Etiology and prognosis of fulminant hepatitis and late‐onset hepatic failure in <scp>J</scp>apan: Summary of the annual nationwide survey between 2004 and 2009

Oketani, Makoto; Ido, Akio; Nakayama, Nobuaki; Takikawa, Yasuhiro; Naiki, Taku; Yamagishi, Yuka; Ichida, Takafumi; Mochida, Satoshi; Onishi, Saburo; Tsubouchi, Hirohito

doi:10.1111/j.1872-034x.2012.01105.x

Cited by 117 publications

(119 citation statements)

References 33 publications

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“…Chronic inflammation in the liver can progress to liver cirrhosis (3). One major problem of AIH is that an acute presentation or exacerbation of the disease can progress to liver failure (4,5). Furthermore, patients with AIH can be susceptible to hepatocellular carcinoma (6); therefore, patients should be followed-up for exacerbation and hepatocellular carcinoma (7).…”

Section: Introductionmentioning

confidence: 99%

Anti-mitochondrial M2 antibody-positive autoimmune hepatitis

Tomizawa

Shinozaki

Fugo

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Anti-mitochondrial M2 antibody (AMA-M2) is specific to primary biliary cirrhosis (PBC), but can also be found in certain patients with autoimmune hepatitis (AIH). Effective methods of differentiating between PBC and AIH are required, as their clinical course and management are different. Titers of AMA-M2 were analyzed before and after follow-up in patients with PBC or AIH. Patients who underwent liver biopsy and were diagnosed with either AIH (10 patients) or PBC (3 patients) were enrolled in the study. The AMA-M2 antibody titers of these patients were analyzed upon hospital admission. AMA-M2 reacted with the pyruvate dehydrogenase complex-E2, branched-chain 2-oxo acid dehydrogenase complex and 2-oxoglutaric acid dehydrogenase complex in the assay utilized for this study. The cut-off value for AMA-M2 was 5. Six AIH patients were AMA-M2(-) and 4 were AMA-M2(+). The titer for the AIH patients who were AMA-M2(+) was 24.8±14.8, compared with 324±174 in the patients with PBC (P= 0.0138). Three AMA-M2(+) AIH patients were followed-up after liver biopsy. The AMA-M2 levels had decreased in all 3 patients, becoming undetectable in 2 of them. In conclusion, certain patients with AIH in this study were found to be AMA-M2(+), but the titers were significantly lower than those in the patients with PBC. At follow-up, the AIH patients exhibited decreased AMA-M2 titers. IntroductionAutoimmune hepatitis (AIH) is caused by an immune attack on the hepatocytes (1). Patients with AIH are positive for auto-antibodies, such as anti-nuclear, anti-smooth muscle and liver-kidney microsomal type 1 antibodies (2). Chronic inflammation in the liver can progress to liver cirrhosis (3). One major problem of AIH is that an acute presentation or exacerbation of the disease can progress to liver failure (4,5). Furthermore, patients with AIH can be susceptible to hepatocellular carcinoma (6); therefore, patients should be followed-up for exacerbation and hepatocellular carcinoma (7). Primary biliary cirrhosis (PBC) is characterized by nonsuppurative cholangitis and autoimmune-mediated destruction of the small or medium-sized bile ducts (8). Inflammation causes cholestasis and the liver develops cirrhosis (9). AIH is treated with immunosuppressive drugs, such as prednisolone or azathioprine (10,11), while PBC is treated with ursodeoxycholic acid (10). It is important to differentiate AIH from PBC due to the differences in the clinical course and management of the two diseases.Anti-mitochondrial antibody (AMA) can be tested via indirect immunofluorescence (12). In this technique, unfixed sections of the kidney and stomach of Wistar rats are used. AMA is used for the diagnosis of PBC (13), as 90-95% of patients with PBC are positive for AMA (14); however, the use of AMA as a differential test is problematic, as 5% of patients with AIH are positive for AMA (15), and the interpretation of a positive AMA result in AIH is difficult.The auto-antigens of AMA have been identified as pyruvate dehydrogenase complex-E2 (PDC-E2), branched-chain 2-oxo...

