key: cord-0726522-f08se2nu
authors: de Sousa Moreira, Jorge Lucas; Barbosa, Sarah Maria Bacurau; Vieira, Jacyanne Gino; Chaves, Nicolly Castelo Branco; Gonçalves Júnior, Jucier
title: LIVER HISTOPATHOLOGICAL CHANGES AND COVID-19: WHAT DOES LITERATURE HAVE TO TELL US?
date: 2022-01-12
journal: Dig Liver Dis
DOI: 10.1016/j.dld.2022.01.001
sha: 3b32076cfc62535aeb1603ffa346233ec9ab2c78
doc_id: 726522
cord_uid: f08se2nu

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In this context, regarding the changes triggered by the new coronavirus in the liver, the result of a study with 11 autopsies showed that Kupffer cells were activated in all patients, having a nodular proliferation of 70% [7] . Furthermore, data from a systematic review and meta-analysis found that Kupffer cell hyperplasia was present in 13.5% of the reports, being the 5th most relevant histological finding [2] Regarding the ability of SARS-CoV-2 to cause cholestasis the literature points out that in patients with COVID-19, histopathological signs that suggest cholestasis are frequently described, such as the proliferation of the bile ducts and intra-canalicular bile Finally, it is important to emphasize that the quality of published studies still lacks greater and better theoretical support. Thus, there is weakness in the data presented. Therefore, the objective of this publication is to stimulate the discussion and carry out more robust research aiming to map the most relevant liver histopathological alterations caused by COVID-19.

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Pulmonary Arterial Thrombosis in COVID-19 With Fatal Outcome

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Macrovesicular and microvesicular steatoses are demonstrated with platelet-fibrin thrombi are present in the sinusoidal spaces and central vein (H&E, ×400)

Ductular (black arrowhead) and canalicular (white arrowheads) cholestasis (H&E; scale bar 50µm)

A: Example of genuine thrombosis: portal with clearly enlarged lumen obliterated by red cell mixed andstratified with lymphocytes and granulocytes

B: smooth musde layer of portal vein lamina media extremely irregular fragmented (SMA, 100×)

SAR-CoV-2 virions are demonstrated within vessel lumen and onendothelial cells (ISH) (inset); C: medium layer of a portal vein, partially lost and infiltrated by inflammatory cellslymphocytes, also attaching endothelial layer

D: severe confluent haemorrhagic necrosis in a patient with elevation of ALT> 10 N(H&E, 100×)

The authors declare that they have no competing interests in paper "LIVER .