Literature DB >> 34425021

Elevated levels of circulating mitochondrial DNA predict early allograft dysfunction in patients following liver transplantation.

Osamu Yoshino1, Boris Ka Leong Wong2,3, Daniel R A Cox1,2, Eunice Lee1, Graham Hepworth4, Christopher Christophi1, Robert Jones1, Alexander Dobrovic1,2, Vijayaragavan Muralidharan1, Marcos V Perini1.   

Abstract

BACKGROUND AND AIM: The role of circulating mitochondrial DNA (cmtDNA) in transplantation remains to be elucidated. cmtDNA may be released into the circulation as a consequence of liver injury; yet recent work also suggests a causative role for cmtDNA leading to hepatocellular injury. We hypothesized that elevated cmtDNA would be associated with adverse events after liver transplantation (LT) and conducted an observational cohort study.
METHODS: Twenty-one patients were enrolled prospectively prior to LT.
RESULTS: Postoperative complications were observed in 47.6% (n = 10). Seven patients (33.3%) had early allograft dysfunction (EAD), and six patients (28.5%) experienced acute cellular rejection within 6 months of LT. cmtDNA levels were significantly elevated in all recipients after LT compared with healthy controls and preoperative samples (1 361 937 copies/mL [IQR 586 781-3 399 687] after LT; 545 531 copies/mL [IQR 238 562-1 381 015] before LT; and 194 562 copies/mL [IQR 182 359-231 515] in healthy controls) and returned to normal levels by 5 days after transplantation. cmtDNA levels were particularly elevated in those who developed EAD in the early postoperative period (P < 0.001). In all patients, there was initially a strong overall positive correlation between cmtDNA and plasma hepatocellular enzyme levels (P < 0.05). However, the patients with EAD demonstrated a second peak in cmtDNA at postoperative day 7, which did not correlate with liver function tests.
CONCLUSIONS: The early release of plasma cmtDNA is strongly associated with hepatocellular damage; however, the late surge in cmtDNA in patients with EAD appeared to be independent of hepatocellular injury as measured by conventional tests.
© 2021 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.

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Keywords:  Allograft dysfunction; Cell-free DNA; Ischemia/reperfusion; Liver immunobiology; Liver transplantation; Mitochondrial DNA

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Year:  2021        PMID: 34425021     DOI: 10.1111/jgh.15670

Source DB:  PubMed          Journal:  J Gastroenterol Hepatol        ISSN: 0815-9319            Impact factor:   4.029


  1 in total

1.  Developing a new nomogram to predict early allograft dysfunction after liver transplantation: a nudge in the right direction.

Authors:  Gang Xu; Chen-Hao Jiang; Tao Lv; Jiu-Lin Song; Yong-Jie Zhou; Jian Yang; Li Jiang; Lyu-Nan Yan; Kui Luo; Jia-Yin Yang
Journal:  Hepatobiliary Surg Nutr       Date:  2022-06       Impact factor: 8.265

  1 in total

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