今日の臨床サポート

A型肝炎

著者: 山本敏樹1) 日本大学医学部 内科学系消化器肝臓内科学分野

著者: 林順平2) はやし内科クリニック

著者: 森山光彦3) 日本大学医学部 内科学系消化器肝臓内科学分野

監修: 金子周一 金沢大学大学院

著者校正/監修レビュー済:2020/11/06
患者向け説明資料

概要・推奨   

  1. 重症化は、感染初期の高度なウイルス複製力に対する過度な宿主免疫反応に関連する。
  1. ALT高値、PT延長、総ビリルビン高値のA型肝炎患者は、急性腎不全の合併に注意が必要。
  1. まれに、A型肝炎にタイプ1自己免疫性肝炎を合併することがある。
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
山本敏樹 : 特に申告事項無し[2021年]
林順平 : 未申告[2021年]
森山光彦 : 特に申告事項無し[2021年]
監修:金子周一 : 研究費・助成金など(バイエル薬品株式会社,株式会社キュービクス,アボットジャパン合同会社,日東電工株式会社,株式会社スギ薬局,株式会社サイトパスファインダー),奨学(奨励)寄付など(小野薬品工業株式会社,エーザイ株式会社,株式会社ツムラ,アッヴィ合同会社,大日本住友製薬株式会社,ゼリア新薬工業株式会社,塩野義製薬株式会社,大塚製薬株式会社,アステラス製薬株式会社,田辺三菱製薬株式会社,マイランEPD合同会社,EAファーマ株式会社,大鵬薬品工業株式会社,中外製薬株式会社,協和キリン株式会社,持田製薬株式会社,日本ケミファ株式会社,LifeScan Japan株式会社)[2021年]

改訂のポイント:
  1. 定期レビューを行い、2018年のブレイクアウトについて加筆した。

病態・疫学・診察

疾患情報(疫学・病態)  
  1. A型肝炎はA型肝炎ウイルス(HAV)の経口感染により発症し、急性肝障害を引き起こす一般的に予後良好な疾患で、世界中で散発的に発生している。感染症予防法では4類感染症に分類されており、ただちに届け出る必要がある。
  1. HAVの主な感染経路はfecal-oral(糞便―経口)感染であり、感染者の糞便中に排泄されたHAVが、飲料水や食物などの感染源を介して未感染者に摂取され、感染が成立する[1]。また最近では、男性同性愛者(MSM)での感染が増加している。
 
A型肝炎の分布

A型肝炎の流行状況は地域によって異なり、衛生環境が不十分な地域で多く発生する。

 
  1. 国立感染症研究所の調査によると、2000~2017年までは年平均266例(範囲115~502例)のA型肝炎患者が報告されていたが、2018年は届出患者数が926例(暫定値)に達し、2019年は3月現在で115例(暫定値)であったと報告されており、アウトブレイクが確認された。この流行の原因は、2015年以降、台湾、ヨーロッパでアウトブレイクを引き起こしたRIVM-HAV16-090株(遺伝子型IA)であることが確認されている[2]
  1. 以前はウイルスに汚染したカキなどの貝類の摂取により感染していたが、最近では、汚染された輸入食品による散発例、海外旅行者のA型肝炎流行地での感染、ドラッグ使用者間の感染や、男性同性愛者(MSM)での性行為感染症としての流行など、従来とは異なる感染様式を持つようになっている。
 
  1. HAV-RNA検出法(参考文献:[3]
  1. 発症前より患者の糞便に多量に排出されたウイルスは、発症時に最大となり発症後1~2カ月後にも認められる。
問診・診察のポイント  
  1. 衛生環境が整っていない地域への渡航経験、カキなどの貝類の摂取の有無を確認する。

これより先の閲覧には個人契約のトライアルまたはお申込みが必要です。

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文献 

著者: Anthony E Fiore
雑誌名: Clin Infect Dis. 2004 Mar 1;38(5):705-15. doi: 10.1086/381671. Epub 2004 Feb 11.
Abstract/Text Hepatitis A is caused by hepatitis A virus (HAV). Transmission occurs by the fecal-oral route, either by direct contact with an HAV-infected person or by ingestion of HAV-contaminated food or water. Foodborne or waterborne hepatitis A outbreaks are relatively uncommon in the United States. However, food handlers with hepatitis A are frequently identified, and evaluation of the need for immunoprophylaxis and implementation of control measures are a considerable burden on public health resources. In addition, HAV-contaminated food may be the source of hepatitis A for an unknown proportion of persons whose source of infection is not identified.

