RESUMO
INTRODUCTION: COVID-19 caused by the SARS-CoV-2 continues to spread rapidly across the world. In our study, we aim to investigate the relationship between the liver enzymes on admission (AST, ALT, ALP, GGT) and severity of COVID-19. We evaluated course of disease, hospital stay, liver damage and mortality. MATERIALS AND METHODS: Our study included 614 patients who were hospitalized with the diagnosis of COVID-19 between 03.16.20 and 05.12.20. Patients with liver disease, hematological and solid organ malignancy with liver metastases were excluded, resulting in 554 patients who met our inclusion criteria. We retrospectively evaluated liver transaminase levels, AST/ALT ratio, cholestatic enzyme levels and R ratio during hospital admission and these were compared in terms of morbidity, mortality and clinical course. RESULTS: Mean age of 554 subjects were 66.21±15.45 years, 328 (59.2%) were men. The mean values of liver enzymes on admission were AST (36.2±33.6U/L), ALT (34.01±49.34U/L), ALP (78.8±46.86U/L), GGT (46.25±60.05U/L). Mortality rate and need for intensive care unit were statistically significant in subjects that had high ALT-AST levels during their admission to the hospital (p=0.001). According to the ROC analysis AST/ALT ratio was a good marker of mortality risk (AUC=0.713: p=0.001) and expected probability of intensive care unit admission (AUC=0.636: p=0.001). R ratio, which was used to evaluate prognosis, showed a poor prognosis rate of 26.5% in the cholestatic injury group, 36.1% in the mixed pattern group and 30% in the hepato-cellular injury group (p 0.001). CONCLUSIONS: ALT-AST elevation and AST/ALT ratio >1 was associated with more severe course and increased mortality in COVID-19.
Assuntos
Alanina Transaminase/metabolismo , Aspartato Aminotransferases/metabolismo , Betacoronavirus , Infecções por Coronavirus/enzimologia , Infecções por Coronavirus/mortalidade , Hepatopatias/virologia , Pneumonia Viral/enzimologia , Pneumonia Viral/mortalidade , Adulto , Idoso , COVID-19 , Infecções por Coronavirus/complicações , Feminino , Hospitalização , Humanos , Hepatopatias/diagnóstico , Hepatopatias/mortalidade , Testes de Função Hepática , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/complicações , Prognóstico , Estudos Retrospectivos , SARS-CoV-2 , Sensibilidade e Especificidade , Taxa de Sobrevida , TurquiaRESUMO
INTRODUCCIÓN: Las alteraciones del perfil hepático durante el embarazo ocurren en 3-5% de las gestantes. Una nueva etiología que se ha presentado en el contexto de pandemia actual es el síndrome respiratorio agudo severo relacionado con el nuevo coronavirus (SARS-CoV-2). Éste es responsable de alteraciones hepáticas en 2 a 11% de la población general infectada por este virus, y de hasta un 30% en las embarazadas que se infectan con SARS-CoV-2. Con el objetivo de mostrar una presentación poco frecuente del SARS-CoV-2 se expone un caso clínico de elevación de transaminasas en embarazada inducida por este nuevo virus. CASO CLÍNICO: Paciente de 36 años, cursando embarazo de 20+6 semanas, consulta por dolor abdominal asociado a ictericia y coluria. Se solicita estudio donde destaca elevación de transaminasas. Ecografía abdominal con vía biliar fina. Se descartan diferentes etiologías de hepatitis aguda y crónica (dada la falta de antecedentes). Finalmente se solicita PCR para COVID-19 que resulta positiva. CONCLUSIÓN: Luego de un estudio exhaustivo de diferentes etiologías de elevación de transaminasas, se atribuye esta alteración enzimática a SARS-CoV-2. Se decide seguimiento ambulatorio estricto con pruebas hepáticas cada dos semanas. La paciente evoluciona estable con exámenes normales luego de un mes desde que se indica el alta hospitalaria. Después de descartar etiologías frecuentes de elevación de transaminasas durante el embarazo, sugerimos solicitar el estudio de este virus con PCR para COVID-19, ya que podría ser una presentación poco frecuente de SARS-CoV-2.
