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• W2148647478 abstract "Objective: To determine whether there is a correlation between liver MR find-ings and the clinical manifestations and severity of liver dysfunction in patientswith Wilson’s disease.Materials and Methods: Two radiologists retrospectively evaluated MRimages of the liver in 50 patients with Wilson’s disease. The Institutional ReviewBoard approved this retrospective study and informed consent was waived. MRimages were evaluated with a focus on hepatic contour abnormalities and thepresence of intrahepatic nodules. By using Fisher’s exact test, MR findings werecompared with clinical presentations (neurological and non-neurological) andhepatic dysfunction, which was categorized by the Child-Pugh classification sys-tem (A, B and C). Follow-up MR images were available for 17 patients.Results: Contour abnormalities of the liver and intrahepatic nodules wereobserved in 31 patients (62%) and 25 patients (50%), respectively. Each MR find-ing showed a statistically significant difference ( p < 0.05) among the three groupsof Child-Pugh classifications (A, n = 36; B, n = 5; C, n = 9), except forsplenomegaly ( p = 0.243). The mean age of the patients with positive MR find-ings was higher than that of patients with negative MR findings. For patients withChild-Pugh class A (n = 36) with neurological presentation, intrahepatic nodules,surface nodularity, and gallbladder fossa widening were more common.Intrahepatic nodules were improved (n = 8, 47%), stationary (n = 5, 29%), oraggravated (n = 4, 24%) on follow-up MR images.Conclusion: MR imaging demonstrates the contour abnormalities andparenchymal nodules of the liver in more than half of the patients with Wilson’sdisease, which correlates with the severity of hepatic dysfunction and clinicalmanifestations. ilson’s disease or progressive hepatolenticular degeneration is an autoso-mal recessive disorder of copper metabolism (1). The gene that causesWilson’s disease, located at chromosome 13 band q14.3, is known tocode for a copper-transporting P-type ATPase (2-4). A mutation of the gene associ-ated with Wilson’s disease results in deficient biliary excretion of copper, leading toexcessive copper accumulation in many tissues. Copper accumulation occurs mainly inthe liver, but also in the brain, cornea, and kidney (1-5). The principal clinical manifes-tations of Wilson’s disease are either hepatic or neurological disease (6, 7). Ultrasound (US), CT, and MR findings of the liver in Wilson’s disease usually reflectnonspecific hepatic injury including fatty infiltration, acute hepatitis, chronic activehepatitis, and cirrhosis (8-12). In advanced Wilson’s disease, nodular infiltrationssuggesting the presence of copper-containing nodules and contour abnormalities consis-Jung-Eun Cheon, MD" @default.
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• W2148647478 date "2010-01-01" @default.
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• W2148647478 title "Clinical Application of Liver MR Imaging in Wilson's Disease" @default.
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