PMID 14986256  Clin Infect Dis. 2004 Mar 1;38(5):705-15. doi: 10.1086/・・・
著者: S Vento, T Garofano, G Di Perri, L Dolci, E Concia, D Bassetti
雑誌名: Lancet. 1991 May 18;337(8751):1183-7.
Abstract/Text To identify factors contributing to the pathogenesis of autoimmune chronic active hepatitis (CAH) healthy relatives of 13 patients with the disorder were followed prospectively for 4 years. 58 relatives were monitored for various serological markers and for T-lymphocyte migration inhibitory activity every 2 months. 3 cases of subclinical acute hepatitis A occurred during the study. In 2 of the 3 subjects, before hepatitis A virus (HAV) infection, there was a defect in suppressor-inducer T lymphocytes specifically controlling immune responses to the asialoglycoprotein receptor, an antigen expressed on the hepatocyte surface. In these 2 subjects, specific helper T cells and antibodies to the asialoglycoprotein receptor persisted and increased after acute hepatitis A, and autoimmune CAH type 1 developed within 5 months. Thus, in susceptible individuals HAV is a trigger for autoimmune CAH.

PMID 1673738  Lancet. 1991 May 18;337(8751):1183-7.
著者: T Ide, M Sata, R Nouno, F Yamashita, H Nakano, K Tanikawa
雑誌名: Am J Gastroenterol. 1994 Feb;89(2):257-62.
Abstract/Text Four patients with acute viral hepatitis complicated by pure red cell aplasia were clinically evaluated. Two patients with hepatitis type A, one with hepatitis type B, and one with posttransfusion non-A non-B hepatitis had pure red cell aplasia. Only the patient with posttransfusion hepatitis was female, and the mean age of the four patients was 37.8 yr (31-51 yr.) The mean interval from the onset of hepatitis to the appearance of pure red cell aplasia was 30.5 days (27-37 days), and the development of hematopoietic disorders coincided with decreases in transaminase levels. Laboratory findings included peak serum glutamate pyruvate transaminase levels of 1305-3160 KU and decreases in the prothrombin time to about 50% in the two patients with hepatitis type A. Pure red cell aplasia was successfully treated by prednisolone or transfusion in all patients.

PMID 8304314  Am J Gastroenterol. 1994 Feb;89(2):257-62.
著者: Masamitsu Nakao, Nobuaki Nakayama, Yoshihito Uchida, Tomoaki Tomiya, Makoto Oketani, Akio Ido, Hirohito Tsubouchi, Hajime Takikawa, Satoshi Mochida
雑誌名: Hepatol Res. 2019 Aug;49(8):844-852. doi: 10.1111/hepr.13345. Epub 2019 May 29.
Abstract/Text AIM: A nationwide survey of acute liver failure (ALF) and late-onset hepatic failure (LOHF) has revealed that the outcomes of recent patients whose diseases were caused by infection with hepatitis A virus (HAV) have worsened, compared with those of previously reported patients. The factors associated with this deterioration were evaluated.
METHODS: A total of 83 patients with HAV infection seen between 1998 and 2015 were enrolled. All the patients had a prothrombin time-international normalized ratio of 1.5 or more and hepatic encephalopathy of grade 2 or more severe. The demographic and clinical features of 45 patients seen prior to 2003 (cohort 1) and 38 patients seen during 2004 and thereafter (cohort 2) were compared.
RESULTS: Three and four patients in cohort 1 and cohort 2, respectively, received liver transplantations; the survival rates among the remaining patients were 56% for cohort 2 and 79% for cohort 1 (P < 0.05). The mean age (±standard deviation) of the patients was higher in cohort 2 than in cohort 1 (58 ± 11 vs. 48 ± 13 years; P < 0.01). The percentages of patients with underlying metabolic diseases were 22% in cohort 1 and 61% in cohort 2 (P < 0.01). Diabetic mellitus was more common among deceased patients than among rescued patients (29% vs. 8%; P < 0.05) among patients who did not receive liver transplantations, and a multivariate analysis revealed that patient age and disease type were significantly and independently associated with the outcome.
CONCLUSION: The outcomes of recent patients with ALF or LOHF caused by HAV infection have recently worsened mainly because of an increase in underlying metabolic diseases as a consequence of aging.

