Liver injury in COVID-19: Detection, pathogenesis, and treatment

Cai, Yue; Ye, Liping; Song, Yu; Mao, Xin-Li; Wang, Li; Jiang, Yanrui; Que, Weitao; Li, Shaowei

doi:10.3748/wjg.v27.i22.3022

Cited by 25 publications

(24 citation statements)

References 79 publications

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“…SARS-CoV-2 infection induces inflammation of the vascular endothelium, thereby causing vascular dysfunction, especially in capillaries. Subsequently, microvascular dysfunction leads to a hypercoagulable state, tissue edema, and organ ischemia [12,16,17]. All these evidence support that SARS-CoV-2 may directly or indirectly cause acute cholecystitis.…”

Section: Discussionmentioning

confidence: 77%

“…This viral RNA detection in the gallbladder indicates direct vesicular involvement [14]. Otherwise, inflammatory cytokine storm generated by the excessive immune response could also be one of the key factors in hepatobiliary injury [12]. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which plasma levels are high in severe inflammatory response, may activate the coagulation cascade, explaining the presence of thrombosed vessels in the gallbladder and the occurrence of ischemic cholecystitis [11,15].…”

Section: Discussionmentioning

confidence: 88%

“…It is well known that SARS-CoV2 have a tropism not only to the lungs but also to the liver and the gallbladder. The intracellular entry of the virus occurs through interaction with the angiotensin-converting enzyme 2 receptor (ACE2), which expresses in relatively high amounts in lungs, vascular endothelium and gallbladder [11,12]. Therefore, patients with SARS-CoV-2 infection may be at increased risk from direct viral effects on the vascular endothelium and infection to the biliary tissue [13].…”

Section: Discussionmentioning

confidence: 99%

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"Acute Acalculous Cholecystitis Due to Covid-19: A Case Report"

Ferjaoui¹

2022

BJSTR

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Introduction:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was discovered in Wuhan, China, in late December 2019. It has emerged worldwide, with the consequent declaration of a pandemic disease (COVID-19). Besides pulmonary involvement, SARS-CoV-2 may affect other organs such as the liver, and rarely the gallbladder.Case Presentation: We report a case of a healthy 52-year-old man who was diagnosed with mild COVID-19 pneumonia. He developed progressive onset of rightsided hypochondrial pain during his hospital stay. Abdominal ultrasound and CT scan revealed acute acalculous cholecystitis (AAC). IV antibiotics were initiated but there was no clinical improvement, so surgery was decided. Intraoperative exploration revealed a distended gallbladder with gangrenous and thickened wall and emergent cholecystectomy was performed.Discussion: COVID-19 infection presenting with gallbladder involvement with acute acalculous cholecystitis is extremely rare. To our knowledge, only 10 cases were reported in the medical literature, since the pandemic declaration. While most of these cases were described in critically ill patients with long intensive care unit (ICU) stays, we report the third case of AAC on a healthy patient with mild COVID-19 pneumonia, who did not develop acute respiratory distress syndrome. By reviewing the recent literature, we noticed that the potential mechanisms of COVID-19-associated acalculous cholecystitis in non-ICU setting patients may include the direct effects of viral infection, inflammatory storm and endotheliitis. Conclusion:Through our case, we aim to highlight the importance of early detection and prompt management of biliary complications such as acute acalculous cholecystitis. As the pandemic continues to spread, further data are necessary to accurately assess the physiopathogenesis of hepatobiliary injury.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

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"Acute Acalculous Cholecystitis Due to Covid-19: A Case Report"

Ferjaoui¹

2022

BJSTR

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“…Current perspectives on the potential pathophysiological mechanisms of COVID-19 induced HRS are that of a multifactorial process (Figure 1 ). COVID-19 induced liver injury can be the result of direct viral cytopathic hepatocyte injury, systemic inflammatory cytokine storms causing hepatocyte cell death, endothelitis and dysfunction of the liver vasculature leading to widespread cell damage and ischemia, and drug-associated exacerbations in COVID-19 induced liver injury[ 25 , 26 ]. Subsequently, these multiple pathways of liver injury may result in circulatory dysfunction, progressing to HRS with vasoconstriction and hypoperfusion of the kidneys amongst other mechanisms[ 17 - 19 ].…”

