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1.
Sci Rep ; 11(1): 21514, 2021 11 02.
Article in English | MEDLINE | ID: covidwho-1500512

ABSTRACT

Coronavirus disease 2019 (COVID-19) is associated with systemic inflammation. A wide range of adipokines activities suggests they influence pathogenesis and infection course. The aim was to assess concentrations of chemerin, omentin, and vaspin among COVID-19 patients with an emphasis on adipokines relationship with COVID-19 severity, concomitant metabolic abnormalities and liver dysfunction. Serum chemerin, omentin and vaspin concentrations were measured in serum collected from 70 COVID-19 patients at the moment of admission to hospital, before any treatment was applied and 20 healthy controls. Serum chemerin and omentin concentrations were significantly decreased in COVID-19 patients compared to healthy volunteers (271.0 vs. 373.0 ng/ml; p < 0.001 and 482.1 vs. 814.3 ng/ml; p = 0.01, respectively). There were no correlations of analyzed adipokines with COVID-19 severity based on the presence of pneumonia, dyspnea, or necessity of Intensive Care Unit hospitalization (ICU). Liver test abnormalities did not influence adipokines levels. Elevated GGT activity was associated with ICU admission, presence of pneumonia and elevated concentrations of CRP, ferritin and interleukin 6. Chemerin and omentin depletion in COVID-19 patients suggests that this adipokines deficiency play influential role in disease pathogenesis. However, there was no relationship between lower adipokines level and frequency of COVID-19 symptoms as well as disease severity. The only predictive factor which could predispose to a more severe COVID-19 course, including the presence of pneumonia and ICU hospitalization, was GGT activity.


Subject(s)
Adipokines/blood , Chemokines/blood , Cytokines/blood , Lectins/blood , Serpins/blood , Aged , Body Mass Index , C-Reactive Protein/analysis , COVID-19/complications , COVID-19/metabolism , COVID-19/pathology , COVID-19/virology , Case-Control Studies , Female , GPI-Linked Proteins/blood , Hospitalization , Humans , Liver/metabolism , Male , Metabolic Syndrome/complications , Middle Aged , SARS-CoV-2/isolation & purification , gamma-Glutamyltransferase/metabolism
2.
Arch Med Res ; 52(7): 738-745, 2021 10.
Article in English | MEDLINE | ID: covidwho-1491707

ABSTRACT

BACKGROUND: It has been observed that subjects with comorbidities related to metabolic syndrome (MetS) as hypertension, obesity, cardiovascular disease (CVD), and diabetes mellitus (DM2) show severe cases and a higher mortality by COVID-19. To date, there is little information available on the impact of the interaction between these comorbidities in the risk of death by COVID-19. AIM OF THE STUDY: To evaluate the impact of the combinations of MetS components in overall survival (OS) and risk of death among COVID-19 patients. METHODS: Using public data of the Ministry of Health, suspected, and confirmed COVID-19 cases from February 25-June 6, 2020 was analyzed. Mortality odds ratio (OR) was calculated with a univariate analysis (95% CI) and attributable risk. Interactions between components and survival curves were analyzed and a multivariate logistics regression analysis was conducted. RESULTS: The analysis included 528,651 cases out of which 202,951 were confirmed for COVID-19. Probabilities of OS among confirmed patients were 0.93, 0.89, 0.87, 0.86, and 0.83 while the OR of multivariate analysis was 1.83 (1.77-1.89), 2.58 (2.48-2.69), 2.83 (2.66-3.01), and 3.36 (2.83-3.99) for zero, one, two, three, and four MetS components, respectively. The combination with the highest risk was DM2 + hypertension at 2.22 (2.15-2.28), and the attributable risk for any component was 9.35% (9.21-9.49). Only the combination obesity + CVD showed no significant interaction. CONCLUSION: The presence of one MetS component doubles the risk of death by COVID-19, which was higher among patients with DM2 + hypertension. Only obesity and CVD do not interact significantly.


