The Domino Effect: Two Donor Livers Serve Four Patients
Jan. 13, 2000 (Boston) -- With typical New England thrift, surgeons from the Lahey Clinic in Burlington, Mass., last week performed two rare "domino" transplants, implanting livers from two cadavers into two patients with liver damage from a metabolic disease. The diseased but still functional livers removed from the recipients were then given to two other patients with livers irreparably damaged by hepatitis C infections.
The novel domino transplant technique, which has been performed only about 40 times throughout the world, holds the promise of a new lease on life for patients who might otherwise not be good candidates for liver transplants, and at least partially addresses the critical problem of a shortage of donor organs, says Frederick Gordon, MD. Gordon is the director of hepatology and medical director of the liver transplant program at the Lahey Clinic.
"The number of patients on the transplant waiting list is increasing exponentially, but if you look at the number of donors nationally and in New England, it's the same thing year after year," says Gordon in an interview with WebMD. "Any way that we can increase the donor pool is beneficial, whether it's with domino transplants, living donor transplants, or split livers, it can certainly have a positive affect upon the organ supply."
The donor-recipients were a 66-year-old man and a 28-year-old woman with familial amyloid polyneuropathy (FAP), a rare inherited disorder in which a genetic mutation within the liver causes the organ to manufacture a mutated version of a normal protein called amyloid transthyretin (ATTR). The mutated protein builds up within the liver, nervous system, and other organs, causing numbness and tingling in the arms and legs, dizziness on standing, and diarrhea, among other symptoms. Removing the liver and replacing it with a donor organ -- the only treatment known to be effective for FAP -- removes the source of the mutated protein and allows the donor liver to manufacture the normal protein, thereby halting disease progression. It is still not known, however, what happens to existing ATTR deposits in the bodies of patients with FAP.