Moreover, the survising decrease of extrahepatic deposits of amylopectin in glycogen storage disease type IV and of glucocerebroside in Gaucher's disease type I after liver transplantation opens the possibility that the microchimerism due to migration of lymphocytes/macrophages from the donor's liver tothe host's extrahepatic sites result in cell-to-cell enzyme transmission; this may not be true in all instances, however, as shown by some lipid storage diseases, where neurological involvement may not be prevented by liver transplatation.
In diseases that do not result in severe liver damage, gene theraphy my provide a less risky solution in the future; auxiliary transplantation leaving the recipient's right lobe in place might prove a satisfactory way of awaiting the availability of gene theraphy.
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