Subject(s)
COVID-19 , Diabetes Mellitus , Hypertension , Metabolic Syndrome , Comorbidity , Diabetes Mellitus/epidemiology , Humans , Hypertension/complications , Hypertension/epidemiology , Metabolic Syndrome/complications , Metabolic Syndrome/epidemiology , Risk Factors , SARS-CoV-2
3.
Sci Rep ; 11(1): 19752, 2021 10 05.
Article in English | MEDLINE | ID: covidwho-1454813

ABSTRACT

Although metabolic syndrome (MetS) is linked to an elevated risk of cardiovascular disease (CVD), the cardiac-specific risk mechanism is unknown. Obesity, hypertension, and diabetes (all MetS components) are the most common form of CVD and represent risk factors for worse COVID-19 outcomes compared to their non MetS peers. Here, we use obese Yorkshire pigs as a highly relevant animal model of human MetS, where pigs develop the hallmarks of human MetS and reproducibly mimics the myocardial pathophysiology in patients. Myocardium-specific mass spectroscopy-derived metabolomics, proteomics, and transcriptomics enabled the identity and quality of proteins and metabolites to be investigated in the myocardium to greater depth. Myocardium-specific deregulation of pro-inflammatory markers, propensity for arterial thrombosis, and platelet aggregation was revealed by computational analysis of differentially enriched pathways between MetS and control animals. While key components of the complement pathway and the immune response to viruses are under expressed, key N6-methyladenosin RNA methylation enzymes are largely overexpressed in MetS. Blood tests do not capture the entirety of metabolic changes that the myocardium undergoes, making this analysis of greater value than blood component analysis alone. Our findings create data associations to further characterize the MetS myocardium and disease vulnerability, emphasize the need for a multimodal therapeutic approach, and suggests a mechanism for observed worse outcomes in MetS patients with COVID-19 comorbidity.


Subject(s)
COVID-19/pathology , Disease Susceptibility , Metabolic Syndrome/pathology , Animals , Blood Coagulation Factors/genetics , Blood Coagulation Factors/metabolism , COVID-19/complications , COVID-19/virology , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Diet, High-Fat/veterinary , Disease Models, Animal , Humans , Immunity, Innate/genetics , Metabolic Syndrome/complications , Metabolic Syndrome/metabolism , Methyltransferases/genetics , Methyltransferases/metabolism , Myocardium/metabolism , Oxidative Stress/genetics , Platelet Aggregation , Receptors, Purinergic P2Y1/genetics , Receptors, Purinergic P2Y1/metabolism , Renin-Angiotensin System , Risk Factors , SARS-CoV-2/isolation & purification , Swine , Urokinase-Type Plasminogen Activator/genetics , Urokinase-Type Plasminogen Activator/metabolism
4.
BMC Endocr Disord ; 21(1): 144, 2021 Jul 03.
Article in English | MEDLINE | ID: covidwho-1295459