© 2019 The Japan Society of Hepatology.
PMID 30957325  Hepatol Res. 2019 Aug;49(8):844-852. doi: 10.1111/hepr.・・・
著者: Advisory Committee on Immunization Practices (ACIP), Anthony E Fiore, Annemarie Wasley, Beth P Bell
雑誌名: MMWR Recomm Rep. 2006 May 19;55(RR-7):1-23.
Abstract/Text Routine vaccination of children is an effective way to reduce hepatitis A incidence in the United States. Since licensure of hepatitis A vaccine during 1995-1996, the hepatitis A childhood immunization strategy has been implemented incrementally, starting with the recommendation of the Advisory Committee on Immunization Practices (ACIP) in 1996 to vaccinate children living in communities with the highest disease rates and continuing in 1999 with ACIP's recommendations for vaccination of children living in states, counties, and communities with consistently elevated hepatitis A rates. These updated recommendations represent the final step in the childhood hepatitis A immunization strategy, routine hepatitis A vaccination of children nationwide. Implementation of these recommendations will reinforce existing vaccination programs, extend the benefits associated with hepatitis A vaccination to the rest of the country, and create the foundation for eventual consideration of elimination of indigenous hepatitis A virus transmission. This report updates ACIP's 1999 recommendations concerning the prevention of hepatitis A through immunization (CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices [ACIP]. MMWR 1999:48[No. RR-12]:1-37) and includes 1) new data on the epidemiology of hepatitis A in the era of hepatitis A vaccination of children in selected U.S. areas, 2) results of analyses of the economics of nationwide routine vaccination of children, and 3) recommendations for the routine vaccination of children in the United States. Previous recommendations for vaccination of persons in groups at increased risk for hepatitis A or its adverse consequences and recommendations regarding the use of immune globulin for protection against hepatitis A are unchanged from the 1999 recommendations.

PMID 16708058  MMWR Recomm Rep. 2006 May 19;55(RR-7):1-23.
著者: Tara M Vogt, Matthew E Wise, Beth P Bell, Lyn Finelli
雑誌名: J Infect Dis. 2008 May 1;197(9):1282-8. doi: 10.1086/586899.
Abstract/Text BACKGROUND: Since the mid-1990s, hepatitis A vaccine has been recommended for US children living in historically high-incidence states and for persons with other risk factors or chronic liver disease (CLD). The incidence of hepatitis A has declined dramatically during the era of vaccination, but trends in mortality are largely unknown.
METHODS: US death certificates from 1990 to 2004 for which hepatitis A was listed as the underlying cause of death were analyzed. Average annual age-adjusted mortality rates during the prevaccine (1990-1995) and post-vaccination recommendation (2000-2004) periods were compared using a Mantel-Haenszel test of association. The number of deaths for which CLD was listed as a contributing cause was determined.
RESULTS: Overall, 1436 deaths due to hepatitis A occurred, averaging 96 annually (range, 142 in 1995 to 54 in 2003). CLD contributed to nearly half of these deaths. Mortality rates paralleled incidence rates, beginning to decline in the mid-1990s and achieving low points in 2003 and 2004. Average rates were 32% lower in the post-vaccination recommendation period than in the prevaccine period (P < .01). The decline was more dramatic for states with (45%; P < .001) than without (23%; P = .002) recommendations.
CONCLUSIONS: Hepatitis A mortality rates have declined over the past decade. CLD remains an important and preventable contributing cause of death due to hepatitis A.

