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Available from: James D Gorham,
    • "Various autoantibodies have been reported in patients with autoimmune liver diseases (ALD), however, their diagnostic and clinical relevance is still a matter of debate [1] [2] [3] [4]. Liver asialoglycoprotein receptor (ASGPR) being a hepatic C-type lectin and the main transmembrane glycoprotein within the liver specific membrane lipoprotein fraction has been demonstrated to be the only organ-specific autoantigenic target in ALD so far [1] [5]. "
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    ABSTRACT: The liver asialoglycoprotein receptor (ASGPR) is the only organ-specific autoantigenic target in autoimmune hepatitis (AIH) patients and corresponding autoantibodies (Abs) have been suggested aiding in the serology of autoimmune liver diseases (ALD). A novel enzyme-linked immunosorbent assay (ELISA) employing purified rabbit ASGPR was used to detect ASGPR Abs in patients with ALD and controls. ASGPR Ab was determined in sera from 172 patients with AIH type 1, AIH type 2 (n=42), primary biliary cirrhosis (PBC) (n=113), cryptogenic liver disease (n=30), toxic liver disease (n=11), primary sclerosing cholangitis (PSC) (n=27), HCV infection (n=25), non-alcoholic steatohepatitis (n=43) and 100 blood donors. ASGPR Ab positivity was compared with AIH-related Abs (ANA, ASMA, Abs to LKM-1, LC-1, and SLA/LP) in patients with AIH. Patients with AIH-1 and AIH-2 demonstrated an ASGPR Ab prevalence of 29.1% and 16.7%, respectively. ASGPR Ab positivity in patients with AIH-1 and AIH-2 was not significantly different to those in patients with PSC and HCV (p > 0.05, respectively). ASGPR Ab levels in all study cohorts were significantly different with the highest medians in patients with AIH, PSC, and HCV infection (p < 0.0001). ASGPR Ab can be found as only AIH-specific Ab determined by LIA and ELISA in 24.4% of AIH patients (48/197). The novel ASGPR Ab ELISA is a specific diagnostic tool for ASGPR Ab detection in AIH. In addition to AIH, patients with PSC can demonstrate elevated ASGPR Ab amongst those with ALD suggesting a tolerance break to ASGPR in PSC. Copyright © 2015. Published by Elsevier B.V.
    Clinica chimica acta; international journal of clinical chemistry 07/2015; 450. DOI:10.1016/j.cca.2015.07.021 · 2.82 Impact Factor
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    • "Immunofluorescence remains therefore the gold standard for ANA testing, as recently surmised by the American College of Rheumatology ANA Task Force [41]. However, according to the AALSD clinical practice guidelines for autoimmune hepatitis practicing hepatologists in the US often use EIAs with recombinant nuclear antigens in their everyday clinical practice [33]. The immunofluorescent staining of SMA is detected in the arterial walls of rodent kidney, liver and stomach. "

    Journal of Hepatology 04/2015; 62(1S):S100-S111. DOI:10.1016/j.jhep.2015.03.005 · 11.34 Impact Factor
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    • "We observed prompt biochemical remission after immunosuppressive therapy in all cases of DI-AIH. In particular, all our patients had a better prognosis and a more complete response to therapy than typical idiopathic AIH patients, in whom, even if there is an initial normalization of LFTs, relapse after withdrawal of immunosuppression is almost the rule [24] [25]. All these data support the importance of a correct distinction of DI-AIH in the group of DILI, emphasizing the key role of liver biopsy in the diagnosis, prognosis and follow-up of the disease. "
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    ABSTRACT: Background: Drugs and herbal products can induce autoimmune hepatitis. We assessed frequency and clinical outcomes of patients suffering from drug-induced autoimmune hepatitis. Methods: All patients with drug-induced liver injury admitted between 2000 and 2011 were retrospectively studied. Diagnoses of drug-induced autoimmune hepatitis and idiopathic autoimmune hepatitis were made according to simplified criteria. After discharge, all patients had regular follow-up and were contacted to update outcomes. Results: Among 10,270 in-hospital patients, 136 (1.3%) were diagnosed with drug-induced liver injury. Among them, 12 (8.8%) were diagnosed as drug-induced autoimmune hepatitis (41.7% males, age range 17-73); 8 (66.7%) were with jaundice at admission. Liver biopsies showed a pattern compatible with drug-induced autoimmune hepatitis, featured by severe portal inflammation and lymphoplasmacytic infiltrate. Drug-induced autoimmune hepatitis group had a shorter duration of drug intake, and higher values of transaminases and gamma globulins. All patients received immunosuppressive therapy with subsequent clinical remission, and five achieved a steroid-free long-term remission. Conclusions: A diagnosis of drug-induced autoimmune hepatitis was quite rare in our cohort, and clinical pattern was similar to idiopathic autoimmune hepatitis. Severe portal inflammation, prominent portal-plasma cells, rosette formation and severe focal necrosis were significantly more frequent in drug-induced autoimmune hepatitis as compared to drug-induced liver injury.
    Digestive and Liver Disease 09/2014; 46(12). DOI:10.1016/j.dld.2014.08.040 · 2.96 Impact Factor
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