ABSTRACT

BACKGROUND: Although obesity, defined by body mass index (BMI), has been associated with a higher risk of hospitalisation and more severe course of illness in Covid-19 positive patients amongst the British population, it is unclear if this translates into increased mortality. Furthermore, given that BMI is an insensitive indicator of adiposity, the effect of adipose volume on Covid-19 outcomes is also unknown. METHODS: We used the UK Biobank repository, which contains clinical and anthropometric data and is linked to Public Health England Covid-19 healthcare records, to address our research question. We performed age- and sex- adjusted logistic regression and Chi-squared test to compute the odds for Covid-19-related mortality as a consequence of increasing BMI, and other more sensitive indices of adiposity such as waist:hip ratio (WHR) and percent body fat, as well as concomitant cardiometabolic illness. RESULTS: 13,502 participants were tested for Covid-19 (mean age 70 ± 8 years, 48.9% male). 1582 tested positive (mean age 68 ± 9 years, 52.8% male), of which 305 died (mean age 75 ± 6 years, 65.5% male). Increasing adiposity was associated with higher odds for Covid-19-related mortality. For every unit increase in BMI, WHR and body fat, the odds of death amongst Covid19-positive participants increased by 1.04 (95% CI 1.01-1.07), 10.71 (95% CI 1.57-73.06) and 1.03 (95% CI 1.01-1.05), respectively (all p < 0.05). Referenced to Covid-19 positive participants with a normal weight (BMI 18.5-25 kg/m2), Covid-19 positive participants with BMI > 35 kg/m2 had significantly higher odds of Covid-19-related death (OR 1.70, 95% CI 1.06-2.74, p < 0.05). Covid-19-positive participants with metabolic (diabetes, hypertension, dyslipidaemia) or cardiovascular morbidity (atrial fibrillation, angina) also had higher odds of death. CONCLUSIONS: Anthropometric indices that are more sensitive to adipose volume and its distribution than BMI, as well as concurrent cardiometabolic illness, are associated with higher odds of Covid-19-related mortality amongst the UK Biobank cohort that tested positive for the infection. These results suggest adipose volume may contribute to adverse Covid-19-related outcomes associated with obesity.


Subject(s)
Adiposity/physiology , COVID-19/mortality , Cardiovascular Diseases/epidemiology , Metabolic Syndrome/epidemiology , Obesity/epidemiology , Aged , Aged, 80 and over , Biological Specimen Banks/statistics & numerical data , Body Mass Index , COVID-19/complications , COVID-19/pathology , Cardiometabolic Risk Factors , Cardiovascular Diseases/complications , Cardiovascular Diseases/mortality , Cohort Studies , Databases, Factual , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/epidemiology , Diabetes Mellitus, Type 2/mortality , Female , Hospital Mortality , Humans , Male , Metabolic Syndrome/complications , Metabolic Syndrome/mortality , Middle Aged , Morbidity , Mortality , Obesity/complications , Obesity/mortality , Risk Factors , SARS-CoV-2/physiology , United Kingdom/epidemiology
5.
Cells ; 10(6)2021 06 06.
Article in English | MEDLINE | ID: covidwho-1259430

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) gave rise to the coronavirus disease 2019 (COVID-19) pandemic. A strong correlation has been demonstrated between worse COVID-19 outcomes, aging, and metabolic syndrome (MetS), which is primarily derived from obesity-induced systemic chronic low-grade inflammation with numerous complications, including type 2 diabetes mellitus (T2DM). The majority of COVID-19 deaths occurs in people over the age of 65. Individuals with MetS are inclined to manifest adverse disease consequences and mortality from COVID-19. In this review, we examine the prevalence and molecular mechanisms underlying enhanced risk of COVID-19 in elderly people and individuals with MetS. Subsequently, we discuss current progresses in treating COVID-19, including the development of new COVID-19 vaccines and antivirals, towards goals to elaborate prophylactic and therapeutic treatment options in this vulnerable population.


Subject(s)
Aging/physiology , COVID-19/prevention & control , COVID-19/therapy , Chemoprevention/trends , Metabolic Syndrome/therapy , Aging/drug effects , Aging/immunology , COVID-19/diagnosis , COVID-19/epidemiology , Chemoprevention/methods , History, 21st Century , Humans , Metabolic Syndrome/complications , Metabolic Syndrome/diagnosis , Metabolic Syndrome/epidemiology , Patient Care Planning/trends , Prevalence , Prognosis , Severity of Illness Index , Vulnerable Populations
6.
J Am Heart Assoc ; 10(12): e018451, 2021 06 15.
Article in English | MEDLINE | ID: covidwho-1259045

