2022
DOI: 10.5501/wjv.v11.i5.310
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COVID-19 and hemolysis, elevated liver enzymes and thrombocytopenia syndrome - association or causation?

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Cited by 5 publications
(3 citation statements)
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“…Recent research revealed several associations between SARS-CoV-2 infection and medical conditions that may lead to liver dysfunction[ 43 ]. Moreover, studies have demonstrated that there is an increased risk of decompensation and mortality in COVID-19 patients with pre-existing cirrhosis[ 44 ].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Recent research revealed several associations between SARS-CoV-2 infection and medical conditions that may lead to liver dysfunction[ 43 ]. Moreover, studies have demonstrated that there is an increased risk of decompensation and mortality in COVID-19 patients with pre-existing cirrhosis[ 44 ].…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, studies have demonstrated that there is an increased risk of decompensation and mortality in COVID-19 patients with pre-existing cirrhosis[ 44 ]. This can possibly be attributed to cirrhosis-related immunological modulation, insufficient physiological reserves, and an increased risk of severe COVID-19 disease[ 43 , 44 ]. The underlying mechanism of liver injury secondary to COVID-19 is multifactorial.…”
Section: Discussionmentioning
confidence: 99%
“…COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been rapidly spreading around the world since its emergence and is mainly transmitted by droplets and contact, leading to its strong infectivity and fast propagation speed. After people become infected with SARS-CoV-2, the S-spike protein binds to angiotensin-converting enzyme 2 on the alveolar epithelial cell surface by mediating transmembrane serine protease 2[ 3 ], viral pneumonia occurs, and a hyperinflammatory syndrome or “cytokine storm” may develop, further leading to many complications such as acute respiratory distress syndrome (ARDS), thromboembolic events, septic shock, and multiple organ failure. Virologists assumed[ 1 ] that the virus attaches to and penetrates the hosts’ airway epithelial cells, leading to cellular dysfunction and apoptosis via many mechanisms; weakens the hosts’ immune system, contributing to the proliferation, colonisation and invasive infection of opportunistic pathogens or normal respiratory flora; obstructs the innate immune response; compresses the airway mucus; and destroys the cilia, promoting virus transmission and adhesion.…”
Section: Discussionmentioning
confidence: 99%