Reply
Authors: Martin Krüger, Simon C. Robson, Jan Schulte am Esch
Journal: Clinical Gastroenterology and Hepatology (2021)

We thank Mr Ng for his insightful remarks related to COVID-19, liver injury, and regeneration in our recent article.1Kaltschmidt B. et al.Clin Gastroenterol Hepatol. 2021 Jan 29; (S1542-3565(21)00094-X. https://doi.org/10.1016/j.cgh.2021.01.044. Online ahead of print)PubMed Google Scholar These additional comments will help to open up commentary on the possible long-term consequences with COVID-19 in liver transplant (LT) recipients, particularly in the setting of severe disease and/or reinfection. However, it is hoped that widespread and early use of COVD-19 vaccines in these patients may preclude some of these concerns.2Fix O.K. et al.Hepatology. 2021 Feb 12; (10.1002/hep.31751. https://doi.org/10.1002/hep.31751. Online ahead of print)PubMed Google Scholar,3Cornberg M. et al.J Hepatol. 2021; 74: 944-951Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar In our own work, we investigated patterns of liver injury, vascular involvement, and regeneration in 60 patients who died of COVID-19 pneumonia, along with 13 patients who died of non-COVID fatal pneumonia (serving as disease control subjects). There are other autopsy studies where COVID-19 has been likewise significantly associated with liver involvement and thromboembolic complications.4Wichmann D. et al.Ann Intern Med. 2020; 173: 268-277Crossref PubMed Scopus (1754) Google Scholar Additional recent publications indicate that the presence of underlying liver disease can provoke worse outcomes in COVID-19 disease.5Kim D. et al.Clin Gastroenterol Hepatol. 2021; 19: 1469-1479Abstract Full Text Full Text PDF PubMed Scopus (152) Google Scholar COVID-19 in LT recipients results in higher numbers of intensive care unit admission and rates of mechanical ventilation.6Rabiee A. et al.Hepatology. 2020; 72: 1900-1911Crossref PubMed Scopus (55) Google Scholar,7Jayant K. et al.Clin Transplant. 2021; e14246PubMed Google Scholar LT patients with COVID-19 do exhibit a higher risk of acute liver injury, which may mirror the histopathologic findings we have noted in nontransplant patients. We might postulate, that direct damage of liver cells by SARS-CoV-2 and changes of immunometabolic responses might provoke severe liver injury especially in immunosuppressed LT recipients with coexistent metabolic syndrome, as noted previously. Our data on regenerative responses in fatal COVID-19 revealed increased frequency of hepatic stem/progenitor cells. The relevance of such histopathologic changes of hepatic repair for patients in the course of LT or other concomitant pathophysiological scenarios of the liver in COVID-19 remains unclear. We agree that adverse possibilities may be afforded by SARS-CoV-2 "long-haul" outcomes, reinfection, and emergence of variant viruses. These do raise the spectra of irreversible graft disease, which might increase risks of retransplantation. This area of clinical endeavor requires further research with elucidation of pathogenic mechanisms and better determination of risk to help answer the provocative questions raised by Mr. Ng. Fatty Liver and Type 2 Diabetes Mellitus Regression: The Weight, the Fat, and the AlcoholClinical Gastroenterology and HepatologyVol. 20Issue 2PreviewI read with interest the results reported by Yamazaki et al.1 Type 2 diabetes mellitus (T2D) remission was less frequent in patients with fatty liver (adjusted odds ratio, 0.51; 95% confidence interval [CI], 0.37–0.72). Moreover, fatty liver improvement was independently associated with T2D remission. Full-Text PDF