喫煙は,肝硬変患者の炎症,線維形成,血管新生およびがんリスクを悪化させる

Nina Dominik^1,2, Benedikt Simbrunner^1,2,3, Bernhard Scheiner^1,2

¹Division of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Liver international : official journal of the International Association for the Study of the Liver

|September 3, 2025

まとめ

進行性慢性肝疾患 (ACLD) の患者の喫煙は炎症,線維生成,血管生成を高めます. 肝臓外悪性腫瘍のリスクを高め禁煙プログラムが必要であることを強調しています

科学分野:

ヘパトロジー
腫瘍学
内科医学

背景:

喫煙は炎症を誘発することが知られている.
進行性慢性肝疾患 (ACLD) のメカニズムとアウトカムに対するその特定の影響については,さらなる調査が必要である.

研究の目的:

喫煙がACLDの病気を誘発するメカニズムに及ぼす影響を評価する.
ACLD患者における喫煙と臨床結果の関連性を評価する.

主な方法:

この研究では,肝臓静脈圧グラデント測定を受けた339人のACLD患者さんを対象とした.
喫煙状態と炎症,線維生成,血管生成のバイオマーカーとの関連が分析された.
肝細胞癌 (HCC) の発生率,肝外悪性腫瘍,および死亡率を喫煙に関連して調べました.

主要な成果:

喫煙者の白血球数とC反応性タンパク質の濃度が喫煙者以前と比べるとかなり高かった.
活性喫煙者において,線維生殖 (TIMP-1,P3NP) と血管生殖 (PLGF) のアップレギュレーションが観察されました.
常喫煙者では肝臓外悪性腫瘍の発生率が高く,特にチャイルド・プーA患者では,HCCの発生率が上昇する傾向がありました.

結論:

喫煙は,ACLDにおける炎症,線維生成,血管生成の増加と関連しています.
喫煙は,ACLD患者の肝臓外悪性腫瘍の発症リスクを高めます.
禁煙戦略はACLD患者の管理に不可欠です.

キーワード:

HCC について血管新生肝硬変繊維生成炎症喫煙

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