Clinical features and mechanism of liver injury in patients with mild or moderate coronavirus disease 2019.
coronavirus disease 2019
liver injury
liver‐infiltrating lymphocytes
severe acute respiratory syndrome coronavirus 2
Journal
JGH open : an open access journal of gastroenterology and hepatology
ISSN: 2397-9070
Titre abrégé: JGH Open
Pays: Australia
ID NLM: 101730833
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
received:
14
05
2021
accepted:
11
06
2021
entrez:
13
8
2021
pubmed:
14
8
2021
medline:
14
8
2021
Statut:
epublish
Résumé
We aimed to identify clinical features that suggest that coronavirus disease 2019 (COVID-19) should be a differential diagnosis in patients presenting with a chief complaint of fever and abnormal liver function. We retrospectively studied the presence or absence of abnormal liver function in 216 patients diagnosed with mild-moderate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection between February and September 2020. Abnormal liver function was observed in 51 patients with mild-moderate COVID-19. The median peak aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels were 57.5, 75.5, and 332.5 U/L, respectively. The median number of days from symptom onset to peak AST, ALT, and LDH were 8.5, 9, and 8.5, respectively. The median peak LDH/AST ratio was 9.0. Low lymphocyte-to-white blood cell ratio and elevated LDH were found to be independent contributing factors for intensive care unit (ICU) admission on a multivariate analysis. AST-predominant AST/ALT/LDH elevation peaking 8-9 days after symptom onset and not accompanied by elevated alkaline phosphatase or gamma-glutamyl transferase may be a useful clinical feature for differentiating COVID-19 from other diseases. Since the median LDH/AST ratio was 9.0, it seems that the abnormal liver function caused by SARS-CoV-2 is an indirect damage to liver cells due to elevated cytokine levels caused by liver-infiltrating lymphocytes. SARS-CoV-2 infection should be considered in patients presenting with a chief complaint of fever and liver injury; those with a high lymphocyte-to-white blood cell ratio or and a high LDH/AST ratio may be admitted to the ICU.
Sections du résumé
BACKGROUND AND AIM
OBJECTIVE
We aimed to identify clinical features that suggest that coronavirus disease 2019 (COVID-19) should be a differential diagnosis in patients presenting with a chief complaint of fever and abnormal liver function.
METHODS
METHODS
We retrospectively studied the presence or absence of abnormal liver function in 216 patients diagnosed with mild-moderate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection between February and September 2020.
RESULTS
RESULTS
Abnormal liver function was observed in 51 patients with mild-moderate COVID-19. The median peak aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels were 57.5, 75.5, and 332.5 U/L, respectively. The median number of days from symptom onset to peak AST, ALT, and LDH were 8.5, 9, and 8.5, respectively. The median peak LDH/AST ratio was 9.0. Low lymphocyte-to-white blood cell ratio and elevated LDH were found to be independent contributing factors for intensive care unit (ICU) admission on a multivariate analysis.
CONCLUSIONS
CONCLUSIONS
AST-predominant AST/ALT/LDH elevation peaking 8-9 days after symptom onset and not accompanied by elevated alkaline phosphatase or gamma-glutamyl transferase may be a useful clinical feature for differentiating COVID-19 from other diseases. Since the median LDH/AST ratio was 9.0, it seems that the abnormal liver function caused by SARS-CoV-2 is an indirect damage to liver cells due to elevated cytokine levels caused by liver-infiltrating lymphocytes. SARS-CoV-2 infection should be considered in patients presenting with a chief complaint of fever and liver injury; those with a high lymphocyte-to-white blood cell ratio or and a high LDH/AST ratio may be admitted to the ICU.
Identifiants
pubmed: 34386596
doi: 10.1002/jgh3.12599
pii: JGH312599
pmc: PMC8341189
doi:
Types de publication
Journal Article
Langues
eng
Pagination
888-895Informations de copyright
© 2021 The Authors. JGH Open published by Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.
Références
Lancet Gastroenterol Hepatol. 2020 May;5(5):428-430
pubmed: 32145190
Hepatology. 1988 Sep-Oct;8(5):1138-9
pubmed: 3417236
N Engl J Med. 2020 Apr 30;382(18):1708-1720
pubmed: 32109013
Arch Intern Med. 1987 Jun;147(6):1111-3
pubmed: 3592876
BMJ. 2020 Feb 19;368:m606
pubmed: 32075786
Lancet Infect Dis. 2020 Apr;20(4):425-434
pubmed: 32105637
J Adolesc Health Care. 1988 May;9(3):203-7
pubmed: 3372286
Arch Intern Med. 1983 Apr;143(4):674-7
pubmed: 6838292
Rinsho Byori. 2001 Nov;Suppl 116:81-9
pubmed: 11797384
Lancet. 2020 Feb 15;395(10223):507-513
pubmed: 32007143
Lancet Respir Med. 2020 May;8(5):475-481
pubmed: 32105632
JAMA. 2020 May 26;323(20):2052-2059
pubmed: 32320003
Lancet. 2020 Mar 28;395(10229):1054-1062
pubmed: 32171076
Liver Int. 2020 May;40(5):998-1004
pubmed: 32170806
Lancet. 2020 Feb 15;395(10223):497-506
pubmed: 31986264
Gut. 2021 Apr;70(4):733-742
pubmed: 32641471