DILI/HDS on top of AIH |
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Can be misinterpreted as an aggressive course of AIH if the causative agent is not identified
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In most cases of AIH, IgG/gammaglobulins parallel the increase of transaminases; this helps to differentiate AIH from DILI/HDS
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Drug-induced AIH |
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Second episode of DILI mimics relapsing course of AIH |
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According to current studies, this scenario is rare
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Repeated drug history is helpful to identify the causative agents
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Chronic DILI mimics AIH |
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Chronic DILI/HDS through sustained intake of the causative drug is possible
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Underreporting (especially of analgetics, HDS, etc.) hampers identification of the causative drug
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However, the presence of cirrhosis favours the diagnosis of AIH and makes DILI/HDS less likely
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DILI/HDS with characteristics of AIH (“autoimmune(-like)” DILI/HDS, “immune-mediated” DILI/HDS) |
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The terms are used for DILI/HDS cases characterized by the presence of autoantibodies and/or infiltration of the liver by immune competent cells
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However, most of the autoantibodies (e.g., ANA and anti-SMA) are not disease-specific
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Demarcation of “autoimmune(-like)” DILI/HDS from AIH is difficult
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Features supporting the diagnosis of AIH are a relapse of transaminases and IgG/gammaglobulins after steroid withdrawal and a chronic, fluctuating course
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Close monitoring of transaminases (weekly for the first 1–2 months, every 2–3 weeks for the next 2–3 months, every 3 months for the next 1–2 years) and IgG/gammaglobulins is necessary to confirm the correct diagnosis
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