ABSTRACT

Background Although chronic cardio-metabolic disease is a common comorbidity among patients with COVID-19, its effects on the clinical characteristics and outcome are not well known. Methods and Results This study aimed to explore the association between underlying cardio-metabolic disease and mortality with COVID-19 among hospitalized patients. This multicenter, retrospective, and real-world study was conducted from January 22, 2020 to March 25, 2020 in China. Data between patients with and without 5 main cardio-metabolic diseases including hypertension, diabetes mellitus, coronary heart disease, cerebrovascular disease, and hyperlipidemia were compared. A total of 1303 hospitalized patients were included in the final analysis. Of them, 520 patients (39.9%) had cardio-metabolic disease. Compared with patients without cardio-metabolic disease, more patients with cardio-metabolic disease had COVID-related complications including acute respiratory distress syndrome (9.81% versus 3.32%; P<0.001), acute kidney injury (4.23% versus 1.40%; P=0.001), secondary infection (13.9% versus 9.8%; P=0.026), hypoproteinemia (12.1% versus 5.75%; P<0.001), and coagulopathy (19.4% versus 10.3%; P<0.001), had higher incidences of the severe type of COVID-19 (32.9% versus 16.7%; P<0.001), more were admitted to the intensive care unit (11.7% versus 7.92%; P=0.021), and required mechanical ventilation (9.8% versus 4.3%; P<0.001). When the number of the patients' cardio-metabolic diseases was 0, 1, and >2, the mortality was 4.2%, 11.1%, and 19.8%, respectively. The multivariable-adjusted hazard ratio of mortality among patients with cardio-metabolic disease was 1.80 (95% CI, 1.17-2.77). Conclusions Cardio-metabolic disease was a common condition among hospitalized patients with COVID-19, and it was associated with higher risks of in-hospital mortality.


Subject(s)
COVID-19/complications , Hospitalization , Metabolic Syndrome/complications , Adult , Aged , COVID-19/diagnosis , COVID-19/mortality , COVID-19/therapy , China , Chronic Disease , Comorbidity , Disease Progression , Female , Hospital Mortality , Humans , Incidence , Male , Metabolic Syndrome/diagnosis , Metabolic Syndrome/mortality , Metabolic Syndrome/therapy , Middle Aged , Prognosis , Retrospective Studies , Risk Assessment , Risk Factors , Severity of Illness Index , Time Factors
7.
Exp Dermatol ; 30 Suppl 1: 18-22, 2021 06.
Article in English | MEDLINE | ID: covidwho-1258931

ABSTRACT

The reported incidence of COVID-19 among cohorts of patients with inflammatory bowel and skin diseases under treatment with biologicals is low. Treatment may further modify disease severity as some biological modifiers, such as anakinra, are also proposed for the management of COVID-19 patients potentially providing HS patients with an advantage. The above preliminary evidence suggests that hidradenitis suppurativa (HS) does probably not provide an increased susceptibility for COVID-19 and that any susceptibility is unlikely to be modified negatively by treatment with biologicals. On the occasion of its 10th International Conference, experts of the European Hidradenitis Suppurativa Foundation e.V. have prepared a consensus statement regarding anti-COVID-19 measurements for HS patients. Based on the available knowledge, patients with HS may be vaccinated against SARS-CoV2 and patients affected by metabolic syndrome constitute a high-risk group for COVID-19 and should be vaccinated at the earliest convenient point in time. HS patients on treatment with adalimumab can be vaccinated with non-living virus anti-SARS-CoV2 vaccines. A possible suboptimal effect of the vaccine may be suspected but might not be expected universally. The management of the biological treatment in HS patients is at the discretion of the dermatologist / responsible physician.