PMID 18422440  J Infect Dis. 2008 May 1;197(9):1282-8. doi: 10.1086/58・・・
著者: Keiichi Fujiwara, Osamu Yokosuka, Fumio Imazeki, Hiromitsu Saisho, Naoki Saotome, Kazuyuki Suzuki, Kiwamu Okita, Eiji Tanaka, Masao Omata
雑誌名: Hepatol Res. 2003 Feb;25(2):124-134.
Abstract/Text Although hepatitis A is still a considerable problem in Japan, correlation of genomic differences of hepatitis A virus (HAV) and the clinical status of hepatitis A has not been studied. To examine whether the HAV genotype is associated with the disease severity, we analyzed the HAV genotype-determining region in sera from patients with hepatitis A of various clinical degrees. Serum samples from 47 Japanese patients with sporadic hepatitis A from 4 different areas in Japan, including 8 with fulminant hepatitis, 11 with severe acute hepatitis (AHs), and 28 with AHs, were examined for HAV RNA. The 168 base pair sequence of the genotype-determining region, which is located at the VP1/2A junction, was amplified by reverse transcription-polymerase chain reaction, and the nucleotide sequence was determined by direct sequencing. By comparing sequences for VP1/2A, we determined that 44 of 47 cases examined were of subgenotype IA, two were of subgenotype IB, and one was of subgenotype IIIA. With respect to subgenotype IA strains, individuals who were infected between 1990 and 1996 tended to show similar sequences, whereas those infected between 1997 and 1999 showed sequences slightly different from those of the 1990-1996 cases. There were no apparent associations between disease severity and sequences of the genotype-determining region. Hepatitis A of our study was caused by a variety of subgenotype IA strains, consistent with the sporadic spread of infection. Disease severity was not associated with the nucleotide sequence of the HAV genotype-determining region.

PMID 12644048  Hepatol Res. 2003 Feb;25(2):124-134.
著者: Zahid Hussain, Syed A Husain, Fahad N Almajhdi, Premashis Kar
雑誌名: Virol J. 2011 May 23;8:254. doi: 10.1186/1743-422X-8-254. Epub 2011 May 23.
Abstract/Text BACKGROUND: Hepatitis A virus is an infection of liver; it is hyperendemic in vast areas of the world including India. In most cases it causes an acute self limited illness but rarely fulminant. There is growing concern about change in pattern from asymptomatic childhood infection to an increased incidence of symptomatic disease in the adult population.
OBJECTIVE: In-depth analysis of immunological, viral quantification and genotype of acute and fulminant hepatitis A virus.
METHODS: Serum samples obtained from 1009 cases of suspected acute viral hepatitis was employed for different biochemical and serological examination. RNA was extracted from blood serum, reverse transcribed into cDNA and amplified using nested PCR for viral quantification, sequencing and genotyping. Immunological cell count from freshly collected whole blood was carried out by fluorescence activated cell sorter.
RESULTS: Fulminant hepatitis A was mostly detected with other hepatic viruses. CD8+ T cells count increases in fulminant hepatitis to a significantly high level (P = 0.005) compared to normal healthy control. The immunological helper/suppressor (CD4+/CD8+) ratio of fulminant hepatitis was significantly lower compared to acute cases. The serologically positive patients were confirmed by RT-PCR and total of 72 (69.2%) were quantified and sequenced. The average quantitative viral load of fulminant cases was significantly higher (P < 0.05). There was similar genotypic distribution in both acute and fulminant category, with predominance of genotype IIIA (70%) compared to IA (30%).
CONCLUSIONS: Immunological factors in combination with viral load defines the severity of the fulminant hepatitis A. Phylogenetic analysis of acute and fulminant hepatitis A confirmed genotypes IIIA as predominant against IA with no preference of disease severity.

