Elevated liver enzymes in hospitalized patients with COVID-19 in Singapore

Abstract

Liver dysfunction in patients with COVID-19 (coronavirus disease 2019) has been described. However, it is not clear if the presence of abnormal liver function tests at presentation was related to underlying undiagnosed liver disease, or a result of the viral infection.We retrospectively examined the first 554 consecutive polymerase chain reaction positive SARS-CoV-2 patients admitted from February 2020 to April 2020 to our academic medical centre. We reviewed their clinical data, chest radiography and laboratory studies obtained within 24 hour of admission.Despite similar hemodynamic parameters, we found significant aspartate transaminase elevation (64 ± 141 vs 35 ± 23 U/L, P < .001) in those with pneumonia compared to those without. Elevated liver enzymes were seen in 102 patients (18.4%). They presented with higher temperatures (38.5 ± 0.9 vs 37.5 ± 0.8 degC, P = .011), higher total white cell counts (6.95 ± 2.29 vs 6.39 ± 2.19 x10 9 /L, P = .021), serum ferritin (240 ± 274 vs 165 ± 198 ng/ml, P = .002) and lactate dehydrogenase (632 ± 912 vs 389 ± 107 U/ L, P < .001). These patients were more likely to require intensive care (6.9% vs 2.7% P = .036) and mechanical ventilation (5.9% vs 2.2%, P = .046). Migrant workers from dormitories had a higher rate of baseline liver function test abnormalities (88/425 vs 14/129, P = .01), which were more likely to persist at the time of discharge.Despite relatively mild COVID-19 disease, there was a significant prevalence of liver dysfunction, particularly amongst migrant workers. Elevated liver enzymes were associated with more severe disease, despite similar haemodynamic characteristics. Future studies should explore whether pre-existing liver disease may predispose to more severe COVID-19 disease.Abbreviations: ALP = alkaline phosphatase, ALT = alanine transaminase, AST = aspartate transaminase, COVID-19 = coronavirus disease 2019, LDH = lactate dehydrogenase, LFT = liver function test, NAFLD = non-alcoholic fatty liver disease, ULN = upper limit of normal.

Inflammatory phenotypes may be more important than age and comorbidities in predicting clinical outcomes in hospitalised patients with COVID-19

“…Our findings showed that SARS-CoV-2 has different effects on individual patients, and we found these can be predicted more accurately by their inflammatory status than by age, comorbidities, and viral load, which were consistently associated with severe disease in the COVID-19 literature [25] . That the hyperinflammatory phenotype is a stronger predictor of progression to more severe disease may be explained by the association of inflammation with dysfunction in other organ systems beyond the respiratory system, such as the heart, lungs, and kidneys [26 , 27] .…”

Response to comments on: Silent hypoxia: pulse oximetry and its relation to COVID-19 in Singapore

“…In a moderately sized, retrospective cohort of hospitalised patients with mild COVID-19, consisting of primarily young and immunocompetent migrant workers in Singapore, we had observed that the infection can present with multi-system involvement, including cardiac manifestations,[ 4 ] kidney injury,[ 5 ] altered haematological profile[ 6 ] and elevated liver enzymes. [ 7 ] While some of these organ-specific complications may be related to the uncontrolled host inflammatory response to the viral infection, a majority of the patients we had examined were largely afebrile, asymptomatic and with relatively mild disease. As a result, direct viral invasion into these specific tissues may also be possible and contributes to the organ-specific manifestations.…”