Risk factors for severe and critically ill COVID‐19 patients: A review

Allergy, Год журнала: 2020, Номер 76(2), С. 428 - 455

Опубликована: Ноя. 13, 2020

The pandemic of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome 2 (SARS-CoV-2), has an unprecedented global social and economic impact, high numbers deaths. Many risk factors have been identified in progression COVID-19 into a critical stage, including old age, male gender, underlying comorbidities such as hypertension, diabetes, obesity, chronic lung diseases, heart, liver kidney tumors, clinically apparent immunodeficiencies, local early type I interferon secretion capacity, pregnancy. Possible complications include injury, coagulation disorders, thoromboembolism. development lymphopenia eosinopenia are laboratory indicators COVID-19. Laboratory parameters to monitor lactate dehydrogenase, procalcitonin, high-sensitivity C-reactive protein, proinflammatory cytokines interleukin (IL)-6, IL-1β, Krebs von den Lungen-6 (KL-6), ferritin. cytokine storm extensive chest computed tomography imaging patterns disease. In addition, socioeconomic status, diet, lifestyle, geographical differences, ethnicity, exposed viral load, day initiation treatment, quality health care reported influence individual outcomes. this review, we highlight scientific evidence on severity

Язык: Английский

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Biomarkers associated with COVID-19 disease progression

Critical Reviews in Clinical Laboratory Sciences, Год журнала: 2020, Номер 57(6), С. 389 - 399

Опубликована: Июнь 5, 2020

The coronavirus disease 2019 (COVID-19) pandemic is a scientific, medical, and social challenge. complexity of the severe acute respiratory syndrome 2 (SARS-CoV-2) centered on unpredictable clinical course that can rapidly develop, causing deadly complications. identification effective laboratory biomarkers able to classify patients based their risk imperative in being guarantee prompt treatment. analysis recently published studies highlights role systemic vasculitis cytokine mediated coagulation disorders as principal actors multi organ failure with COVID-19 following have been identified: hematological (lymphocyte count, neutrophil neutrophil–lymphocyte ratio (NLR)), inflammatory (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), procalcitonin (PCT)), immunological (interleukin (IL)-6 biochemical (D-dimer, troponin, creatine kinase (CK), aspartate aminotransferase (AST)), especially those related cascades disseminated intravascular (DIC) distress (ARDS). New could be identified through accurate multicentric case series; particular, homocysteine angiotensin II play significant role.

Язык: Английский

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COVID-19 in people with diabetes: understanding the reasons for worse outcomes

The Lancet Diabetes & Endocrinology, Год журнала: 2020, Номер 8(9), С. 782 - 792

Опубликована: Июль 17, 2020

Язык: Английский

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In-Hospital Use of Statins Is Associated with a Reduced Risk of Mortality among Individuals with COVID-19

Cell Metabolism, Год журнала: 2020, Номер 32(2), С. 176 - 187.e4

Опубликована: Июнь 24, 2020

Язык: Английский

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COVID-19 and multiorgan failure: A narrative review on potential mechanisms

Journal of Molecular Histology, Год журнала: 2020, Номер 51(6), С. 613 - 628

Опубликована: Окт. 4, 2020

The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) in December 2019 form Wuhan, China leads to disease (COVID-19) pandemic. While the common cold symptoms are observed mild cases, COVID-19 is accompanied by multiorgan failure patients. involvement different organs patients results lengthening hospitalization duration and increasing mortality rate. In this review, we aimed investigate patients, particularly cases. Also, tried define potential underlying mechanisms SARS-CoV2 induced failure. multi-organ dysfunction characterized lung failure, liver kidney injury, cardiovascular disease, as well a wide spectrum hematological abnormalities neurological disorders. most important related direct indirect pathogenic features SARS-CoV2. Although presence angiotensin-converting enzyme 2, receptor lung, heart, kidney, testis, liver, lymphocytes, nervous system was confirmed, there controversial findings about observation RNA these organs. Moreover, organ may be cytokine storm, result increased levels inflammatory mediators, endothelial dysfunction, coagulation abnormalities, infiltration cells into Therefore, further investigations needed detect exact pathogenesis. Since several for clinicians, their knowledge help improve outcomes decrease rate morbidity.