PMID 21605420  Virol J. 2011 May 23;8:254. doi: 10.1186/1743-422X-8-25・・・
著者: Keiichi Fujiwara, Hiroshige Kojima, Shin Yasui, Koichiro Okitsu, Yutaka Yonemitsu, Masao Omata, Osamu Yokosuka
雑誌名: J Med Virol. 2011 Feb;83(2):201-7. doi: 10.1002/jmv.21958.
Abstract/Text A correlation between hepatitis A virus (HAV) genomes and the clinical severity of hepatitis A has not been established. The viral load in sera of hepatitis A patients was examined to determine the possible association between hepatitis A severity and HAV replication. One hundred sixty-four serum samples from 91 Japanese patients with sporadic hepatitis A, comprising 11 patients with fulminant hepatitis, 10 with severe acute hepatitis, and 70 with self-limited acute hepatitis, were tested for HAV RNA. The sera included 83 serial samples from 20 patients. Viral load was measured by real-time RT-PCR. The detection rates of HAV RNA from fulminant, severe acute, and acute hepatitis were 10/11 (91%), 10/10 (100%), and 55/70 (79%), respectively. Mean values of HAV RNA at admission were 3.48 ± 1.30 logcopies/ml in fulminant, 4.19 ± 1.03 in severe acute, and 2.65 ± 1.64 in acute hepatitis. Patients with severe infection such as fulminant hepatitis and severe acute hepatitis had higher initial viral load than patients with less severe infection (P < 0.001). Viremia persisted for 14.2 ± 5.8 days in patients with severe infection and 21.4 ± 10.6 days in those with acute hepatitis after clinical onset (P = 0.19). HAV RNA was detectable quantitatively in the majority of the sera of hepatitis A cases during the early convalescent phase by real-time PCR. Higher initial viral replication was found in severely infected patients. An excessive host immune response might follow, reducing the viral load rapidly as a result of the destruction of large numbers of HAV-infected hepatocytes, and in turn severe disease might be induced.

2010 Wiley-Liss, Inc.
PMID 21181913  J Med Virol. 2011 Feb;83(2):201-7. doi: 10.1002/jmv.219・・・
著者: Volker Fensterl, Dajana Grotheer, Iris Berk, Stefanie Schlemminger, Angelika Vallbracht, Andreas Dotzauer
雑誌名: J Virol. 2005 Sep;79(17):10968-77. doi: 10.1128/JVI.79.17.10968-10977.2005.
Abstract/Text Hepatitis A virus (HAV) antagonizes the innate immune response by inhibition of double-stranded RNA (dsRNA)-induced beta interferon (IFN-beta) gene expression. In this report, we show that this is due to an interaction of HAV with the intracellular dsRNA-induced retinoic acid-inducible gene I (RIG-I)-mediated signaling pathway upstream of the kinases responsible for interferon regulatory factor 3 (IRF-3) phosphorylation (TBK1 and IKKepsilon). In consequence, IRF-3 is not activated for nuclear translocation and gene induction. In addition, we found that HAV reduces TRIF (TIR domain-containing adaptor inducing IFN-beta)-mediated IRF-3 activation, which is part of the Toll-like receptor 3 signaling pathway. As IRF-3 is necessary for IFN-beta transcription, inhibition of this factor results in efficient suppression of IFN-beta synthesis. This ability of HAV seems to be of considerable importance for HAV replication, as HAV is not resistant to IFN-beta, and it may allow the virus to establish infection and preserve the sites of virus production in later stages of the infection.

