RESUMEN
Kaposi sarcoma (KS) can develop following organ transplantation through reactivation of recipient human herpesvirus 8 (HHV-8) infection or through donor-derived HHV-8 transmission. We describe 6 cases of donor-derived HHV-8 infection and KS investigated from July 2018 to January 2020. Organs from 6 donors, retrospectively identified as HHV-8-positive, with a history of drug use disorder, were transplanted into 22 recipients. Four of 6 donors had risk factors for HHV-8 infection reported in donor history questionnaires. Fourteen of 22 organ recipients (64%) had evidence of posttransplant HHV-8 infection. Lung recipients were particularly susceptible to KS. Four of the 6 recipients who developed KS died from KS or associated complications. The US opioid crisis has resulted in an increasing number and proportion of organ donors with substance use disorder, and particularly injection drug use history, which may increase the risk of HHV-8 transmission to recipients. Better awareness of the risk of posttransplant KS for recipients of organs from donors with HHV-8 infection risk could be useful for recipient management. Testing donors and recipients for HHV-8 is currently challenging with no validated commercial serology kits available. Limited HHV-8 antibody testing is available through some US reference laboratories and the Centers for Disease Control and Prevention.
Asunto(s)
Herpesvirus Humano 8 , Trasplante de Riñón , Sarcoma de Kaposi , Humanos , Estudios Retrospectivos , Sarcoma de Kaposi/etiología , Donantes de TejidosRESUMEN
BACKGROUND: The impact of pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD) on survival after lung transplantation (LTx) is not known. MATERIAL AND METHODS: First-time adult LTx recipients with COPD transplanted between May 2005 and September 2013 were identified in the United Network for Organ Sharing Registry database, and tracked from transplant date until death or censoring. Right heart catheterization (RHC) measurements at time of wait listing were used to predict all-cause mortality after LTx, with multivariable analyses stratified by transplant type. RESULTS: Of 3362 COPD LTx recipients, 3105 were included in the analytic sample, with multiple imputation used to complete missing data on covariates. Multivariable analysis found the hazard of death to increase with a 10 mmHg increase in mean pulmonary artery pressure (mPAP) among recipients of bilateral LTx (HR = 1.12; 95% CI = 1.01, 1.24; p = 0.032), but not among recipients of single LTx (HR = 0.92; 95% CI = 0.80, 1.06; p = 0.234). CONCLUSION: PH prior to bilateral LTx in patients with COPD is associated with higher mortality risk.