Takeshi Yokoo, Akira Sakamaki, Hiroteru Kamimura, Shuji Terai

Biochemical and biophysical research communications 625 116 - 121 2022年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD) is associated with metabolic dysregulation and is linked with various cardiovascular complications, which often lead to poor prognostic outcomes. To develop a standard therapy for NAFLD and to urgently address its complications, the current study aimed to investigate the mechanisms of NAFLD-related heart disease and the therapeutic effects of drugs targeting various metabolic pathways. METHODS: To explore the mechanism of NAFLD-related heart disease, a medaka model of high-fat diet-induced NAFLD was utilized. The gross structural, histological, and inflammatory changes in the myocardium were evaluated in a time-dependent manner. In addition, the therapeutic effects of medicines used for NAFLD treatment including, selective peroxisome proliferator-activated receptor α modulator (SPPARMα, pemafibrate), sodium-glucose cotransporter 2 (SGLT2) inhibitor (tofogliflozin), and statin (pitavastatin), and their combinations on heart pathology were evaluated. To determine the mechanisms underlying the therapeutic effects, the expression of genes related to liver inflammation was assessed via whole transcriptome sequencing analysis. RESULTS: The fish with NAFLD-related heart injury presented with cardiomyocyte hypertrophy, which led to cardiac hypertrophy. This morphological change was caused by the infiltration of inflammatory cells, including macrophages and CD4- and CD8-positive lymphocytes, in the cardiac wall and the expression of transforming growth factor beta 1 in the cardiomyocytes. Further, the livers of the fish had upregulated expressions of senescence-associated secretory phenotype-related genes. Treatment with pemafibrate, tofogliflozin, and pitavastatin reduced these changes and, consequently, cardiomyopathy. CONCLUSION: Our results demonstrated that NAFLD-related heart disease was attributed to the senescence-associated secretory phenotype-induced inflammatory activity in the cardiac wall, which resulted in myocardial hypertrophy. Moreover, the effects of SPPARMα, SGLT2 inhibitor, and statin on NAFLD-related heart disease were evident in the medaka NAFLD model.

DOI： 10.1016/j.bbrc.2022.07.117

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機械学習を用いた慢性心不全に続発した肝臓への障害(Cardiac Hepatopathy)の画像解析

三井田秀, 上村博輝, 山崎文紗子, 渡邉雄介, 荒生祥尚, 木村成宏, 薛徹, 横尾健, 坂牧僚, 土屋淳紀, 藤木伸也, 猪又孝元, 寺井崇二

日本門脈圧亢進症学会雑誌 28 ( 3 ) 152 - 152 2022年8月

Cumulative risk of developing a new symptom in patients with primary biliary cholangitis and its impact on prognosis. 国際誌

Naruhiro Kimura, Toru Setsu, Yoshihisa Arao, Norihiro Sakai, Yusuke Watanabe, Hiroyuki Abe, Hiroteru Kamimura, Akira Sakamaki, Takeshi Yokoo, Kenya Kamimura, Atsunori Tsuchiya, Akihiko Osaki, Kentarou Igarashi, Nobuo Waguri, Masahiko Yanagi, Toru Takahashi, Soichi Sugitani, Yuka Kobayashi, Masaaki Takamura, Akira Yoshikawa, Toru Ishikawa, Toshiaki Yoshida, Toshiaki Watanabe, Hitoshi Bannai, Tomoyuki Kubota, Kazuhiro Funakoshi, Hiroto Wakabayashi, So Kurita, Norio Ogata, Masashi Watanabe, Yuhsaku Mita, Shigeki Mori, Motoya Sugiyama, Toru Miyajima, Sumio Takahashi, Shuichi Sato, Kisei Ishizuka, Hironobu Ohta, Yutaka Aoyagi, Shuji Terai

JGH open : an open access journal of gastroenterology and hepatology 6 ( 8 ) 577 - 586 2022年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

