| Literature DB >> 31155601 |
Keisuke Nonaka1, Yoko Matsuda1, Mototsune Kakizaki1, Shoichiro Takakuma1, Akihiko Hamamatsu1, Yasuhiro Sakashita2, Tomoyasu Matsubara2, Shigeo Murayama2, Toshiyuki Ishiwata3, Noriko Yamanaka4, Mitsuyo Itabashi4, Takashi Takei4, Noriko Nakajima5, Hideki Hasegawa5, Tomio Arai1.
Abstract
An 84-year-old man with chronic renal failure, anemia, and diabetes was admitted for hemodialysis initiation. His vital signs were stable until the eighteenth hospital day, before acquiring an influenza A virus infection. Three days later, he died of septic shock with severe liver impairment. His leukocyte count, prothrombin time (PT-INR), and liver enzyme levels such as aspartate transaminase and alanine aminotransferase, were significantly increased. Hypercytokinemia was also observed. Autopsy revealed bilateral diffuse pneumonia with neutrophil infiltration. The liver showed extensive centrilobular hepatocyte necrosis. Immunohistochemistry for influenza A nucleoprotein revealed positivity in the ciliated columnar epithelium of the bronchi and negativity in the trachea, lungs, and liver. Hypoxic hepatitis is characterized by an abrupt and massive increase in aminotransferase levels (> 20 times upper normal limit) due to anoxic centrilobular hepatocyte necrosis. The occurrence of hypoxic hepatitis requires a pre-existing, chronic condition, such as anemia, causing reduced oxygen supply to the liver, followed by an acute decrease in hepatic oxygen supply, such as septic shock. Therefore, this report suggests that hypoxic hepatitis can be an important causative factor for acute liver failure associated with influenza virus infection.Entities:
Keywords: acute liver failure; hypercytokinemia; hypoxic hepatitis; influenza A virus
Mesh:
Year: 2019 PMID: 31155601 DOI: 10.7883/yoken.JJID.2018.494
Source DB: PubMed Journal: Jpn J Infect Dis ISSN: 1344-6304 Impact factor: 1.362