Язык: Английский

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COVID-19: Specific and Non-Specific Clinical Manifestations and Symptoms: The Current State of Knowledge

Journal of Clinical Medicine, Год журнала: 2020, Номер 9(6), С. 1753 - 1753

Опубликована: Июнь 5, 2020

Coronavirus disease 2019 (COVID-19), due to the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become an epidemiological threat and a worldwide concern. SARS-CoV-2 spread 210 countries more than 6,500,000 confirmed cases 384,643 deaths have been reported, while number of both fatal is continually increasing. COVID-19 viral that can affect every age group-from infants elderly-resulting in wide spectrum various clinical manifestations. might present different degrees severity-from mild or even asymptomatic carriers, cases. The most common complications include pneumonia distress syndrome. Fever, dry cough, muscle weakness, chest pain are prevalent typical symptoms COVID-19. However, patients also atypical occur alone, which indicate possible infection. aim this paper review summarize all findings regarding manifestations patients, respiratory, neurological, olfactory gustatory, gastrointestinal, ophthalmic, dermatological, cardiac, rheumatologic manifestations, as well specific pediatric patients.

Язык: Английский

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COVID-19 and liver disease: mechanistic and clinical perspectives

Nature Reviews Gastroenterology & Hepatology, Год журнала: 2021, Номер 18(5), С. 348 - 364

Опубликована: Март 10, 2021

Our understanding of the hepatic consequences severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its resultant disease 2019 (COVID-19) has evolved rapidly since onset pandemic. In this Review, we discuss hepatotropism SARS-CoV-2, including differential expression viral receptors on liver cell types, describe histology features present in patients with COVID-19. We also provide an overview pattern relevance abnormal biochemistry during COVID-19 possible underlying direct indirect mechanisms for injury. Furthermore, large international cohorts have been able to characterize course pre-existing chronic disease. Patients cirrhosis particularly high rates decompensation death following SARS-CoV-2 outline hypotheses explain these findings, role cirrhosis-associated immune dysfunction. This finding contrasts outcome data pharmacologically immunosuppressed after transplantation who seem comparatively better outcomes from than those advanced Finally, approach vaccination predict how changes social behaviours clinical care pathways pandemic might lead increased incidence severity. Review provides mechanistic insights into context disease, discussing potential biology conditions. The management is discussed, strategies.

Язык: Английский

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Abnormal Liver Function Tests in Patients With COVID‐19: Relevance and Potential Pathogenesis