Subject(s)
COVID-19/complications , Hidradenitis Suppurativa/complications , Hidradenitis Suppurativa/drug therapy , SARS-CoV-2 , Adalimumab/therapeutic use , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines/immunology , COVID-19 Vaccines/pharmacology , Cohort Studies , Disease Susceptibility , Europe , Foundations , Hidradenitis Suppurativa/immunology , Humans , Incidence , Interleukin 1 Receptor Antagonist Protein/therapeutic use , Metabolic Syndrome/complications , Metabolic Syndrome/immunology , Pandemics , Severity of Illness Index
8.
World J Gastroenterol ; 27(5): 377-390, 2021 Feb 07.
Article in English | MEDLINE | ID: covidwho-1081093

ABSTRACT

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has undoubtedly revolutionized the whole globe and given a new point of view on respiratory tract infections. Nevertheless, coronavirus disease 2019 (COVID-19) cannot be perceived as a disease limited only to pneumonia with diverse severity. More and more reports have demonstrated a wide range of possible systemic symptoms, including hepatic complications. Liver injury has been observed in a significant proportion of patients, especially in those with a severe or critical illness. COVID-19 might provoke a deterioration of liver function in patients with already diagnosed chronic liver diseases and without pre-existing liver disorders. The deterioration of liver function worsens the prognosis, increases the risk of a severe course of SARS-CoV-2 infection and prolongs the hospital stay. In general, patients who develop liver dysfunction in COVID-19 are mainly males, elderly people, and those with higher body mass index. The underlying mechanisms for hepatic failure in patients infected with SARS-CoV-2 are still unclear, nevertheless liver damage appears to be directly connected with virus-induced cytopathic effects. A liver injury observed during hospitalization might be simultaneously caused by the use of potentially hepatotoxic drugs, mainly antiviral agents. This minireview focuses on a possible relationship between COVID-19 and the liver, potential molecular mechanisms of liver damage, the characteristics of liver injury and suggested factors predisposing to hepatic manifestations in COVID-19 patients.


Subject(s)
COVID-19/complications , Liver Failure/virology , Antiviral Agents/adverse effects , COVID-19/drug therapy , COVID-19/pathology , COVID-19/physiopathology , Gastrointestinal Tract/physiopathology , Host-Pathogen Interactions , Humans , Inflammation/complications , Liver/pathology , Liver Failure/chemically induced , Metabolic Syndrome/complications , Prognosis , SARS-CoV-2/physiology
10.
Int J Obes (Lond) ; 44(8): 1793-1799, 2020 08.
Article in English | MEDLINE | ID: covidwho-1023842

ABSTRACT

OBJECTIVE: Recent clinical trials have demonstrated that colchicine may have metabolic and cardiovascular and benefits in at-risk patients; however, the mechanisms through which colchicine may improve outcomes are still unclear. We sought to examine colchicine's effects on circulating inflammatory and metabolic molecules in adults with obesity and metabolic syndrome (MetS). METHODS: Blood samples were collected pre- and post-intervention during a double-blind randomized controlled trial in which 40 adults with obesity and MetS were randomized to colchicine 0.6 mg or placebo twice-daily for 3 months. Serum samples were analyzed for 1305 circulating factors using the SomaScan Platform. The Benjamini-Hochberg procedure was used to adjust the false discovery rate (FDR) for multiple testing. RESULTS: At baseline, age (48.0 ± 13.8 vs. 44.7 ± 10.3 years) and BMI (39.8 ± 6.4 vs. 41.8 ± 8.2 kg/m2) were not different between groups. After controlling for the FDR, 34 molecules were significantly changed by colchicine. Colchicine decreased concentrations of multiple inflammatory molecules, including C-reactive protein, interleukin 6, and resistin, in addition to vascular-related proteins (e.g., oxidized low-density lipoprotein receptor, phosphodiesterase 5A). Conversely, relative to placebo, colchicine significantly increased concentrations of eight molecules including secreted factors associated with metabolism and anti-thrombosis. CONCLUSIONS: In adults with obesity, colchicine significantly affected concentrations of proteins involved in the innate immune system, endothelial function and atherosclerosis, uncovering new mechanisms behind its cardiometabolic effects. Further research is warranted to investigate whether colchicine's IL-6 suppressive effects may be beneficial in COVID-19.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Colchicine/therapeutic use , Coronavirus Infections/immunology , Metabolic Syndrome/complications , Metabolic Syndrome/immunology , Obesity/immunology , Pneumonia, Viral/immunology , Adult , Anti-Inflammatory Agents/pharmacology , Betacoronavirus/drug effects , C-Reactive Protein , COVID-19 , Colchicine/pharmacology , Coronavirus Infections/drug therapy , Double-Blind Method , Female , Humans , Interleukin-6 , Male , Metabolic Syndrome/drug therapy , Middle Aged , Obesity/complications , Obesity/drug therapy , Pandemics , Pilot Projects , Pneumonia, Viral/drug therapy , SARS-CoV-2 , Treatment Outcome , Young Adult
11.
BMJ Open Respir Res ; 7(1)2020 12.
Article in English | MEDLINE | ID: covidwho-983651

