Altered metal metabolism in patients with HCV-related cirrhosis and hepatic encephalopathy

Dysfunctional metal homeostasis contributes to oxidativestress and neuronal damage. These have been implicatedin hepatic encephalopathy pathogenesis. To investigatewhether altered metal metabolism is associated with hepaticencephalopathy. Twenty-one controls and 34 HCV-cirrhoticpatients (ENC/NEC patients according to presence/absenceof previous overt episodes of hepatic encephalopathy) and acontrol group were studied. Serum iron, copper, ceruloplasmin,ceruloplasmin activity, transferrin, and ceruloplasmin/transferrin ratio were determined. Neuropsychological testswere performed by the repeatable battery of neuropsychologicalstatus. Magnetic resonance assessed basal ganglia volumesand metal deposition (pallidal index and T2*). Cirrhoticpatients performed worse than controls at cognitive tests, especiallyENC patients,. At biochemical analysis copper concentrations,ceruloplasmin activity and transferrin levels werelower in ENC than in NEC patients and controls (p<0.05 andp<0.01, respectively). Ceruloplasmin/transferrin ratio washigher in ENC compared to NEC patients (p<0.05), and controls(p<0.01). By brain magnetic resonance, ENC patientsshowed reduced caudate and globus pallidus volumes comparedto controls (p<0.05), and ENC and NEC patients anincreased pallidal index compared to controls (p<0.01). InENC patients, ceruloplasmin activity correlated with caudatevolume and pallidal index (ρ=0.773 and ρ=−0.683, p<0.05).Altered metal metabolism likely contributes to cirrhotic hepaticencephalopathy.