Hepatology, Год журнала: 2020, Номер 72(5), С. 1864 - 1872

Опубликована: Июль 23, 2020

Potential conflict of interest: Dr. Bodewes advises Vertex. Strazzabosco Bayer and Engitix. The current pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has led to over 6 million cases 370,000 deaths as June 1, 2020.(1) Although most patients infected with SARS‐CoV‐2 develop only mild symptoms, a minority require hospitalization intensive care.(2) Based on available clinical data, abnormal liver function tests (LFTs) are frequently observed in disease 2019 (COVID‐19), which underlying pathogenesis is incompletely understood. We reviewed information prevalence, nature, relevance, potential altered LFTs COVID‐19. Epidemiology Abnormal Patients With COVID‐19 Liver include measures hepatocyte injury (aspartate transferase [AST] alanine [ALT]), bile duct or cholestasis (alkaline phosphatase [ALP] gamma‐glutamyltransferase [GGT]), markers hepatic clearance/biliary secretion capacity (bilirubin), well synthetic (prothrombin time albumin). not necessarily liver‐specific. It been suggested that elevated aminotransferases could also originate from myositis rather than injury.(3) In large descriptive study, muscle damage marker creatinine kinase was 14% COVID‐19.(4) Hypoalbuminemia reported 55% hospitalized COVID‐19(5) associated severity.(6) an independent predictor mortality.(7) Lower levels pre‐albumin were reported, suggesting decreased synthesis.(5) context inflammation, hypoalbuminemia may reflect albumin extravasation consequence increased capillary permeability.(8) Additional factors explain catabolism malnutrition. prevalence ALT elevations among ranged between 4% 33% Chinese cohorts (weighted average: 19%), but high 39% cohort New York City area(5,9‐21) (Fig. 1). generally mild, defined less 5 times upper reference limit.(9,10,14‐19,21‐34) AST 53% 21%) 58% US cohort(4,5,9‐16,18,19,21,22,24,25,29,34,35) similarly limit.(9,10,14‐16,18,19,21‐31,34,36) had SARS SARS‐CoV.(37) Several case reports have described LFT abnormalities(18,38,39) acute‐on‐chronic(40,41) failure Zhang et al.(33) 1 82 deceased cause death, although it clear whether this patient pre‐existing disease.FIG. 1: Percentage admission. studies summarized included all severity. size dots reflects relative number each study. panels represent cohorts, whereas lower panel represents cohort. weighted averages represented vertical black lines refer cohorts.Elevated ALP 2%‐5% patients,(5,11,25,42) GGT 13%‐54% 23%).(5,11,19,42) total bilirubin 1% 18% admission.(4,5,15,16,18,25,35,43) should be realized, however, comprehensively any these studies. Stratification according severity, including extent distress need for care unit (ICU) admission, indicated plasma more greater compared those disease.(4,5,9,14,22,23,29,31,43‐47) This during 2002‐2004 outbreak.(37) prognostic value unclear. Some found LFTs, particularly (peak) ALT, severity mortality,(17,20,46,47) other did find association mortality,(48) progression,(5) ICU admission,(27,48) length hospital stay.(11) Pathogenesis Function Tests Hepatic Infection uses angiotensin‐converting enzyme (ACE2) docking entry receptor host cells.(49) Transmembrane serine protease (TMPRSS2) involved its cellular entry.(50) Theoretically, direct virus‐induced cytopathic effects play role abnormalities COVID‐19.(51) To determine able infect liver, ACE2 expression studied cells. Single‐cell RNA‐sequencing approaches mRNA expressed subpopulation cholangiocytes, minimally hepatocytes, cell type.(52‐55) line this, at protein level, visualized immunohistochemistry subset hepatocytes.(56,57) TMPRSS2 hepatocytes cholangiocytes.(58) Zhao al. human ductal organoids showed viral 24 hours after infection.(59) organoids, 3% cells co‐expressed biliary markers, these, 68% TMPRSS2. endothelial debated.(56,57) highly brush border small intestinal enterocytes.(56,57) Accordingly, infection intestine organoids,(60) nucleocapsid detected cytoplasm biopsies COVID‐19.(61) gastrointestinal symptoms likely LFTs.(62) (<15%) COVID‐19, RNA blood PCR low amounts.(29,63,64) Assuming brisk replication intestine, appears plausible viruses enter portal circulation reach liver. Kupffer would attempt virus initiate inflammatory response. possible mediators system sinusoids. Evidence provided showing particles without membrane‐bound vesicles abnormalities.(45) However, no confirmatory testing nucleic acids performed, leaving possibility "spiked" inclusions different origin.(65) Role Host Inflammatory Response Following infection, immune response can rapid controlled, resulting resolution delayed dysregulated, host‐damaging complications. complications syndrome, coagulopathy reminiscent disseminated intravascular coagulation (DIC) thrombotic microangiopathy, multi‐organ (MOF), ultimately death.(66) An excessive release early‐response factors, especially IL‐6, IL‐10, IL‐2 interferon gamma, correlates severity(67) cytokine storm (CSS). CSS uncontrolled pro‐inflammatory cytokines MOF.(68) cascade events leading MOF includes early phase mediators, later amplification inflammation damage, affect various organs (bystander effect).(68) Additionally, result DIC.(69) DIC critical nonsurvivor evidenced raised D‐dimer prolonged prothrombin time,(70) autopsy findings pulmonary embolism microangiopathy multiple organs.(71) Endothelitis COVID‐19,(72) fibrin microthrombi sinusoids.(73) largest series taken (48 cases) massive dilation vein branches, luminal thrombosis, tract fibrosis, sinusoids.(74) therefore related shock coagulopathy, perfusion death. Indeed, several higher admission disease, concomitantly markers.(4,5,9,11,14,22,23,29,31,44,46,75) general inflammation. al.(19) pneumonia non‐COVID‐19 comparable There differences C‐reactive IL‐6 two groups. While none AST, 28%, 44% respectively, independently status. One explanation specific elicited pathogens. Whether present asymptomatic paucisymptomatic who do unknown. Drug‐Induced Injury Alterations implying before starting drug treatment. comprehensive description conditions prior medication use lacking. Many medications used management such acetaminophen, antivirals, antibiotics, corticosteroids immune‐modulators, potentially hepatotoxic. Fan al.(11) retrospectively relationship 148 Among 48% developed them about week Whereas received lopinavir‐ritonavir, 31% normal it. due retrospective nature lack treatment randomization into account. Cai 7 odds alterations lopinavir‐ritonavir.(20) contrast, trial 199 frequent lopinavir‐ritonavir group given standard care. excluded trial. Remdesivir recently superior placebo shortening recovery COVID‐19.(76) comparing remdesivir either 10 days, immediately life‐threatening ALT/AST 4%‐6% patients, AST/ALT 2%‐3% necessitating discontinuation.(77) Acetaminophen symptom relief even therapeutic doses.(78) assessed specifically. Preliminary data associate hydroxychloroquine significant abnormalities.(79,80) Pre‐existing Diseases (chronic) diseases. Reported rates vary 1%‐11%.(42,47,81,82) As reporting retrospective, aforementioned numbers subject underreporting, unlikely accounts LFTs. presence course vice versa largely Plasma chronic diseases,(44,47) mortality.(83) comprises spectrum differentially outcomes. advanced risk cirrhosis‐associated dysfunction.(84) Another category raises concerns transplant recipients auto‐immune receiving immunosuppressant drugs. based currently there reason believe population.(85,86) study mortality recipients, displayed comorbidities.(87) speculated immunosuppression beneficial, might reduce developing hyper‐inflammatory state CSS. Conversely, increase bacterial fungal superinfection. Metabolic Dysfunction–Associated Fatty Disease Severity identified obesity factor co‐morbidities age, type diabetes mellitus, hypertension.(51,88‐93) Nonalcoholic fatty (NAFLD), known nonalcoholic lean individuals.(94) initial characterizing NAFLD rarely common (and possibly asymptomatic) condition, account some Moreover, United States (24%) China (15%).(95) closely lifestyle‐related metabolic disorders (e.g., diabetes). U.S. cohort, 42% obese 34% diabetes.(10) 15%.(4) progression longer shedding NAFLD.(96) Increased if alongside obesity,(97) diabetes,(98) younger patients,(99) fibrosis scores.(100) unclear how similar pathways relating response, macrophage activation (low‐grade) often both conditions, thought key role.(100‐103) increases hepatotoxicity certain drugs, aggravate COVID‐19.(104,105) Other Causes Elevations Critically Ill changes hemodynamics oxygen delivery. Hypoxic hepatitis sharp setting failure, shock, cardiac failure.(106) During occur COVID‐19,(107) systemic arterial pressure suddenly drops, reduction hepatocellular hypoxia. ischemia, venous congestion central pressure, predispose hypoxic injury.(108) Similar hemodynamic mechanically ventilated positive end‐respiratory (PEEP).(109,110) alter unclear.(110) Importantly, PEEP usually unnecessary lung compliance relatively high.(111) Conclusions Mildly markers. general, lead impairment liver‐directed unnecessary. pathogenetic mechanisms fully understood: They multifactorial and, while and/or cholangiocytes unlikely, microthrombotic endothelialitis, dysregulation, drug‐induced injury, ischemia hypoxia role. Author Contributions A.B.: conceptualization, formal analysis, curation, investigation, visualization, writing – original draft; I.P.P.: F.A.J.A.B., H.M., A.F., F.F., R.F., M.S., H.J.V.: review & editing; G.P.: editing, supervision.