ABSTRACT

BACKGROUND: Several characteristics of the metabolic syndrome, such as obesity and hypertension, have emerged as risk factors for a poor clinical outcome in COVID-19. However, most reports lack data on the metabolic syndrome itself. This study investigated prospectively the relationship between respiratory deterioration and the presence of metabolic syndrome or abdominal adiposity in patients with COVID-19. METHODS: A prospective observational cohort study analysing patients with respiratory symptoms who presented at a local emergency department in the Netherlands. The influence of abdominal adiposity-assessed by an increased waist-hip ratio-and metabolic syndrome on respiratory deterioration and the length of hospital stay were analysed with multivariable logistic regressions and Kaplan-Meier analyses. RESULTS: In total, 166 patients were analysed, of whom 86 (52%) tested positive for COVID-19. The prevalence of metabolic syndrome did not differ between patients with COVID-19 with and without the need for intubation or level of supportive care (37.5% vs 48.4%, p=0.338). In contrast, abdominal adiposity is an independent risk factor for respiratory distress in COVID-19, adjusted for metabolic syndrome, age, gender and BMI (OR 1.11, 95% CI 1.02 to 1.20, p=0.014). CONCLUSION: This study shows that abdominal adiposity, and not the presence of metabolic syndrome, is associated with clinical deterioration in COVID-19. This prospective study provides further insight into the risk stratification of patients with COVID-19 based on a simple measurement as the waist and hip circumference. TRIAL REGISTRATION NUMBER: NL8580.


Subject(s)
COVID-19/complications , Metabolic Syndrome/complications , Obesity, Abdominal/complications , Respiratory Distress Syndrome/etiology , Adiposity , Adult , Aged , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/virology , Female , Humans , Hypertension/complications , Length of Stay/statistics & numerical data , Male , Metabolic Syndrome/diagnosis , Metabolic Syndrome/epidemiology , Middle Aged , Netherlands/epidemiology , Obesity/complications , Obesity, Abdominal/epidemiology , Prevalence , Prospective Studies , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/mortality , Risk Factors , SARS-CoV-2/genetics , Waist-Hip Ratio/methods
13.
Cells ; 9(11)2020 11 13.
Article in English | MEDLINE | ID: covidwho-927551

ABSTRACT

The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was declared a pandemic by the WHO on 19 March 2020. This pandemic is associated with markedly elevated blood glucose levels and a remarkable degree of insulin resistance, which suggests pancreatic islet ß-cell dysfunction or apoptosis and insulin's inability to dispose of glucose into cellular tissues. Diabetes is known to be one of the top pre-existing co-morbidities associated with the severity of COVID-19 along with hypertension, cardiocerebrovascular disease, advanced age, male gender, and recently obesity. This review focuses on how COVID-19 may be responsible for the accelerated development of type 2 diabetes mellitus (T2DM) as one of its acute and suspected long-term complications. These observations implicate an active role of metabolic syndrome, systemic and tissue islet renin-angiotensin-aldosterone system, redox stress, inflammation, islet fibrosis, amyloid deposition along with ß-cell dysfunction and apoptosis in those who develop T2DM. Utilizing light and electron microscopy in preclinical rodent models and human islets may help to better understand how COVID-19 accelerates islet and ß-cell injury and remodeling to result in the long-term complications of T2DM.


