| 1 | Statin-induced Liver Injury Patterns: A Clinical Review显示文摘Since their introduction in 1987,hydroxymethyl glutaryl coenzyme A reductase(HMG-CoA)inhibitors,more commonly known as statins,have become some of the most widely prescribed medications in the world.Though generally considered to be safe and well tolerated,statins have been associated with several side effects including mild liver dysfunction manifested by increases in aminotransferases.Rarely,statins have been noted to induce more serious hepatic injury,including liver injury with autoimmune features.Current literature supports statin induced liver injury presenting in either hepatocellular or cholestatic patterns,though with the former being the prevailing pattern of injury.Fortunately,severe liver injury is uncommon with statin use and is generally reversible without any intervention other than offending statin cessation.When evaluating cases of suspected statininduced liver injury,a complete medical history,laboratory tests including a complete metabolic panel,autoimmune markers,and viral panel,as well as hepatic imaging,are crucial for a complete causality analysis with validated tools such as Roussel Uclaf Causality Assessment Method.The aim of this review is to review the current evidence for statininduced liver injury and cholestasis. | Leon D.Averbukh Alla Turshudzhyan David C.Wu George Y.Wu | 2022 | Journal of Clinical and Translational Hepatology2022，10，3： | 1 |
| 3 | Primary Non-HFE Hemochromatosis:A Review显示文摘Iron homeostasis is a complex process in which iron uptake and use are tightly balanced.Primary Type 1 or HFE hemochromatosis results from homozygous mutations in the gene that encodes human homeostatic iron regulator(known as human factors engineering,HFE)protein,a regulator of hepcidin,and makes up approximately 90%of all hemochromatosis cases.However,four types of hemochromatosis do not involve the HFE gene.They are non-HFE hemochromatosis type 2A(HFE2,encoding HJV),type 2B(HAMP,encoding hepcidin),type 3(TFR2,encoding transferring receptor-2),and types 4A and B(SLC40A1,encoding ferroportin.NonHFE hemochromatosis is extremely rare.Pathogenic allele frequencies have been estimated to be 74/100,000 for type 2A,20/100,000 for type 2B,30/100,000 for type 3,and 90/100,000 for type 4 hemochromatosis.Current guidelines recommend that the diagnosis be made by ruling out HFE mutations,history,physical examination,laboratory values(ferritin and transferrin saturation),magnetic resonance or other imaging,and liver biopsy if needed.While less common,non-HFE hemochromatosis can cause iron overload as severe as the HFE type.In most cases,treatment involves phlebotomy and is successful if started before irreversible damage occurs.Early diagnosis and treatment are important because it prevents chronic liver disease.This review updates the mutations and their pathogenetic consequences,the clinical picture,diagnostic guidelines,and treatment of hemochromatosis. | Alla Turshudzhyan David C.Wu George Y.Wu | 2023 | Journal of Clinical and Translational Hepatology2023，11，4： | 0 |
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