The Lewis blood group system in liver transplantation.

THE LEWIS blood group antigens Lea and Leb have been found on red blood cells (RBCs), in secretions and fluids such as saliva, alimentary tract juice, and urine, and in various tissues including renal tubular cells, collecting ducts, urothelium, and ductal or mucosal epithelium of the sweat glands, salivary glands, gastrointestinal tract, pancreas, uterus, cervix, and breast. l .s Hepatic bile duct epithelium also contains Lewis antigens.9 Lewis antigens in secretions are glycoproteins. RBC Lewis antigens are glycolipids acquired from plasma and are not intrinsic to the RBCs.6,lo Transfused RBCs have been found to assume the recipient's Lewis phenotype by absorption or loss of antigens within two to seven days,B.12 and bone marrow transplant patients retain their own RBC Lewis phenotype, not that of their donors. 13,14 The site of origin of Lewis plasma glycolipids is uncertain. Evans et aI's proposed the small intestine as a possible source. Crookstonl6 suggested that the study of RBC Lewis phenotypes in liver transplants would shed light on this issue. Lewis antibodies are generally clinically insignificant in RBC compatibility, in part because of the shift of transfused RBCs to the recipient's phenotype. 12 However, in renal transplantation, Lewis incompatibility has been reported to adversely affect graft survival. l7•l9 Some Lewis antibodies are lymphocytotoxicl9 and others are not detected by routine hemagglutination techniques. IS In one case an anti-host Lewis antibody of bone marrow graft origin was associated with renal failure in the recipient.20 However, other clinical studies have not found a significant adverse effect of Lewis incompatibility in renal transplantation.21.23 On a random basis by prediction from Lewis phenotype frequencies,24 an estimated 20% of whites and 35% of blacks getting transplants from unrelated donors receive Lewis-incompatible organs. These figures are derived from the sum of approximately 5% of whites and 20% of blacks who are Le(ab-) and predicted to receive Lewis-positive grafts, plus another 15% in each group who are Le(a + b -) and predicted to receive Le(a-b+) organs. We studied Lewis-incompatible liver transplants with regard to the subsequent recipient RBC Lewis phenotype and the graft outcome. Our goals were twofold: (1) to assess the role of the Lewis blood group system in hepatic transplant compatibility, and (2) to determine whether the liver is the source of RBC Lewis antigens.