Background and Aim: Symptoms of primary biliary cholangitis (PBC) frequently impair one's quality of life (QOL). Nonetheless, with improved treatment, the prognosis of PBC also improves. QOL plays an important role in patients with PBC. In this study, we aimed to reevaluate the transition of new symptom development in PBC and its predictive factors. Methods: This retrospective multicenter study enrolled 382 patients with PBC for symptom analysis. The impact of a newly developed symptom on PBC prognosis was investigated by Kaplan-Meier analysis with propensity score matching and logistic progression analysis. Results: The cumulative risk of developing a new symptom after 10 and 20 years of follow-up was 7.6 and 28.2%, and specifically that of pruritus, which was the most common symptom, was 6.7 and 23.3%, respectively. In Cox hazard risk analysis, serum Alb level (hazard ratio [HR], 1.097; 95% confidence interval [CI], 1.033-1.165; P = 0.002), the serum D-Bil level (HR, 6.262; 95% CI, 2.522-15.553, P < 0.001), and Paris II criteria (HR, 0.435; 95% CI, 0.183-1.036; P = 0.037) were significant independent predictors of a new symptom. Kaplan-Meier analysis showed that the overall survival and liver-related death were not significant between patients with and without a new symptom. Conclusion: The cumulative risk of new symptom development is roughly 30% 20 years after diagnosis and could be predicted by factors including serum albumin levels, serum D-Bil level, and Paris II criteria.

DOI： 10.1002/jgh3.12789

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機械学習を用いた慢性心不全に続発した肝臓への障害(Cardiac Hepatopathy)の画像解析

三井田秀, 上村博輝, 山崎文紗子, 渡邉雄介, 荒生祥尚, 木村成宏, 薛徹, 横尾健, 坂牧僚, 土屋淳紀, 藤木伸也, 猪又孝元, 寺井崇二

日本門脈圧亢進症学会雑誌 28 ( 3 ) 152 - 152 2022年8月

上村顕也, 永山逸夫, 大脇崇史, 高昌良, 名古屋拓郎, 井上良介, 坂牧僚, 寺井崇二

日本アルコール・薬物医学会雑誌 57 ( 4 ) 121 - 121 2022年8月

Allograft liver failure awaiting liver transplantation in Japan.

Takuya Genda, Takafumi Ichida, Eiji Tanaka, Satoshi Mochida, Yoshiyuki Ueno, Shuji Terai, Ayano Inui, Yoshihide Ueda, Hideki Ohdan, Hiroto Egawa, Koji Umeshita, Hiroyuki Furukawa, Yukihiro Inomata

Journal of gastroenterology 57 ( 7 ) 495 - 504 2022年7月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Following liver transplantation (LT), allograft liver failure can be developed by various causes and requires re-LT. Hence, this study aimed to clarify the characteristics and prognostic factors of patients with allograft liver failure awaiting deceased donor LT (DDLT) in Japan. METHODS: Of the 2686 DDLT candidates in Japan between 2007 and 2016, 192 adult patients listed for re-LT were retrospectively enrolled in this study. Factors associated with waitlist mortality were assessed using the Cox proportional hazards model. The transplant-free survival probabilities were evaluated using the Kaplan-Meier analysis and log-rank test. RESULTS: The median period from the previous LT to listing for re-LT was 1548 days (range, 4-8449 days). Primary sclerosing cholangitis (PSC), which was a primary indication, showed a higher listing probability for re-LT as compared with other primary etiologies. Recurrent liver disease was a leading cause of allograft failure and was more frequently observed in the primary indication of hepatitis C virus (HCV) infection and PSC in contrast with other etiologies. Multivariate analysis identified the following independent risk factors associated with waitlist mortality: age, Child-Turcotte-Pugh (CTP) score, mode for end-stage liver disease (MELD) score, alanine aminotransferase (ALT), and causes of allograft failure. CONCLUSIONS: Recurrent HCV and PSC were major causes of allograft liver failure in Japan. In addition to CTP and MELD scores, either serum ALT levels or causes of allograft failure should be considered as graft liver allocation measures.

DOI： 10.1007/s00535-022-01880-w

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(II章)肝肝硬変に対する再生医療

寺井崇二, 土屋淳紀

消化器内科学レビュー 2022-'23 213 - 216 2022年7月

記述言語：日本語出版者・発行元：(株)総合医学社

＜最近の動向とガイドライン＞●現在までに、C型肝炎に対する有効な治療薬が開発され、またB型肝炎に対して核酸アナログ製剤を中心にコントロールが良好な症例が増え、なお制圧に向け薬剤開発が進んでいる状況である。●一方、アルコールや生活習慣を背景とした肝硬変は増えてきており、肝移植以外の肝硬変に対する治療法の開発は喫緊の課題である。●本項では肝臓再生医療で2019～2021年に著された臨床論文を解説すると同時にその背景や、現在行われている将来の治療の基盤となる基礎研究についても一部述べる。(著者抄録)

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肝性腹水が腹部コンパートメント症候群を介して腎機能へ与える影響の検討

