Liver dysfunction as a cytokine storm manifestation and prognostic factor for severe COVID-19

Taneva, Gergana T; Dimitrov, Dimitar; Velikova, Tsvetelina

doi:10.4254/wjh.v13.i12.2005

Cited by 18 publications

(13 citation statements)

References 35 publications

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“…The molecular biology behind hepatic impairment is currently being explored since researchers are starting to recognize that ALI emerges as a clinically significant consequence of COVID-19. The hyperinflammation resulting from the cytokine storm and immune dysfunction provoked by COVID-19 contributes to ALI[ 17 , 18 ]. Pathological evidence of typical viral infection lesions with scarce CD4 + and CD8 + lymphocytes indicates that SARS-CoV-2 directly infects the liver[ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Acute liver injury in a COVID-19 infected woman with mild symptoms: A case report

Lai¹,

Ding²

2023

World J Clin Cases

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BACKGROUND Coronavirus disease 2019 (COVID-19) has spread rapidly, resulting in a pandemic in January 2020. Few studies have focused on the natural history and consequences of acute liver injury (ALI) in mild or asymptomatic COVID-19 patients, manifested by elevated aminotransferase levels. ALI is usually expected for severe COVID-19 cases. Here, we present a COVID-19 case with mild respiratory symptoms and significantly elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. CASE SUMMARY A 60-year-old woman without medical history or chronic illness received three COVID-19 vaccinations since the start of the pandemic. The patient was infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and presented with mild symptoms on July 12 th , 2022. Post-recovery, she underwent an examination at our hospital on August 30 th , 2022. AST and ALT levels in the liver function test were 207 U/L (normal value < 39, 5.3-fold increase) and 570 U/L (normal value < 52, 10.9-fold increase), respectively. The patient was diagnosed with ALI, and no treatment was prescribed. The following week, blood tests showed a reduction in both levels (ALT 124 U/L, AST 318 U/L). Two weeks later, AST and ALT levels had decreased to near the expected upper limits (ALT 40 U/L, AST 76 U/L). CONCLUSION Clinicians should pay attention to liver function testing during COVID-19 recovery regardless of the disease’s severity.

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Section: Discussionmentioning

confidence: 99%

Acute liver injury in a COVID-19 infected woman with mild symptoms: A case report

Lai¹,

Ding²

2023

World J Clin Cases

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“…Therefore, just ACE2 increase alone is not the only explanation for tissue virus infection, corroborating our previously published finding that although ACE2 is increased in the liver of COVID-19 patients, no SARS-CoV-2 was found in the identical specimens ( Santana et al, 2021 ). Moreover, cytokine storms can occur in severe SARS-CoV-2 infection ( Mangalmurti and Hunter, 2020 ), and it is higher in subjects with liver dysfunction than those with normal hepatic tests ( Premkumar and Kedarisetty, 2021 ; Taneva et al, 2021 ). Besides the pro-inflammatory role ( Fara et al, 2020 ), cytokines regulate the expression level of several molecules, including the bradykinin receptors ( Ricciardolo et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

The des-Arg9-bradykinin/B1R axis: Hepatic damage in COVID-19

et al. 2022

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Patients infected by the SARS-CoV-2 virus are commonly diagnosed with threatening liver conditions associated with drug-induced therapies and systemic viral action. RNA-Seq data from cells in bronchoalveolar lavage fluid from COVID-19 patients have pointed out dysregulation of kallikrein-kinin and renin-angiotensin systems as a possible mechanism that triggers multi-organ damage away from the leading site of virus infection. Therefore, we measured the plasma concentration of biologically active peptides from the kallikrein-kinin system, bradykinin and des-Arg9-bradykinin, and liver expression of its proinflammatory axis, bradykinin 1 receptor (B1R). We measured the plasma concentration of bradykinin and des-Arg9-bradykinin of 20 virologically confirmed COVID-19 patients using a liquid chromatography-tandem mass spectrometry-based methodology. The expression of B1R was evaluated by immunohistochemistry from post-mortem liver specimens of 27 COVID-19 individuals. We found a significantly higher blood level of des-Arg9-bradykinin and a lower bradykinin concentration in patients with COVID-19 compared to a healthy, uninfected control group. We also observed increased B1R expression levels in hepatic tissues of patients with COVID-19 under all hepatic injuries analyzed (liver congestion, portal vein dilation, steatosis, and ischemic necrosis). Our data indicate that des-Arg9-bradykinin/B1R is associated with the acute hepatic dysfunction induced by the SARS-CoV-2 virus infection in the pathogenesis of COVID-19.

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“…The lack of direct evidence of adenovirus on immunostaining of liver tissue points towards a possible virus-induced hyperimmunologic reaction rather than direct viral cytotoxicity, but the specific pathogenesis of liver injury remains unknown. Cytokine storm has been identified as a likely major factor in COVID-19 infected patients who developed liver failure [ 16 ]. The role of SARS-CoV-2 as a potential cofactor remains an important clinical focus, either as a postinfectious sequela like multisystem inflammatory syndrome in children, or potentially due to SARS-CoV-2 superantigen-mediated immune activation [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

Use of Cidofovir for Safe Transplantation in a Toddler with Acute Liver Failure and Adenovirus Viremia

Christian

Sarwar

Resch

et al. 2022

Case Reports in Transplantation

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Background. Since October 2021, there have been more than 500 cases of severe hepatitis of unknown origin in children reported worldwide, including 180 cases in the U.S. The most frequently detected potential pathogen to date has been adenovirus, typically serotype 41. Adenovirus is known to cause a self-limited infection in the immunocompetent host. However, in immunosuppressed individuals, severe or disseminated infections may occur. Method. We present the case of a two-year-old female who presented with cholestatic hepatitis and acute liver failure (ALF). Work up for etiologies of ALF was significant for adenovirus viremia, but liver biopsy was consistently negative for the virus. The risk for severe adenoviral infection in the setting of anticipated immunosuppression prompted us to initiate cidofovir to decrease viral load prior to undergoing liver transplantation. Result. Our patient received a successful liver transplant, cleared the viremia after 5 doses of cidofovir, and continues to maintain allograft function without signs of infection at the time of this report, 5 months posttransplant. Conclusion. Recent reports of pediatric hepatitis cases may be associated with adenoviral infection although the exact relationship is unclear. There is the possibility of the ongoing SARS-CoV-2 environment, or other immunologic modifying factors. All patients presenting with hepatitis or acute liver failure should be screened for adenovirus and reported to state health departments. Cidofovir may be used to decrease viral load prior to liver transplantation, to decrease risk of severe adenoviral infection.

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Liver dysfunction as a cytokine storm manifestation and prognostic factor for severe COVID-19

Cited by 18 publications

References 35 publications

Acute liver injury in a COVID-19 infected woman with mild symptoms: A case report

Acute liver injury in a COVID-19 infected woman with mild symptoms: A case report

The des-Arg9-bradykinin/B1R axis: Hepatic damage in COVID-19

Use of Cidofovir for Safe Transplantation in a Toddler with Acute Liver Failure and Adenovirus Viremia

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