INTRODUCTION: Approximately 3-5% of women present alterations of hepatic enzymes during pregnancy. Under the new circumstances that the world is facing with the SARS-COV2 pandemic, a new etiology for hepatic enzyme alterations has risen. The severe acute respiratory syndrome that the novel coronavirus causes is responsible for hepatic enzyme alterations in 2 to 11% of the sick population that did not have a previous underlying hepatic condition. Furthermore, hepatic enzyme alterations in pregnant women infected with SARS-COV2 presents in up to 30% of the cases. An infrequent presentation of SARS-COV2 is presented as our clinical case. CLINICAL CASE: A 36-year-old patient with a 20+6 week pregnancy presents abdominal pain, jaundice and choluria. General blood workup shows elevated transaminases. The abdominal ultrasound revealed a thin bile duct. Acute and chronic hepatitis etiologies were discarded. Finally, a PCR of COVID-19 was solicited, which turned out to be positive. CONCLUSIÓN: After an exhaustive study to determine the etiology of the elevated transaminases, the hepatic alterations were attributed to SARS-COV2 infection. A conservative management was adopted, with outpatient follow-up with liver testing every two weeks. The patient progresses with a stable steady decline in hepatic enzyme levels, and one-month post hospital discharge, her transaminases had reached normal values. Based on this clinical case, after ruling out frequent etiologies for elevated transaminases during pregnancy, it seems reasonable to request a PCR for COVID-19, since it could be a rare presentation of SARS-CoV-2.
Assuntos
Humanos , Feminino , Gravidez , Adulto , Pneumonia Viral/complicações , Complicações Infecciosas na Gravidez/enzimologia , Complicações Infecciosas na Gravidez/etiologia , Infecções por Coronavirus/complicações , Betacoronavirus , Pneumonia Viral/enzimologia , Transferases/análise , Infecções por Coronavirus/enzimologia , Fosfatase Alcalina/análise , Pandemias , Icterícia , Hepatopatias/enzimologia , Hepatopatias/etiologiaRESUMO
In light of the outbreak of the 2019 novel coronavirus disease (COVID-19), the international scientific community has joined forces to develop effective treatment strategies. The Angiotensin-Converting Enzyme (ACE) 2, is an essential receptor for cell fusion and engulfs the SARS coronavirus infections. ACE2 plays an important physiological role, practically in all the organs and systems. Also, ACE2 exerts protective functions in various models of pathologies with acute and chronic inflammation. While ACE2 downregulation by SARS-CoV-2 spike protein leads to an overactivation of Angiotensin (Ang) II/AT1R axis and the deleterious effects of Ang II may explain the multiorgan dysfunction seen in patients. Specifically, the role of Ang II leading to the appearance of Macrophage Activation Syndrome (MAS) and the cytokine storm in COVID-19 is discussed below. In this review, we summarized the latest research progress in the strategies of treatments that mainly focus on reducing the Ang II-induced deleterious effects rather than attenuating the virus replication.
Assuntos
Betacoronavirus/isolamento & purificação , Infecções por Coronavirus/fisiopatologia , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/fisiopatologia , Enzima de Conversão de Angiotensina 2 , COVID-19 , Infecções por Coronavirus/enzimologia , Infecções por Coronavirus/virologia , Citocinas/metabolismo , Regulação para Baixo , Humanos , Síndrome de Ativação Macrofágica/virologia , Insuficiência de Múltiplos Órgãos/virologia , Pandemias , Peptidil Dipeptidase A/genética , Pneumonia Viral/enzimologia , Pneumonia Viral/virologia , SARS-CoV-2RESUMO
Coronavirus disease 2019 (COVID-19) is a global pandemic affecting the world, seen in more than 1,300,000 patients. COVID-19 acts through the angiotensin-converting enzyme 2 (ACE2) receptor. Cardiovascular comorbidities are more common with COVID-19, and nearly 10% of cases develop myocarditis (22% of critical patients). Further research is needed to continue or discontinue ACE inhibitors and angiotensin receptor blockers, which are essential in hypertension and heart failure in COVID-19. Intensive research is promising for the treatment and prevention of COVID-19.
A doença de coronavírus 2019 (COVID-19) é uma pandemia global afetando o mundo, estando presente em mais de 1.300.000 pacientes. O COVID-19 age pelo receptor da enzima conversora de angiotensina 2 (ECA2). As comorbidades cardiovasculares são mais frequentes com COVID-19, e cerca 10% de casos desenvolvem miocardite (22% de pacientes críticas). Mais pesquisas serão necessárias para continuar ou descontinuar inibidores de ECA e bloqueadores dos receptores da angiotensina, que são essenciais para hipertensão e insuficiência cardíaca em COVID-19. Pesquisa intensiva é promissora para o tratamento e a prevenção da COVID-19.