PMID 16103148  J Virol. 2005 Sep;79(17):10968-77. doi: 10.1128/JVI.79.・・・
著者: Koen Van Herck, Jeanne-Marie Jacquet, Pierre Van Damme
雑誌名: J Med Virol. 2011 Nov;83(11):1885-91. doi: 10.1002/jmv.22200. Epub 2011 Aug 23.
Abstract/Text Long-term persistence of vaccine-induced immune response in adults was assessed annually for 15 years following primary immunization with a two-dose inactivated hepatitis A vaccine. In 1992, 119 and 194 subjects aged 17-40 years and naïve for hepatitis A virus (HAV) were enrolled in two studies to receive 1,440 ELISA units (El.U) of inactivated hepatitis A vaccine (Havrix™, GlaxoSmithKline Biologicals, Belgium) according to a standard 0, 6 or an extended 0, 12 months schedule, respectively. Serum samples were taken 1 month after the second vaccine dose and every consecutive year up to 15 years after primary vaccination for measurement of anti-HAV antibody concentrations (NCT00291876 and NCT00289757). At year 15, 100% (48/48) and 97.3% (108/111) of subjects vaccinated at 0, 6 or 0, 12 months remained seropositive for anti-HAV antibodies, with geometric mean concentrations (GMCs) of 289.2 and 367.4 mIU/ml, respectively. An additional dose of HAV vaccine (1,440 El.U) was administered to the six subjects who had become seronegative for anti-HAV antibodies since year 11. All subjects mounted a humoral immune response to the additional HAV challenge dose, although post-challenge anti-HAV antibody levels remained low in one subject. These studies represent the longest annual follow-up of hepatitis A vaccine in healthy adults. The immune response induced by two doses of this inactivated HAV vaccine was shown to persist for at least 15 years. No difference in long-term antibody persistence was observed between the two primary vaccination schedules, reinforcing the potential for flexibility in the timing of the second primary vaccine dose.

Copyright © 2011 Wiley-Liss, Inc.
PMID 21915861  J Med Virol. 2011 Nov;83(11):1885-91. doi: 10.1002/jmv.・・・
著者: Umid M Sharapov, Lisa R Bulkow, Susan E Negus, Philip R Spradling, Chriss Homan, Jan Drobeniuc, Michael Bruce, Saleem Kamili, Dale J Hu, Brian J McMahon
雑誌名: Hepatology. 2012 Aug;56(2):516-22. doi: 10.1002/hep.25687. Epub 2012 Jun 11.
Abstract/Text UNLABELLED: Persistence of seropositivity conferred by hepatitis A vaccine administered to children <2 years of age is unknown and passively transferred maternal antibodies to hepatitis A virus (maternal anti-HAV) may lower the infant's immune response to the vaccine. One hundred ninety-seven infants and young children were randomized into three groups to receive a two-dose hepatitis A vaccine: group 1 at 6 and 12 months, group 2 at 12 and 18 months, and group 3 at 15 and 21 months of age. Within each group, infants were randomized by maternal anti-HAV status. Anti-HAV levels were measured at 1 and 6 months and at 3, 5, 7, and 10 years after the second dose of hepatitis A vaccination. Children in all groups had evidence of seroprotection (>10 mIU/mL) at 1 month after the second dose. At 10 years, all children retained seroprotective anti-HAV levels except for only 7% and 11% of children in group 1 born to anti-HAV-negative and anti-HAV-positive mothers, respectively, and 4% of group 3 children born to anti-HAV-negative mothers. At 10 years, children born to anti-HAV-negative mothers in group 3 had the highest geometric mean concentration (GMC) (97 mIU/mL; 95% confidence interval, 71-133 mIU/mL) and children born to anti-HAV-positive mothers in group 1 had the lowest GMC (29 mIU/mL; 95% confidence interval, 20-40 mIU/mL). Anti-HAV levels through 10 years of age correlated with initial peak anti-HAV levels (tested at 1 month after the second dose).
CONCLUSION: The seropositivity induced by hepatitis A vaccine given to children <2 years of age persists for at least 10 years regardless of presence of maternal anti-HAV.