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Section: Introductionmentioning

confidence: 99%

Anti-mitochondrial M2 antibody-positive autoimmune hepatitis

Tomizawa

Shinozaki

Fugo

et al. 2015

Experimental and Therapeutic Medicine

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“…LOHF is classified as a disease related to acute liver failure (ALF) (1,4) and is recognized to be a more critical disease than ALF according to a national survey in Japan covering the period from 2004 to 2009 (1). The survival rate of LOHF patients treated without liver transplantation (LT) is extremely poor compared with that of patients treated with LT (1, 4).…”

Section: Discussionmentioning

confidence: 99%

“…Late-onset hepatic failure (LOHF) has a relatively long precoma period (8-24 weeks), in which liver dysfunction, such as that due to cholestasis, coagulopathy and liver atrophy, progresses consistently, and in most cases, irreversibly (1,2). Because these symptoms are based on the onset of severe and progressive hepatic necrosis and impaired liver regeneration, new methods to detect severe liver tissue damage may be useful for predicting and preventing the development of a coma.…”

Section: Introductionmentioning

confidence: 99%

Hepatic Hemodynamics and Elevation of Liver Stiffness as Possible Predictive Markers of Late-onset Hepatic Failure

et al. 2016

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A 52-year-old Japanese woman admitted to our hospital for the treatment of liver dysfunction due to an undetermined cause developed disorientation on the 58th hospital day and was diagnosed with late-onset liver failure. Abdominal ultrasound examinations were performed several times from the admission. Before the disorientation appeared, the results of the examinations revealed that the portal flow decreased, after which the hepatic arterial flow increased and the degree of liver stiffness became elevated. Although the pathophysiology of these changes remains unclear, hemodynamic changes and elevation of liver stiffness might be predictive markers of severe liver tissue damage.

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“…33,34 The immunopathological damage and microcirculation disturbance could lead to liver cells in ischemia, hypoxia, and edema. As an immunomodulator, corticosteroids suppress the function of CTL to prevent or delay primary liver injury.…”

Section: Discussionmentioning

confidence: 99%

Prognoses of patients with acute-on-chronic hepatitis B liver failure are closely associated with altered SOCS1 mRNA expression and cytokine production following glucocorticoid treatment

et al. 2014

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Suppressor of cytokine signaling (SOCS) 1 plays a crucial role in the immune response and might contribute to the prognoses of liver failure treated with glucocorticoid. We recruited 47 acute-on-chronic hepatitis B liver failure (ACHBLF) patients receiving glucocorticoid treatment and 30 healthy controls to determine the potential effects of glucocorticoid on the transcriptional level of SOCS1 in peripheral blood mononuclear cells. On the third and twenty-eighth days of glucocorticoid treatment, SOCS1 expression was negatively correlated with model for end-stage liver disease (MELD) score. Interleukin-6 (IL-6) and tumor-necrosis factor-a (TNF-a) levels were statistically lower, while the SOCS1 transcription level was higher in survivors than non-survivors both in pre-and post-treatment ACHBLF patients. The methylation rate of the SOCS1 promoter in ACHBLF patients was higher than in healthy control patients as determined by methylation-specific polymerase chain reaction. The mRNA level of SOCS1 in methylated promoters was significantly lower than from patients with unmethylated SOCS1 promoters. interferon (IFN)-c-responsive and STAT1-dependent gene expression was higher in survivors and was dramatically decreased with rising expression of SOCS1 after glucocorticoid treatment. Mortality rates were significantly higher in methylated patients than for those without methylation at the end of a 90-day follow-up. Furthermore, we found that five in six surviving patients displayed demethylated SOCS1 on the twenty-eighth day after treatment, while that number was 3 in 10 in the non-survivors. These findings suggested that ACHBLF patients without SOCS1 methylation may have a favorable response to corticosteroid treatment.

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Etiology and prognosis of fulminant hepatitis and late‐onset hepatic failure in Japan: Summary of the annual nationwide survey between 2004 and 2009

Cited by 117 publications

References 33 publications

Anti-mitochondrial M2 antibody-positive autoimmune hepatitis

Anti-mitochondrial M2 antibody-positive autoimmune hepatitis

Hepatic Hemodynamics and Elevation of Liver Stiffness as Possible Predictive Markers of Late-onset Hepatic Failure

Prognoses of patients with acute-on-chronic hepatitis B liver failure are closely associated with altered SOCS1 mRNA expression and cytokine production following glucocorticoid treatment

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