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DOI 10.1007/s10072-009-0149-0

Медицинская библиотека · Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2009

Progressive necrotic encephalopathy following tacrolimus therapy for liver transplantation.

Aridon Paolo, Ragonese Paolo, Di Benedetto Norma, Grasso Giovanni, Conaldi Pier Giulio, D'Amelio Marco, Savettieri Giovanni

Клинический случайСтатьяПеревод пока не подготовлен

Аннотация

Previously described neurologic damage induced by immunosuppressive treatments includes transient or reversible central nervous system involvement. We describe a 57-year-old man who underwent liver transplantation and was started on immunosuppressive therapy with tacrolimus (FK506). Six months later, he started complaining of a progressive motor and sensory impairment of the left side, together with cognitive impairment. Brain MRI showed an enlarging lesion of the white matter with peripheral contrast enhancement. PET study indicated severe hypometabolism in the right hemisphere and spectroscopic MRI showed a peak of choline and relative reduction of other metabolites. Findings of CSF examinations and cultures, serology, and molecular techniques were normal. Tacrolimus treatment was stopped. A cerebral biopsy of the lesion showed a sub acute necrotizing process. In the following months, cognitive status of the patient tended to improve although he remained hemiplegic, while serial MRI confirmed the tendency to the recovery of the lesion that was still present 1 year after. The present observation describes a progressive encephalopathy associated with immune suppression with an unusual feature and permanent brain damage.

Для цитирования: Aridon Paolo, Ragonese Paolo, Di Benedetto Norma, Grasso Giovanni, Conaldi Pier Giulio, D'Amelio Marco, Savettieri Giovanni. Progressive necrotic encephalopathy following tacrolimus therapy for liver transplantation.. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. 2009. DOI: 10.1007/s10072-009-0149-0.

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