tetano
Editor, Senior Moderator
World J Gastroenterol
. 2021 Sep 21;27(35):5919-5931.
doi: 10.3748/wjg.v27.i35.5919.
Liver-spleen axis dysfunction in COVID-19
Sara Cococcia[SUP] 1 [/SUP], Marco Vincenzo Lenti[SUP] 2 [/SUP], Giovanni Santacroce[SUP] 1 [/SUP], Giovanna Achilli[SUP] 1 [/SUP], Federica Borrelli de Andreis[SUP] 1 [/SUP], Antonio Di Sabatino[SUP] 1 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an acute infectious disease that spreads mainly through the respiratory route. Besides interstitial pneumonia, a number of other clinical manifestations were noticed in COVID-19 patients. In particular, liver and spleen dysfunctions have been described both as complications of COVID-19 and as potential predisposing factors for severe COVID-19. Liver damage is rather common in COVID-19 patients, and it is most likely multifactorial, caused by the direct insult of SARS-CoV-2 to the liver by the cytokine storm triggered by the virus, by the use of hepatotoxic drugs, and as a consequence of hypoxia. Although generally mild, liver impairment has been found to be associated with a higher rate of intensive care unit admission. A higher mortality rate was reported among chronic liver disease patients. Instead, spleen impairment in patients with COVID-19 has been poorly described. The main anatomical changes are the architectural derangement of the B cell compartment, white pulp atrophy, and reduction or absence of lymphoid follicles, while, from a functional point of view, the IgM memory B cell pool is markedly depleted. The outcome of COVID-19 in asplenic or hyposplenic patients is yet to be defined. In this review, we will summarise the current knowledge regarding the impact of SARS-CoV-2 on the liver and spleen function, as well as the outcome of patients with a pre-existent liver disease or defective spleen function.
Keywords: Asplenia; Chronic liver disease; IgM memory B cell; Liver transplantation; Transaminase.
. 2021 Sep 21;27(35):5919-5931.
doi: 10.3748/wjg.v27.i35.5919.
Liver-spleen axis dysfunction in COVID-19
Sara Cococcia[SUP] 1 [/SUP], Marco Vincenzo Lenti[SUP] 2 [/SUP], Giovanni Santacroce[SUP] 1 [/SUP], Giovanna Achilli[SUP] 1 [/SUP], Federica Borrelli de Andreis[SUP] 1 [/SUP], Antonio Di Sabatino[SUP] 1 [/SUP]
Affiliations
- PMID: 34629809
- PMCID: PMC8475007
- DOI: 10.3748/wjg.v27.i35.5919
Abstract
Coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an acute infectious disease that spreads mainly through the respiratory route. Besides interstitial pneumonia, a number of other clinical manifestations were noticed in COVID-19 patients. In particular, liver and spleen dysfunctions have been described both as complications of COVID-19 and as potential predisposing factors for severe COVID-19. Liver damage is rather common in COVID-19 patients, and it is most likely multifactorial, caused by the direct insult of SARS-CoV-2 to the liver by the cytokine storm triggered by the virus, by the use of hepatotoxic drugs, and as a consequence of hypoxia. Although generally mild, liver impairment has been found to be associated with a higher rate of intensive care unit admission. A higher mortality rate was reported among chronic liver disease patients. Instead, spleen impairment in patients with COVID-19 has been poorly described. The main anatomical changes are the architectural derangement of the B cell compartment, white pulp atrophy, and reduction or absence of lymphoid follicles, while, from a functional point of view, the IgM memory B cell pool is markedly depleted. The outcome of COVID-19 in asplenic or hyposplenic patients is yet to be defined. In this review, we will summarise the current knowledge regarding the impact of SARS-CoV-2 on the liver and spleen function, as well as the outcome of patients with a pre-existent liver disease or defective spleen function.
Keywords: Asplenia; Chronic liver disease; IgM memory B cell; Liver transplantation; Transaminase.