Subject(s)
Apoptosis , Coronavirus Infections/pathology , Diabetes Mellitus, Type 2/pathology , Pneumonia, Viral/pathology , Animals , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/virology , Diabetes Mellitus, Type 2/complications , Humans , Insulin-Secreting Cells/cytology , Insulin-Secreting Cells/metabolism , Metabolic Syndrome/complications , Metabolic Syndrome/pathology , Oxidative Stress , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/virology , Renin-Angiotensin System/physiology , SARS-CoV-2
15.
Glob Heart ; 15(1): 58, 2020 08 19.
Article in English | MEDLINE | ID: covidwho-761022

ABSTRACT

Whilst current public health measures focused on good hygiene practices and limiting person-to-person transmission contribute effectively in managing the COVID-19 pandemic, they will not prevent all individuals from becoming infected. Thus, it is of importance to explore what individuals could do to mitigate adverse outcomes. The value of beneficial health behaviours and a healthy lifestyle to improve immune functioning and lower adverse consequences of COVID-19 are increasingly being emphasized. Here we discuss seven key health behaviours and corresponding recommendations that may assist in reducing unfavourable COVID-19 outcomes.


Subject(s)
Cardiovascular Diseases/complications , Cardiovascular Diseases/prevention & control , Coronavirus Infections/complications , Health Behavior , Healthy Lifestyle , Metabolic Syndrome/complications , Metabolic Syndrome/prevention & control , Pneumonia, Viral/complications , COVID-19 , Humans , Pandemics , Practice Guidelines as Topic
17.
J Int Med Res ; 48(7): 300060520939746, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-690568

ABSTRACT

The novel coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 infection is a serious global concern. Increased morbidity and mortality is associated with older age, male gender, cardiovascular disease, diabetes, and smoking. As COVID-19 spreads from coastal borders, both state to state and country to country, our understanding of its pathophysiology has evolved. Age and type 2 diabetes mellitus (T2DM) play especially important roles in COVID-19 progression. T2DM is an age-related disease associated with metabolic syndrome, obesity, insulin resistance (hyperinsulinemia), hyperlipidemia, hypertension, hyperglycemia, and endothelial activation and dysfunction. This review evaluates the relationships and intersection between endothelial cell activation and dysfunction in T2DM and COVID-19. COVID-19 induces multiple injuries of the terminal bronchioles and alveolar blood-gas barrier and associated ultrastructural tissue remodeling. COVID-19 may unmask multiple vulnerabilities associated with T2DM including damage to the endothelial glycocalyx and multiple end-organ macro and microvascular diseases. Unmasking existing vulnerabilities in diabetic patients with COVID-19 is important. Globally, we must come together to better understand why T2DM is associated with increased COVID-19 morbidity and mortality.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Coronavirus Infections/physiopathology , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/physiopathology , Endothelial Cells/physiology , Metabolic Syndrome/complications , Metabolic Syndrome/physiopathology , Pneumonia, Viral/complications , Pneumonia, Viral/physiopathology , Animals , Blood-Air Barrier/pathology , Blood-Air Barrier/physiopathology , Bronchioles/pathology , Bronchioles/physiopathology , COVID-19 , Comorbidity , Coronavirus Infections/epidemiology , Diabetes Mellitus, Type 2/epidemiology , Drug Repositioning , Endothelial Cells/pathology , Humans , Metabolic Syndrome/epidemiology , Models, Biological , Pandemics , Pneumonia, Viral/epidemiology , Pulmonary Alveoli/physiology , Pulmonary Alveoli/physiopathology , Rats , SARS-CoV-2 , Wound Healing/physiology
18.
Expert Rev Gastroenterol Hepatol ; 14(10): 867-872, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-670232

