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Abstract Autoimmune hepatitis (AIH) is an immune-mediated inflammatory disease that requires the integration of histological abnormalities, characteristic laboratory findings, autoantibody positivity, and exclusion of other liver diseases for diagnosis. The case of a 28-year-old female patient with a week-long history of generalized jaundice associated with diffuse and intermittent abdominal pain is presented. Liver tests revealed hepatocellular injury (R factor = 17.6) with severe transaminitis (aspartate aminotransferase [AST]: 1.502 IU/L, alanine aminotransferase [ALT]: 2.029 IU/L) and conjugated hyperbilirubinemia (total serum bilirubin: 10.9 mg/dL, direct bilirubin: 8.50 mg/dL). Serological tests for hepatotropic viruses were negative, as were autoantibodies for autoimmune hepatitis. Percutaneous liver biopsy revealed findings compatible with autoimmune hepatitis. The revised 1999 International Autoimmune Hepatitis Group (IAIHG) score was calculated pretreatment, resulting in a score of 16, thus diagnosing it as definitive severe AIH. The patient was treated with oral steroids, obtaining clinical and biochemical improvement, so she was discharged after seven days of hospitalization without incidents. Maintaining a high index of suspicion for AIH, despite the initial negativity of autoantibodies, and complementing the diagnostic approach with percutaneous liver biopsy allow the timely diagnosis and treatment of this group of patients, thus preventing progression to advanced cirrhosis and its complications.
Resumen La hepatitis autoinmune (HAI) es una enfermedad inflamatoria inmunomediada la cual requiere para su diagnóstico la integración de anomalías histológicas, hallazgos de laboratorio característicos, positividad de autoanticuerpos y exclusión de otras enfermedades hepáticas. Se presenta el caso de una paciente femenina de 28 años con un cuadro de ictericia generalizada de una semana de evolución asociado a dolor abdominal difuso e intermitente. Las pruebas hepáticas revelaron lesión hepatocelular (factor R= 17,6) con transaminasemia grave (aspartato-aminotransferasa [AST]: 1,502 UI/L, alanina-aminotransferasa [ALT]: 2,029 UI/L) e hiperbilirrubinemia conjugada (bilirrubina sérica total: 10,9 mg/dL, bilirrubina directa: 8,50 mg/dL). Las pruebas serológicas para virus hepatotropos fueron negativas, así como los autoanticuerpos para hepatitis autoinmune. La biopsia hepática percutánea reveló hallazgos compatibles de hepatitis autoinmune. Se calculó el puntaje revisado del Grupo Internacional de Hepatitis Autoinmune (IAIHG) de 1999 pretratamiento, en el que se obtuvo un puntaje de 16, por lo que se diagnosticó como HAI grave definitiva. La paciente fue manejada con esteroides orales y se obtuvo una mejoría clínica y bioquímica, por lo que fue egresada a los siete días de hospitalización, sin eventualidades. Mantener un alto índice de sospecha de HAI, a pesar de la negatividad inicial de los autoanticuerpos, y complementar el abordaje diagnóstico con biopsia hepática percutánea permite el diagnóstico y tratamiento oportuno de este grupo de pacientes, de modo que se previene la progresión a cirrosis avanzada y sus complicaciones.
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Objective To study the effects of endoplasmic reticulum stress on liver damage in young rats fed with high-fat diet.Methods We divided 48 male weaned young rats randomly into high-fat diet group and control group,which were separately fed with high-fat diet and normal diet.After feeding 8,12 and 1 6 weeks,the body weight and visceral fat of the rats were measured.The serum liver function was measured.The morphology of livers was observed by HE and transmission electron microscopy. The mRNA expressions of ATF6 and GRP78 in hepatocytes were measured with RT-PCR.Results ① The body weight and visceral fat weight of rats in high-fat diet group increased compared with those in control group (P 0.05);alanine aminotransferase at week 1 6 was increased significantly compared with that in controls (P < 0.05 ).③ Liver cells in high-fat diet group had steatosis at week 8 and the steatosis became more serious between week 12 and week 1 6.④ In high-fat diet group at week 8 there were a large number of lipid droplets in the cytoplasm,and the cell structure was close to that of normal cells;rough endoplasmic reticulum was nearly normal and the ribosome was visible.At week 12 and week 1 6,besides a large number of lipid droplets,we could also see that some substances with line-like structure deposited in rough endoplasmic reticulum pool.⑤ The expressions of ATF6 and GRP78 mRNA in hepatocytes in high-fat group at weeks 8, 12 and 1 6 were significantly increased compared with those in control group (P <0.05). Conclusion High-fat diet in infants can cause visceral fat accumulation,fatty degeneration of hepatocytes and liver injury.ATF6-mediated endoplasmic reticulum may be closely related to the liver injury which results from highfat diet.
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We analyzed the clinical features of 21 cases with drug-induced liver injury due to Kampo medicines between the years 2000 and 2009 in our institute. The mean age in these cases was 55.2 ± 13.4 years. Five of the cases were men, and 16 were women. In 17 of the 21 cases, drug-induced liver injury had occurred within 3 months after beginning Kampo medicines. There were no subjective symptoms in 11 cases. Nine cases of both hepatocellular injury, and of mixed-type injury were seen. Causative Kampo medicines included an Ogon (<i>Scutellariae Radix</i>) component in 19 cases. A drug-induced lymphocyte stimulation test (DLST) was performed in 5 cases. The test was positive for Kampo medicines in only one of the 5 cases. Liver injury improved or normalized in 18 cases (85.7%) after discontinuing causative Kampo medicines. In another 2 cases, liver injury normalized after changing a Kampo medicine to the same prescription without Ogon. These results suggest that even if patients complain of no symptoms we must perform blood tests to check liver function within 3 months of prescribing Kampo medicines, especially those including Ogon, to facilitate early diagnosis of drug-induced liver injury.
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We analyzed the clinical features of 21 cases with drug-induced liver injury due to Kampo medicines between the years 2000 and 2009 in our institute. The mean age in these cases was 55.2 ± 13.4 years. Five of the cases were men, and 16 were women. In 17 of the 21 cases, drug-induced liver injury had occurred within 3 months after beginning Kampo medicines. There were no subjective symptoms in 11 cases. Nine cases of both hepatocellular injury, and of mixed-type injury were seen. Causative Kampo medicines included an Ogon (<I>Scutellariae Radix</I>) component in 19 cases. A drug-induced lymphocyte stimulation test (DLST) was performed in 5 cases. The test was positive for Kampo medicines in only one of the 5 cases. Liver injury improved or normalized in 18 cases (85.7%) after discontinuing causative Kampo medicines. In another 2 cases, liver injury normalized after changing a Kampo medicine to the same prescription without Ogon. These results suggest that even if patients complain of no symptoms we must perform blood tests to check liver function within 3 months of prescribing Kampo medicines, especially those including Ogon, to facilitate early diagnosis of drug-induced liver injury.