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LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T16","span":{"begin":631,"end":658},"obj":"http://purl.obolibrary.org/obo/GO_0002526"},{"id":"T17","span":{"begin":637,"end":658},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T18","span":{"begin":686,"end":696},"obj":"http://purl.obolibrary.org/obo/GO_0007049"},{"id":"T19","span":{"begin":740,"end":749},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T20","span":{"begin":740,"end":749},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T21","span":{"begin":2330,"end":2334},"obj":"http://purl.obolibrary.org/obo/GO_0004111"},{"id":"T22","span":{"begin":2512,"end":2517},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T23","span":{"begin":4634,"end":4639},"obj":"http://purl.obolibrary.org/obo/GO_0004111"},{"id":"T24","span":{"begin":5314,"end":5318},"obj":"http://purl.obolibrary.org/obo/GO_0004111"},{"id":"T25","span":{"begin":6194,"end":6202},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T26","span":{"begin":6194,"end":6202},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T27","span":{"begin":6194,"end":6202},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T28","span":{"begin":6194,"end":6202},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T29","span":{"begin":6462,"end":6483},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"HEPATOBILIARY MANIFESTATIONS\n\nSARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I.\n\nMERS-CoV\nSeveral studies report patients with MERS-CoV and elevated liver enzymes, as well as hypoalbuminemia59 , 60 (Table 2). The degree of hypoalbuminemia also helps to predict disease severity.60 Hepatic findings may resemble SARS-CoV-related changes.61 However, MERS-CoV utilizes dipeptidyl peptidase-4 to infect cells, which is highly expressed in the liver.62 , 63 In transgenic mice, the liver injury occurred within the first week after infection resulting in hepatic necrosis and infiltration of Kupffer cells and macrophages.64 Similar to other coronavirus infections, high concentrations of inflammatory cytokines are noted in the acute phase, including IFN-g, TNF-a, IL-15 and IL-17.65 Future investigations may clarify the role of inflammatory response in causing the liver injury.\n\nCOVID-19\nThe few available studies show that as many as 51% of patients with COVID-19 have abnormal liver function on admission (elevated liver enzymes, bilirubin and lactate dehydrogenase levels) 66 (Table 2). Patients with abnormal LFTs present with a high degree of fever, and their degree of hepatic dysfunction correlates with length of hospitalization.66 New reports suggest that the liver dysfunction in patients with COVID-19 may be related to damage to the cholangiocytes lining the biliary epithelium, likely due to the higher expression of ACE2 receptors on those cells.67 Patients with preexisting metabolic fatty liver disease have been seen to have an about 6-fold higher chance of severe disease in the presence of coexisting obesity.21"}

LitCovid-PD-HP

LitCovid-sentences

LitCovid-PMC-OGER-BB

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2_test

PMC:7212949 / 20822-28087 JSONTXT

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PMC:7212949 / 20822-28087 JSON TXT