Augmenting the Unites States transplant registry with external mortality data: A moving target ripe for further improvement.

The Organ Procurement and Transplantation Network conducts a robust death verification process when augmenting the United States transplant registry with external sources of data. Process enhancements added over 35,000 externally verified deaths across waitlist candidates and transplant recipients for all organs beginning in April 2022. Ninety-four percent of added posttransplant deaths occurred beyond 5 years posttransplant, and over 74% occurred beyond 10 years. Deceased donor solid organ recipients transplanted from January 1, 2010, through October 31, 2020, were analyzed from January and July 2022 Organ Procurement and Transplantation Network Standard Transplant Analysis and Research and the Scientific Registry of Transplant Recipients Standard Analysis Files to quantify the impact of including vs excluding unverified deaths (not releasable to researchers) on posttransplant patient survival estimates. Across all organs, 1- and 5-year posttransplant survival rates were not substantially impacted; meaningful differences were observed in 10-year survival among kidney recipients. These findings bear important implications for anyone who utilized transplant registry data to examine long-term outcomes prior to the updated verification process. Users of transplant surveillance data should interpret results of long-term outcomes cautiously, particularly differences across subpopulations, and the transplant community should identify ways to improve data quality and minimize the reporting burden on transplant institutions.

Proliferative suppression and class I insufficiency on peripheral blood cells from hepatitis C patients overcome by exogenous cytokines or high-dose mitogen.

An abnormal T cell response to HCV viral infection is speculated to cause viral persistence, although the mechanism(s) is not understood. Using a classical in vitro test of T cell vigor, proliferative responses to PHA were determined in PBLs from 92 HCV+ individuals and 35 healthy noninfected controls. In addition, since HLA antigens modulate proliferation, surface HLA content was measured by quantitative flow cytometry. The proliferative response of cells from HCV+ individuals was lower than that of controls (SI of 91 +/- 70 vs 219 +/- 70, P < .0001). In addition, class I content was underexpressed on cells from HCV+ individuals (4540 +/- 1359 vs 13,180 +/- 5511 MESF units, P < .0001) after 5 days of PHA stimulation. Class II content was also lower than that of controls (89 +/- 17 vs 124 +/- 61 MESF units, P < .0001) after PHA stimulation. Treatment of cells from HCV+ individuals with a high dose of PHA corrected proliferative hyporesponsiveness (P < 0.01) and class I and II insufficiency (P = 0.02). Treatment with exogenous IL-2 or IFN-gamma corrected proliferative reduction (P < 0.01) but not HLA antigen content (P = ns). The results show a biochemical and functional abnormality in PBLs from HCV+ individuals, which may contribute to HCV chronicity.