Язык: Английский

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COVID-19 and Sex Differences

Mayo Clinic Proceedings, Год журнала: 2020, Номер 95(10), С. 2189 - 2203

Опубликована: Авг. 4, 2020

Men are consistently overrepresented in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and disease 2019 (COVID-19) outcomes, including higher fatality rates. These differences likely due to gender-specific behaviors, genetic hormonal factors, sex biological pathways related SARS-CoV-2 infection. Several social, behavioral, comorbid factors implicated the generally worse outcomes men compared with women. Underlying their effects on COVID-19 however, have received less attention. The present review summarizes available literature regarding proposed molecular cellular markers of associations health any reported modification by sex. Biological characterized such biomarkers exist within healthy populations also differ age- sex-specific conditions, as pregnancy menopause. In context COVID-19, descriptive biomarker levels often sex, but data pertaining effect patient relationship between severity/outcomes scarce. Such may offer plausible explanations for seen men. There is need larger studies reporting robust analyses elucidate how modifies associated SARS-CoV-2. This will improve interpretation clinical management patients facilitating a personalized medical approach risk stratification, prevention, treatment.

Язык: Английский

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Pre-existing liver disease is associated with poor outcome in patients with SARS CoV2 infection; The APCOLIS Study (APASL COVID-19 Liver Injury Spectrum Study)

Hepatology International, Год журнала: 2020, Номер 14(5), С. 690 - 700

Опубликована: Июль 4, 2020

Язык: Английский

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