| Literature DB >> 27421916 |
Roberto De Giorgio1, Loris Pironi2, Rita Rinaldi3, Elisa Boschetti2, Leonardo Caporali4, Mariantonietta Capristo4, Carlo Casali5, Giovanna Cenacchi6, Manuela Contin4,6, Roberto D'Angelo2,3, Antonietta D'Errico7, Laura Ludovica Gramegna6, Raffaele Lodi6, Alessandra Maresca4, Susan Mohamed4, Maria Cristina Morelli2, Valentina Papa6, Caterina Tonon6, Vitaliano Tugnoli6, Valerio Carelli4,6, Roberto D'Alessandro4, Antonio Daniele Pinna2.
Abstract
Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a fatal, recessive disease caused by mutations in the gene encoding thymidine phosphorylase, leading to reduced enzymatic activity, toxic nucleoside accumulation, and secondary mitochondrial DNA damage. Thymidine phosphorylase replacement has been achieved by allogeneic hematopoietic stem cell transplantation, a procedure hampered by high mortality. Based on high thymidine phosphorylase expression in the liver, a 25-year-old severely affected patient underwent liver transplantation. Serum levels of toxic nucleosides rapidly normalized. At 400 days of follow-up, the patient's clinical conditions are stable. We propose liver transplantation as a new therapy for MNGIE. Ann Neurol 2016;80:448-455.Entities:
Mesh:
Year: 2016 PMID: 27421916 DOI: 10.1002/ana.24724
Source DB: PubMed Journal: Ann Neurol ISSN: 0364-5134 Impact factor: 10.422