3 years ago

Nonhemolytic passenger lymphocyte syndrome

Albert Langeberg, Cal Matsumoto, S. Gerald Sandler, Suhua Han, Thomas M. Fishbein
BACKGROUND An 8-month-old recipient of a liver segment transplant had anti-D detected for the first time in her Day 5 posttransplant plasma and anti-C detected for the first time in her Day 55 posttransplant plasma. The donor's plasma contained anti-C and anti-D. Clinical and laboratory findings established a diagnosis of passenger lymphocyte syndrome (PLS). Hemolysis did not occur, because the recipient's blood group phenotype was, by chance, D– C–. STUDY DESIGN AND METHODS To evaluate contemporary practice for diagnosing PLS, we conducted a retrospective 10-year literature review. RESULTS There were 31 studies (63 cases) of PLS of which eight cases (four studies) were hematopoietic stem cell and 55 (27 studies) were organ transplants. All eight (100%) hematopoietic stem cell and 52 (95%) organ transplants were associated with hemolysis. Of the four studies of hematopoietic stem cell PLS, three actively screened for posttransplant blood group antibodies. Of 27 studies of organ PLS, one actively screened for antibodies. Antibody screens detected five cases of hematopoietic stem cell PLS before hemolysis was apparent and two cases of organ PLS with antibodies without hemolysis. CONCLUSION Focusing on hemolysis, without a comparable effort to detect donor-derived antibodies diverts from the primary pathophysiology of PLS and limits capturing the full scope of the syndrome. Recognition of hemolytic and nonhemolytic subcategories of PLS is recommended. When feasible, an antibody screen performed on the donor's plasma when collecting the hematopoietic stem cells or before an organ harvest could result in an alert that the donor has formed an alloantibody(s) and the recipient is a risk for PLS. Alternatively, a routine antibody screen performed on the recipient's plasma 1 week posttransplant and, if negative, repeated 3 to 5 weeks posttransplant would detect any donor-derived antibodies and improve alignment of clinical practice with the pathophysiology of PLS.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/trf.14383

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