Purpose Of Review: Cases of de-novo autoimmune hepatitis/plasma cell hepatitis (PCH) are increasingly being diagnosed by liver transplant centers. Its pathogenesis is poorly understood but this entity appears to be a variant of rejection. Herein, we review recent clinical reports of patients developing PCH.
Recent Findings: Histologically, PCH is a challenging diagnosis, especially in the setting of recurrent hepatitis C and, in some cases, can be mistaken for acute cellular rejection. Recent case reports and case-control studies have shown that interferon appears to trigger PCH in hepatitis C posttransplant patients. Optimization of the immunosuppression regimen was found to prevent the development of PCH. In the nonhepatitis C posttransplant patient, tacrolimus-based immunosuppression appears to have some protective effect from PCH development. A combination therapy of cyclosporine and everolimus has also been shown to be effective in treating PCH.
Summary: PCH is a variant of rejection and is a cause of late graft loss post liver transplantation, especially in patients with hepatitis C. It should be part of the differential diagnosis of abnormal liver enzyme tests occurring in the post-liver transplant setting.
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http://dx.doi.org/10.1097/MOT.0b013e3283536622 | DOI Listing |
Hepatol Commun
February 2025
University Grenoble Alpes, Inserm U 1209, CNRS UMR 5309, Institute for Advanced Biosciences, Grenoble, France.
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View Article and Find Full Text PDFNiger Med J
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Department of Medical Microbiology, Usman Danfodiyo University Teaching Hospital, Sokoto, Nigeria.
Background: Anthrax is a life-threatening zoonotic disease caused by Gram-positive, spore-forming bacterium . It manifests as a cutaneous, gastrointestinal, and respiratory disease. The cutaneous form ranges from a self-limiting lesion to severe edematous lesions with toxemic shock.
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Front Immunol
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Department of Hepatology, Center for Pathogen Biology and Infectious Diseases, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
The intricate link between cholesterol metabolism and host immune responses is well recognized, but the specific mechanisms by which cholesterol biosynthesis influences hepatitis B virus (HBV) replication remain unclear. In this study, we show that SREBP2, a key regulator of cholesterol metabolism, inhibits HBV replication by interacting directly with the HBx protein, thereby preventing its nuclear translocation. We also found that inhibiting the ER-to-Golgi transport of the SCAP-SREBP2 complex or blocking SREBP2 maturation significantly enhances HBV suppression.
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Hepatopancreatobiliary Center, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing 102218, China.
In human aging, liver aging per se not only increases susceptibility to liver diseases but also increases vulnerability of other organs given its central role in regulating metabolism. Total liver function tends to be well maintained in the healthy elderly, so liver aging is generally difficult to identify early. In response to this critical challenge, the Aging Biomarker Consortium of China has formulated an expert consensus on biomarkers of liver aging by synthesizing the latest scientific literature, comprising insights from both scientists and clinicians.
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