Assuntos
Betacoronavirus , Doenças Cardiovasculares/epidemiologia , Infecções por Coronavirus/epidemiologia , Pneumonia Viral/epidemiologia , Antagonistas de Receptores de Angiotensina/metabolismo , Enzima de Conversão de Angiotensina 2 , Animais , Antirreumáticos/uso terapêutico , Antivirais/uso terapêutico , COVID-19 , Doenças Cardiovasculares/enzimologia , Doenças Cardiovasculares/mortalidade , China/epidemiologia , Cloroquina/uso terapêutico , Comorbidade , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/enzimologia , Infecções por Coronavirus/mortalidade , Humanos , Hipertensão/enzimologia , Hipertensão/epidemiologia , Pandemias , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/enzimologia , Pneumonia Viral/mortalidade , SARS-CoV-2RESUMO
Patients who died from COVID-19 often had comorbidities, such as hypertension, diabetes, and chronic obstructive lung disease. Although angiotensin-converting enzyme 2 (ACE2) is crucial for SARS-CoV-2 to bind and enter host cells, no study has systematically assessed the ACE2 expression in the lungs of patients with these diseases. Here, we analyzed over 700 lung transcriptome samples from patients with comorbidities associated with severe COVID-19 and found that ACE2 was highly expressed in these patients compared to control individuals. This finding suggests that patients with such comorbidities may have higher chances of developing severe COVID-19. Correlation and network analyses revealed many potential regulators of ACE2 in the human lung, including genes related to histone modifications, such as HAT1, HDAC2, and KDM5B. Our systems biology approach offers a possible explanation for increased COVID-19 severity in patients with certain comorbidities.
Assuntos
Infecções por Coronavirus/epidemiologia , Pulmão/enzimologia , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/epidemiologia , Enzima de Conversão de Angiotensina 2 , COVID-19 , Estudos de Casos e Controles , Transtornos Cerebrovasculares/epidemiologia , Transtornos Cerebrovasculares/genética , Comorbidade , Doença das Coronárias/epidemiologia , Doença das Coronárias/genética , Infecções por Coronavirus/enzimologia , Infecções por Coronavirus/genética , Complicações do Diabetes/epidemiologia , Complicações do Diabetes/genética , Epigenômica , Feminino , Humanos , Hipertensão/epidemiologia , Hipertensão/genética , Masculino , Pandemias , Peptidil Dipeptidase A/genética , Pneumonia Viral/enzimologia , Pneumonia Viral/genética , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/genética , Índice de Gravidade de Doença , Biologia de Sistemas , TranscriptomaRESUMO
The world is currently facing a serious SARS-CoV-2 infection pandemic. This virus is a new isolate of coronavirus, and the current infection crisis has surpassed the SARS and MERS epidemics that occurred in 2002 and 2013, respectively. SARS-CoV-2 has currently infected more than 142,000 people, causing 5,000 deaths and spreading across more than 130 countries worldwide. The spreading capacity of the virus clearly demonstrates the potential threat of respiratory viruses to human health, thereby reiterating to the governments around the world that preventive health policies and scientific research are pivotal to overcoming the crisis. Coronavirus disease (COVID-19) causes flu-like symptoms in most cases. However, approximately 15% of the patients need hospitalization, and 5% require assisted ventilation, depending on the cohorts studied. What is intriguing, however, is the higher susceptibility of the elderly, especially individuals who are older than 60 years of age, and have comorbidities, including hypertension, diabetes, and heart disease. In fact, the death rate in this group may be up to 10-12%. Interestingly, children are somehow less susceptible and are not considered as a risk group. Therefore, in this review, we discuss some possible molecular and cellular mechanisms by virtue of which the elderly subjects may be more susceptible to severe COVID-19. Toward this, we raise two main points, i) increased ACE-2 expression in pulmonary and heart tissues in users of chronic angiotensin 1 receptor (AT1R) blockers; and ii) antibody-dependent enhancement (ADE) after previous exposure to other circulating coronaviruses. We believe that these points are pivotal for a better understanding of the pathogenesis of severe COVID-19, and must be carefully addressed by physicians and scientists in the field.
Assuntos
Formação de Anticorpos/imunologia , Anticorpos Facilitadores , Betacoronavirus , Infecções por Coronavirus/enzimologia , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/enzimologia , Idoso , Enzima de Conversão de Angiotensina 2 , Biomarcadores/metabolismo , COVID-19 , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/metabolismo , Humanos , Pandemias , Peptidil Dipeptidase A/imunologia , Pneumonia Viral/imunologia , Pneumonia Viral/metabolismo , SARS-CoV-2 , Regulação para CimaRESUMO
Resumo A doença de coronavírus 2019 (COVID-19) é uma pandemia global afetando o mundo, estando presente em mais de 1.300.000 pacientes. O COVID-19 age pelo receptor da enzima conversora de angiotensina 2 (ECA2). As comorbidades cardiovasculares são mais frequentes com COVID-19, e cerca 10% de casos desenvolvem miocardite (22% de pacientes críticas). Mais pesquisas serão necessárias para continuar ou descontinuar inibidores de ECA e bloqueadores dos receptores da angiotensina, que são essenciais para hipertensão e insuficiência cardíaca em COVID-19. Pesquisa intensiva é promissora para o tratamento e a prevenção da COVID-19.