上村博輝, 酒井規裕, 小島雄一, 川田雄三, 渡邊雄介, 荒生祥尚, 木村成宏, 阿部寛幸, 薛徹, 横尾健, 坂牧僚, 土屋淳紀, 上村顕也, 横山純二, 寺井崇二

日本門脈圧亢進症学会雑誌 28 ( 2 ) 199 - 203 2022年7月

記述言語：日本語出版者・発行元：(一社)日本門脈圧亢進症学会

大量の肝性腹水が腹腔内圧の上昇をもたらし、腹部コンパートメント症候群を発症している状況を腹水前後の膀胱内圧測定、腎静脈流速測定を中心に検討した。対象症例は穿刺前後の膀胱内圧測定、腎静脈の流速測定等が可能であった腹水合併肝硬変8例。穿刺前後の膀胱内圧、尿潜血反応、腎機能、腎静脈流速等を経時的に観察した。末期肝硬変患者が肝腎症候群へ移行する過程で腹水による腹腔内圧の上昇が腎うっ血を併発させ、レニン-アンギオテンシン-アルドステロン系の亢進に関係する可能性が示唆された。(著者抄録)

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『高齢者(75歳以上)の非アルコール性脂肪性肝疾患の現状と課題』非アルコール性脂肪性肝炎を背景とした高齢者肝硬変に対する非侵襲的スコアリングシステムの有用性の検討

坂牧僚, 酒井規裕, 阿部寛幸, 横尾健, 上村顕也, 寺井崇二

日本高齢消化器病学会誌 25 ( 1 ) 74 - 74 2022年7月

【肝性脳症の病態と治療】肝性脳症と腸内細菌病態と治療

坂牧僚, 上村顕也, 横山邦彦, 酒井規裕, 渡邉雄介, 荒生祥尚, 木村成宏, 薛徹, 阿部寛幸, 上村博輝, 横尾健, 土屋淳紀, 寺井崇二

消化器・肝臓内科 12 ( 1 ) 68 - 72 2022年7月

各都道府県における肝疾患対策取り組みの現状新潟県の肝炎対策について

荒生祥尚, 薛徹, 酒井規裕, 寺井崇二

肝臓クリニカルアップデート 8 ( 1 ) 82 - 85 2022年7月

肝性腹水が腹部コンパートメント症候群を介して腎機能へ与える影響の検討

上村博輝, 酒井規裕, 小島雄一, 川田雄三, 渡邊雄介, 荒生祥尚, 木村成宏, 阿部寛幸, 薛徹, 横尾健, 坂牧僚, 土屋淳紀, 上村顕也, 横山純二, 寺井崇二

日本門脈圧亢進症学会雑誌 28 ( 2 ) 199 - 203 2022年7月

記述言語：日本語出版者・発行元：(一社)日本門脈圧亢進症学会

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The liver-gut peripheral neural axis and nonalcoholic fatty liver disease pathologies via hepatic serotonin receptor 2A. 国際誌

Takashi Owaki, Kenya Kamimura, Masayoshi Ko, Itsuo Nagayama, Takuro Nagoya, Osamu Shibata, Chiyumi Oda, Shinichi Morita, Atsushi Kimura, Takeki Sato, Toru Setsu, Akira Sakamaki, Hiroteru Kamimura, Takeshi Yokoo, Shuji Terai

Disease models & mechanisms 15 ( 7 ) 2022年6月

記述言語：英語掲載種別：研究論文（学術雑誌）

Serotonin (5-HT) is one of the key bioamines of nonalcoholic fatty liver disease (NAFLD). Its mechanism via autonomic neural signal pathways remains unexplained; hence, we evaluated the involvement of 5-HT and related-signaling pathways via autonomic nerves in NAFLD. Diet-induced NAFLD animal models were developed using wild-type and melanocortin 4 receptor knockout (MC4RKO) mice, and the effects of autonomic neural axis on NAFLD physiology, 5-HT and its receptors (Htrs), and lipid metabolism-related genes were assessed applying hepatic nerve blockade. Hepatic neural blockade retarded the progression of NAFLD by reducing 5-HT in the small intestine, hepatic Htr2a, and hepatic lipogenic genes expression, and HTR2A antagonist reproduced these effects. The effects were milder in MC4RKO, and brain 5-HT and Htr2c expression did not correlate with peripheral neural blockade. Our study demonstrates that the autonomic liver-gut neural axis is involved in the etiology of diet-induced NAFLD and that 5-HT and HTR2A are key factors, implying that the modulation of the axis and use of HTR2A antagonists are potentially novel therapeutic strategies for NAFLD treatment.

DOI： 10.1242/dmm.049612

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