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Liver failure in mitochondrial DNA depletion syndrome: the importance of serial neuroimaging in liver transplantation evaluation.

Mitochondrial DNA (mtDNA) is inherited maternally and codes for a mitochondrion’s ribosomal proteins, tRNAs, and 13 of its respiratory chain proteins. mtDNA depletion occurs when mtDNA levels are quantitatively significantly decreased, usually with <1 residual molecule per mitochondrion (normal number of 2–10) (1). In a single cell normal and mutated mtDNA may coexist (ie, heteroplasmy). The threshold of mutated mtDNA for a deleterious phenotype is variable and mtDNA depletion is tissue specific. It may be expressed in a single organ or multiple organs, resulting in diverse clinical manifestations. In addition to liver failure in infancy (1), other clinical manifestations of mtDNA deletion syndrome (MDS) include myopathy or encephalomyopathy, lactic acidosis, heart failure, renal tubulopathy, and neurological abnormalities (2). Liver transplantation is a potential treatment option for end-stage liver disease from MDS. Contraindications to transplantation, including involvement of vital organs such as the brain, need to be actively investigated (3). The severity of extrahepatic involvement may be variable. Mild extrahepatic involvement may not be a contraindication to transplantation. We report on a child with