Abstract Coronavirus disease 2019 (COVID-19) is a global pandemic affecting the world, seen in more than 1,300,000 patients. COVID-19 acts through the angiotensin-converting enzyme 2 (ACE2) receptor. Cardiovascular comorbidities are more common with COVID-19, and nearly 10% of cases develop myocarditis (22% of critical patients). Further research is needed to continue or discontinue ACE inhibitors and angiotensin receptor blockers, which are essential in hypertension and heart failure in COVID-19. Intensive research is promising for the treatment and prevention of COVID-19.
Assuntos
Humanos , Animais , Pneumonia Viral/epidemiologia , Doenças Cardiovasculares/epidemiologia , Infecções por Coronavirus/epidemiologia , Betacoronavirus , Antivirais/uso terapêutico , Pneumonia Viral/enzimologia , Pneumonia Viral/mortalidade , Pneumonia Viral/tratamento farmacológico , Doenças Cardiovasculares/enzimologia , Doenças Cardiovasculares/mortalidade , Comorbidade , China/epidemiologia , Cloroquina/uso terapêutico , Infecções por Coronavirus , Infecções por Coronavirus/enzimologia , Infecções por Coronavirus/mortalidade , Infecções por Coronavirus/tratamento farmacológico , Peptidil Dipeptidase A/metabolismo , Antirreumáticos/uso terapêutico , Antagonistas de Receptores de Angiotensina/metabolismo , Pandemias , Hipertensão/enzimologia , Hipertensão/epidemiologiaRESUMO
Abstract We aimed to analyze the expression profile of ACE2 and similar genes with ACE2, predict the number of variations in ACE2, detect the suspected SNPs on ACE2 gene, and perform the pathway analysis of renin-angiotensin system (RAS) and protein absorption-digestion. Moreover, we have predicted the gene-related diseases with ACE2. STRING was used to analyze functionally similar genes with ACE2. Exome Variant Server, SIFT, Polyphen2 were used to predict the number of variations in ACE2 and detect the suspected SNPs on ACE2. KEGG database and STRING were used to draw pathway of ACE2. Then, DISEASES resource, FitSNPs, UniProt, BioXpress, IGV Browser, Ensembl Genome Browser, and UCSC Genome Browser were used to predict the ACE2 gene-related diseases and expression profile in human normal and cancer tissues. We have shown that expression of ACE2 was correlated with AGT, REN, AGTR1, AGRT2, MME2, DPP4, PRCP, MEP1A, XPNPEP2, MEP1BandACE2 is expressed in testis, kidney, heart, thyroid, colon, esophagus, breast, minor salivary gland, pancreas, lung, liver, bladder, cervix, and muscle tissues. We found 99 variations in ACE2 gene, in which no previous study has been performed. In the future, this in silico analysis should be combined with other pieces of evidence including experimental data to assign function.
Assuntos
Humanos , Pneumonia Viral/enzimologia , Infecções por Coronavirus/enzimologia , Peptidil Dipeptidase A/genética , Pandemias , Sistema Renina-Angiotensina/genética , Expressão Gênica , GenótipoRESUMO
The world is currently facing a serious SARS-CoV-2 infection pandemic. </mac_aq>This virus is a new isolate of coronavirus, and the current infection crisis has surpassed the SARS and MERS epidemics</mac_aq> that occurred in 2002 and 2013, respectively. SARS-CoV-2 has currently infected more than 142,000 people, causing </mac_aq>5,000 deaths and spreading across more than 130 </mac_aq>countries worldwide. The spreading capacity of the virus clearly demonstrates the potential threat </mac_aq>of respiratory viruses to human health, thereby reiterating to the governments around the world that preventive </mac_aq>health policies and scientific research are pivotal to overcoming the crisis. Coronavirus disease (COVID-19) causes flu-like symptoms in most cases. However, approximately 15% of the patients need hospitalization, and 5% require assisted ventilation, depending on the cohorts studied. What is intriguing, however, is the higher susceptibility of the elderly, especially individuals who are older than 60 years of age, and have comorbidities, including hypertension, diabetes, and heart disease. In fact, the death rate in this group may be up to 10-12%. Interestingly, children are somehow less susceptible and are not considered as a risk group. Therefore, in this review, we discuss some possible molecular and cellular mechanisms by virtue of which the elderly subjects may be more susceptible to severe COVID-19. Toward this, we raise two main </mac_aq>points, i) increased ACE-2 expression in pulmonary and heart tissues in users of chronic angiotensin 1 </mac_aq>receptor (AT1R) blockers; and ii) antibody-dependent enhancement (ADE) after previous exposure to other circulating coronaviruses. We believe that these points are pivotal for a better understanding of the pathogenesis of severe COVID-19, and must be carefully addressed by physicians and scientists in the field.