Copyright © 2012 American Association for the Study of Liver Diseases.
PMID 22371069  Hepatology. 2012 Aug;56(2):516-22. doi: 10.1002/hep.256・・・
著者: Hyun W Kim, Mi H Yu, Jang H Lee, Jai W Chang, Won S Yang, Soon B Kim, Sang K Lee, Jung S Park, Su-Kil Park
雑誌名: Nephrology (Carlton). 2008 Dec;13(6):451-8. doi: 10.1111/j.1440-1797.2008.00974.x. Epub 2008 Jun 1.
Abstract/Text AIM: To describe the clinical features and to identify factors related to development of acute kidney injury in acute hepatitis A patients.
METHODS: The study and control groups consisted of 21 and 425 patients who did or did not develop acute kidney injury, respectively, after acute hepatitis A from January 1997 to May 2007.
RESULTS: There were 13 men and eight women; their mean age at diagnosis was 28.8 +/- 8.2 years in the study group. Peak values for renal and liver function impairment consisted of a median serum creatinine of 4.6 mg/dL (range, 1.5-15.3 mg/dL) on day 6 (range, days 1-20) and a median total bilirubin of 10.7 mg/dL (range, 2.6-57.5 mg/dL) on day 8 (range, day 1-19). Serum creatinine concentrations returned to baseline level by a median of 16 days and total bilirubin levels returned to normal by a median of 62 days. Six of 21 (29%) patient underwent haemodialysis. Renal biopsies performed in two patients showed acute tubular necrosis and interstitial nephritis, respectively. Logistic regression analysis showed that a lower haematocrit, the presence of coagulopathy and high C-reactive protein concentration on admission, and higher peak bilirubin value during the illness were associated with development of acute kidney injury.
CONCLUSION: Acute hepatitis A should be considered in the differential diagnosis of patients with acute kidney injury, even without fulminant hepatic failure. A lower haematocrit, the presence of coagulopathy and high C-reactive protein level at presentation, and higher peak bilirubin level during the illness were associated with development of acute kidney injury in acute hepatitis A patients.

PMID 18518930  Nephrology (Carlton). 2008 Dec;13(6):451-8. doi: 10.111・・・
著者: Y J Jung, W Kim, J B Jeong, B G Kim, K L Lee, K-H Oh, J-H Yoon, H-S Lee, Y J Kim
雑誌名: J Viral Hepat. 2010 Sep;17(9):611-7. doi: 10.1111/j.1365-2893.2009.01216.x. Epub 2009 Oct 11.
Abstract/Text Acute hepatitis A (AHA) is one of the most common infectious diseases; it is usually a self-limiting disease affecting the liver. Although extrahepatic manifestations are not common, some cases have been reported associated with acute renal failure. We reviewed the clinical features of patients with AHA complicated by acute renal failure (ARF group) and compared them with patients with noncomplicated AHA (non-ARF group). The medical records of 208 consecutive patients with AHA who were diagnosed between January 2003 and October 2008 were reviewed. We identified 15 patients (7.2%) with ARF associated with AHA. There were no differences between the ARF and non-ARF group with regard to gender and age. The peak value of alanine aminotransferase (ALT) (median: 6060 IU/L vs 1792 IU/L, P < 0.001), prothrombin time (PT) (International normalized ratio, median 1.72 vs 1.10, P < 0.001), and total bilirubin level (median: 9.6 mg/dL vs 6.3 mg/dL, P = 0.04) were significantly higher in the ARF than in the non-ARF group. Twelve patients (80%) recovered completely with haemodialysis (seven patients, 46.7%) or only conservative management (five patients, 33.3%), while one patient underwent liver transplantation because of fulminant hepatic failure, and two patients died because of fulminant hepatic failure. There were no deaths among patients with noncomplicated AHA in the non-ARF group. Five patients underwent kidney biopsy; two patients were diagnosed with acute tubular necrosis, two patients with acute interstitial nephritis with IgA nephropathy and one patient with acute tubulointerstitial nephritis. All patients in the ARF group had microscopic haematuria and proteinuria (100%vs 31.1%, P < 0.001). Urine sodium levels were more than 10 mEq/L in 10 patients. The findings of high urinary sodium concentrations, microscopic haematuria and proteinuria did not support the diagnosis of hepatorenal syndrome (HRS). Patients with AHA with ARF had higher ALT levels, more prolonged PTs, and higher total bilirubin levels. The prognosis for these patients was poorer than for those without ARF. However, the patients with ARF and nonfulminant AHA had recovered with proper treatment and should not be confused with patients that have HRS.

PMID 19824944  J Viral Hepat. 2010 Sep;17(9):611-7. doi: 10.1111/j.136・・・

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