Section: Potential Pathophysiological Mechanisms Of Covid-19 Induced Hrsmentioning

confidence: 99%

COVID-19 and hepatorenal syndrome

Wu¹,

Athwal²,

Kalra³

et al. 2022

World J Gastroenterol

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Coronavirus disease 2019 (COVID-19) is a highly infectious disease which emerged into a global pandemic. Although it primarily causes respiratory symptoms for affected patients, COVID-19 was shown to have multi-organ manifestations. Elevated liver enzymes appear to be commonly observed during the course of COVID-19, and there have been numerous reports of liver injury secondary to COVID-19 infection. It has been established that patients with pre-existing chronic liver disease (CLD) are more likely to have poorer outcomes following COVID-19 infection compared to those without CLD. Co-morbidities such as diabetes, hypertension, obesity, cardiovascular and chronic kidney disease frequently co-exist in individuals living with CLD, and a substantial population may also live with some degree of frailty. The mechanisms of how COVID-19 induces liver injury have been postulated. Hepatorenal syndrome (HRS) is the occurrence of kidney dysfunction in patients with severe CLD/fulminant liver failure in the absence of another identifiable cause, and is usually a marker of severe decompensated liver disease. Select reports of HRS following acute COVID-19 infection have been presented, although the risk factors and pathophysiological mechanisms leading to HRS in COVID-19 infection or following COVID-19 treatment remain largely unestablished due to the relative lack and novelty of published data. Evidence discussing the management of HRS in high-dependency care and intensive care contexts is only emerging. In this article, we provide an overview on the speculative pathophysiological mechanisms of COVID-19 induced HRS and propose strategies for clinical diagnosis and management to optimize outcomes in this scenario.

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“…Elevated bilirubin levels have been reported in COVID-19 patients with severe or critical diseases ( 11 , 12 ). There is also evidence of cholangiocyte injury due to higher ACE2 expression—a key receptor targeted by SARS-CoV-2, which leads to DBiL elevation ( 13 ). Elevated DBiL levels indicate the presence of cholestasis.…”

Section: Introductionmentioning

confidence: 99%

Effect of Direct Bilirubin Level on Clinical Outcome and Prognoses in Severely/Critically Ill Patients With COVID-19

Chen

Liu

et al. 2022

Front. Med.

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ObjectivesWe aimed to investigate how changes in direct bilirubin (DBiL) levels in severely/critically ill the coronavirus disease (COVID-19) patients during their first week of hospital admission affect their subsequent prognoses and mortality.MethodsWe retrospectively enrolled 337 severely/critically ill COVID-19 patients with two consecutive blood tests at hospital admission and about 7 days after. Based on the trend of the two consecutive tests, we categorized patients into the normal direct bilirubin (DBiL) group (224), declined DBiL group (44) and elevated DBiL group (79).ResultsThe elevated DBiL group had a significantly larger proportion of critically ill patients (χ2-test, p < 0.001), a higher risk of ICU admission, respiratory failure, and shock at hospital admission (χ2-test, all p < 0.001). During hospitalization, the elevated DBiL group had significantly higher risks of shock, acute respiratory distress syndrome (ARDS), and respiratory failure (χ2-test, all p < 0.001). The same findings were observed for heart damage (χ2-test, p = 0.002) and acute renal injury (χ2-test, p = 0.009). Cox regression analysis showed the risk of mortality in the elevated DBiL group was 2.27 (95% CI: 1.50–3.43, p < 0.001) times higher than that in the normal DBiL group after adjusted age, initial symptom, and laboratory markers. The Receiver Operating Characteristic curve (ROC) analysis demonstrated that the second test of DBiL was consistently a better indicator of the occurrence of complications (except shock) and mortality than the first test in severely/critically ill COVID-19 patients. The area under the ROC curve (AUC) combined with two consecutive DBiL levels for respiratory failure and death was the largest.ConclusionElevated DBiL levels are an independent indicator for complication and mortality in COVID-19 patients. Compared with the DBiL levels at admission, DBiL levels on days 7 days of hospitalization are more advantageous in predicting the prognoses of COVID-19 in severely/critically ill patients.

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Liver injury in COVID-19: Detection, pathogenesis, and treatment

Cited by 25 publications

References 79 publications

"Acute Acalculous Cholecystitis Due to Covid-19: A Case Report"

"Acute Acalculous Cholecystitis Due to Covid-19: A Case Report"

COVID-19 and hepatorenal syndrome

Effect of Direct Bilirubin Level on Clinical Outcome and Prognoses in Severely/Critically Ill Patients With COVID-19

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