ABSTRACT

The pandemic Sars-CoV-2 infection represents a dramatic health challenge worldwide. Pneumonia is considered the major damage caused by the virus. However, recent data have highlighted the impact of the Sars-CoV-2 related disease namely COVID-19 on the liver. Hepatic abnormalities significantly increase during COVID-19 and a more severe infection occurs in patients with pre-existing liver diseases, among which the most frequent is metabolic-associated fatty liver disease (MAFLD). It has been described that MAFLD patients had a higher risk of progression to severe COVID-19, higher abnormal liver tests and longer viral shedding time. The presence of fibrosis in MAFLD patients is another risk factor for severity of COVID-19. Due to the overgrowing prevalence of MAFLD, it could be speculated that a large proportion of the population might be at risk of severe COVID-19 and the identification of these patients possibly by using liver enzymes as risk predictors may be crucial for an early diagnosis and for the management of the infection.


Subject(s)
Betacoronavirus , Coronavirus Infections/epidemiology , Fatty Liver/epidemiology , Metabolic Syndrome/epidemiology , Pandemics , Pneumonia, Viral/epidemiology , Aged , COVID-19 , Comorbidity , Fatty Liver/etiology , Female , Global Health , Humans , Male , Metabolic Syndrome/complications , Prevalence , Risk Factors , SARS-CoV-2
20.
J Pathol ; 251(3): 228-248, 2020 07.
Article in English | MEDLINE | ID: covidwho-604773

ABSTRACT

Angiotensin-converting enzyme 2 (ACE2) has been established as the functional host receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the current devastating worldwide pandemic of coronavirus disease 2019 (COVID-19). ACE2 is abundantly expressed in a variety of cells residing in many different human organs. In human physiology, ACE2 is a pivotal counter-regulatory enzyme to ACE by the breakdown of angiotensin II, the central player in the renin-angiotensin-aldosterone system (RAAS) and the main substrate of ACE2. Many factors have been associated with both altered ACE2 expression and COVID-19 severity and progression, including age, sex, ethnicity, medication, and several co-morbidities, such as cardiovascular disease and metabolic syndrome. Although ACE2 is widely distributed in various human tissues and many of its determinants have been well recognised, ACE2-expressing organs do not equally participate in COVID-19 pathophysiology, implying that other mechanisms are involved in orchestrating cellular infection resulting in tissue damage. Reports of pathologic findings in tissue specimens of COVID-19 patients are rapidly emerging and confirm the established role of ACE2 expression and activity in disease pathogenesis. Identifying pathologic changes caused by SARS-CoV-2 infection is crucially important as it has major implications for understanding COVID-19 pathophysiology and the development of evidence-based treatment strategies. Currently, many interventional strategies are being explored in ongoing clinical trials, encompassing many drug classes and strategies, including antiviral drugs, biological response modifiers, and RAAS inhibitors. Ultimately, prevention is key to combat COVID-19 and appropriate measures are being taken accordingly, including development of effective vaccines. In this review, we describe the role of ACE2 in COVID-19 pathophysiology, including factors influencing ACE2 expression and activity in relation to COVID-19 severity. In addition, we discuss the relevant pathological changes resulting from SARS-CoV-2 infection. Finally, we highlight a selection of potential treatment modalities for COVID-19. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.


Subject(s)
Betacoronavirus/physiology , Cardiovascular Diseases/complications , Coronavirus Infections/physiopathology , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/physiopathology , Renin-Angiotensin System/genetics , Age Factors , Angiotensin-Converting Enzyme 2 , Antiviral Agents/pharmacology , COVID-19 , Coronavirus Infections/pathology , Coronavirus Infections/therapy , Coronavirus Infections/virology , Disease Progression , Humans , Metabolic Syndrome/complications , Morbidity , Pneumonia, Viral/pathology , Pneumonia, Viral/therapy , Pneumonia, Viral/virology , Risk Factors , SARS-CoV-2 , Sex Factors
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