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Sequential measurement of Trypanosoma cruzi parasitic load in endomyocardial biopsies for early detection and follow‐up of Chagas disease reactivation after heart transplantation
Author(s) -
Benvenuti Luiz Alberto,
Roggério Alessandra,
Nishiya Anna Shoko,
Mangini Sandrigo,
Levi José Eduardo
Publication year - 2020
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/tid.13209
Subject(s) - trypanosoma cruzi , chagas disease , heart transplantation , medicine , parasite load , parasitic infection , transplantation , histopathology , endomyocardial biopsy , viral load , biopsy , gastroenterology , immunology , pathology , parasite hosting , immune system , human immunodeficiency virus (hiv) , world wide web , computer science
Abstract Background Reactivation of Chagas disease after heart transplantation is characterized by proliferation and dissemination of Trypanosoma cruzi parasites to several organs. Reactivation affecting the allograft can simulate acute cellular rejection, from which it should be distinguished through the analysis of endomyocardial biopsies (EMB). Methods We evaluated retrospectively 100 EMB collected in the first year of follow‐up from 13 heart‐transplanted, chagasic patients who presented reactivation and were successfully treated. Additionally, 37 EMB from 8 patients who did not present reactivation constituted the control group. We reviewed histopathology and performed a real‐time PCR‐based assay in order to evaluate the T cruzi parasitic load of each EMB. Results The parasitic load of the EMB at the time of reactivation ranged from 22.80 to 190 000/10 6 cells (median: 1555). In 6 patients, none of the EMB obtained prior to reactivation amplified T cruzi DNA. On the other hand, 10 EMB from 7 patients, obtained 9‐105 days before reactivation (median: 26 days), showed parasitic load ranging from 8.25 to 625/10 6 cells (median: 167.55). In all patients, the parasitic load increased at the time of reactivation, usually sharply. After initiation of treatment, all patients showed negative PCR or a dramatic reduction of the parasitic load in the following EMB. None of the EMB from the control group amplified T cruzi DNA. Conclusions Sequential measurement of T cruzi parasitic load in EMB is useful for monitoring Chagas disease reactivation after heart transplantation. Its increase suggests imminent reactivation and its decrease after treatment indicates favorable evolution for cure of the episode of reactivation.