ABSTRACT
BACKGROUND: There is an increasing number of liver injury cases resembling autoimmune hepatitis (AIH) following SARS-CoV-2 vaccination; however, an association has not yet been established. METHODS/MATERIALS: A literature review was performed to identify articles regarding the association of AIH with vaccination, emphasizing on SARS-CoV-2 vaccines, and the proposed mechanisms. We then performed a literature search for AIH-like cases following SARS-CoV-2 vaccination, and we evaluated the included cases for AIH diagnosis using simplified diagnostic criteria (SDC), and for vaccination causality using the Naranjo score for adverse drug reactions. RESULTS: We identified 51 AIH-like cases following SARS-CoV-2 vaccination. Forty cases (80%) were characterized as "probable", "at least probable", or "definite" for AIH diagnosis according to SDC. Forty cases (78.4%) were characterized as "probable", four (7.8%) as "possible", and three (5.8%) as "definite" for vaccine-related AIH according to the Naranjo score. CONCLUSION: SARS-CoV-2 vaccine-related AIH carries several phenotypes and, although most cases resolve, immunosuppressive therapy seems to be necessary. Early diagnosis is mandatory and should be considered in any patient with acute or chronic hepatitis after SARS-CoV-2 vaccination, especially in those with pre-existing liver disease.
ABSTRACT
Since the pandemic's onset, a growing population of individuals has recovered from SARS-CoV-2 infection and its long-term effects in some of the convalescents are gradually being reported. Although the precise etiopathogenesis of post-acute COVID-19 sequelae (PACS) remains elusive, the mainly accepted rationale is that SARS-CoV-2 exerts long-lasting immunomodulatory effects, promotes chronic low-grade inflammation, and causes irreversible tissue damage. So far, several viruses have been causally linked to human oncogenesis, whereas chronic inflammation and immune escape are thought to be the leading oncogenic mechanisms. Excessive cytokine release, impaired T-cell responses, aberrant activation of regulatory signaling pathways (e.g., JAK-STAT, MAPK, NF-kB), and tissue damage, hallmarks of COVID-19 disease course, are also present in the tumor microenvironment. Therefore, the intersection of COVID-19 and cancer is partially recognized and the long-term effects of the virus on oncogenesis and cancer progression have not been explored yet. Herein, we present an up-to-date review of the current literature regarding COVID-19 and cancer cross-talk, as well as the oncogenic pathways stimulated by SARS-CoV-2.