Obese COVID-19 Patients Research Articles

A closer look at utilized radiation doses during chest CT for COVID-19 patients

This study examined radiation exposure from CT scans performed on 500 adult COVID-19 patients at two major university hospitals in Morocco. A robust correlation (r = 0.82) was found between patient size and Size-Specific Dose Estimate (SSDE), which ranged from 10.11 to 17.87 mGy. The mean CTDIvol was 6.7 mGy, contrasting markedly with the mean SSDE of 12.81 mGy. This highlights a substantial difference, with the SSDE-to-CTDIvol ratio being approximately 1.91. Notably, the SSDE was nearly twice as high as the CTDIvol, underscoring the vulnerability of obese COVID-19 patients. Evaluation of different CT scanner models showed higher radiation doses associated with the Siemens Somaton Emotion 16 compared to the GE Optima CT520 Series, emphasizing the need to account for scanner-specific factors in dose optimization protocols. A comparison of chest CT reference doses (DRL) from this study with international data showed a lower mean CTDIvol here (6.7 mGy) than reported in other countries. However, the DRL in terms of DLP is in the same range or lower as compared to others. Using the BEIR VII model, the lifetime attributable risk (LAR) of cancer from COVID-19 chest CTs was estimated. Elevated risks of lung cancer in both genders and increased breast cancer risk in females were projected, albeit with limitations regarding overestimated cancer incidence. The high effective dose values, approaching 15.3 mSv, underscore the need for dose optimization, especially in obese COVID-19 patients receiving chest CTs.

Evaluation of the relationship between disease severity and the leptin, adiponectin, and chemerin levels in overweight and obese COVID-19 patients

Evaluation of the relationship between disease severity and the leptin, adiponectin, and chemerin levels in overweight and obese COVID-19 patients

SARS-CoV-2 specific immune responses in overweight and obese COVID-19 patients.

Obesity is a known risk factor for severe respiratory tract infections. In this prospective study, we assessed the impact of being obese or overweight on longitudinal SARS-CoV-2 humoral and cellular responses up to 18 months after infection. 274 patients provided blood samples at regular time intervals up to 18 months including obese (BMI ≥30, n=32), overweight (BMI 25-29.9, n=103) and normal body weight (BMI 18.5-24.9, n=134) SARS-CoV-2 patients. We determined SARS-CoV-2 spike-specific IgG, IgA, IgM levels by ELISA and neutralising antibody titres by neutralisation assay. RBD- and spike-specific memory B cells were investigated by ELISpot, spike- and non-spike-specific IFN-γ, IL-2 and IFN-γ/IL-2 secreting T cells by FluoroSpot and T cell receptor (TCR) sequencing was performed. Higher BMI correlated with increased COVID-19 severity. Humoral and cellular responses were stronger in overweight and obese patients than normal weight patients and associated with higher spike-specific IgG binding titres relative to neutralising antibody titres. Linear regression models demonstrated that BMI, age and COVID-19 severity correlated independently with higher SARS-CoV-2 immune responses. We found an increased proportion of unique SARS-CoV-2 specific T cell clonotypes after infection in overweight and obese patients. COVID-19 vaccination boosted humoral and cellular responses irrespective of BMI, although stronger immune boosting was observed in normal weight patients. Overall, our results highlight more severe disease and an over-reactivity of the immune system in overweight and obese patients after SARS-CoV-2 infection, underscoring the importance of recognizing overweight/obese individuals as a risk group for prioritisation for COVID-19 vaccination.

Early Treatment and Care of Obese COVID-19 Patients

<p>嚴重特殊傳染性肺炎（COVID-19）造成整個世界健康與經濟重大衝擊與危機，尤其是高齡和慢性病患者更容易產生預後合併症、重症和死亡。然而流行病學證據顯示肥胖者，即使年輕（< 65歲），不論有無慢性疾病史，較非肥胖者易感染SARS-CoV-2病毒和發生感染後的重症與死亡。因此本文整理肥胖者較易感染SARS-CoV-2 的生病理機轉、口服抗病毒藥物（Paxlovid & Molnupiravir）使用相關知識、慢性病藥物調整和居家照護時的生活型態，包括營養攝取及運動方式建議，期待第一線的專科護理師對「肥胖」這個危險因子具有敏感性，可以收集相關病史與身體檢查評估資料，不論在口服抗病毒或慢性病藥物（尤其是高血壓、高血脂和抗凝劑等）使用與生活型態調整、營養補充都能與醫師討論做出最有利的建議，以期早期治療COVID-19，避免重症和死亡的發生。</p> <p> </p><p>The COVID-19 pandemic severely impacted the health and economics of the entire world since De­cember 2019, particularly to the elderly and people with chronic diseases for a higher possibility of aggravations, complications and even death. However, the epidemiological evidence showed that obese people are prone to SARS-CoV-2 infection and post-COVID complications. This review reported the mechanism of SARS-CoV-2 entry into fat cells, COVID-19 medications (Paxlovid & Molnupiravir) and treatments, chronic disease (e.g. hypertension, hyperlipidemia, and anticoagulation etc.) manage­ment, and lifestyle (diet and exercise) modification. Nurse practitioners should consider obese as a significant risk factor while designing management plans with doctors and initiate the anti-COVID-19 treatment plan as soon as possible for complication prevention among obese cases.</p> <p> </p>

Lung Epithelial Cells from Obese Patients Have Impaired Control of SARS-CoV-2 Infection.

Obesity is known to increase the complications of the COVID-19 coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the exact mechanisms of SARS-CoV-2 infection in obese patients have not been clearly elucidated. This study aims to better understand the effect of obesity on the course of SARS-CoV-2 infection and identify candidate molecular pathways involved in the progression of the disease, using an in vitro live infection model and RNA sequencing. Results from this study revealed the enhancement of viral load and replication in bronchial epithelial cells (NHBE) from obese subjects at 24 h of infection (MOI = 0.5) as compared to non-obese subjects. Transcriptomic profiling via RNA-Seq highlighted the enrichment of lipid metabolism-related pathways along with LPIN2, an inflammasome regulator, as a unique differentially expressed gene (DEG) in infected bronchial epithelial cells from obese subjects. Such findings correlated with altered cytokine and angiotensin-converting enzyme-2 (ACE2) expression during infection of bronchial cells. These findings provide a novel insight on the molecular interplay between obesity and SARS-CoV-2 infection. In conclusion, this study demonstrates the increased SARS-CoV-2 infection of bronchial epithelial cells from obese subjects and highlights the impaired immunity which may explain the increased severity among obese COVID-19 patients.

The Importance of Serum Homocysteine as a Biomarker in Diabetic and Obese COVID-19 Patients.

Homocysteine is a possible risk marker in hematological complications of COVID-19 infection. This study aimed to elucidate the significance of homocysteine as a biomarker for COVID-19 infection, and the relation of homocysteine with COVID-19 severity in obese people and diabetic patients. The study groups were 1- COVID-19 patients + Diabetic + Obese (CDO), 2- COVID-19 patients + Diabetic (CD), 3- COVID-19 patients + Obese (CO), 4- Healthy Group (HG). Serum levels of homocysteine, IL-6, D-dimer, vitamin B12, and folate were measured by a fully automated biochemistry device Cobas 6000 analyzer series.The mean serum concentration of homocysteine in the COD, CD, CO and H groups were 32.0114, 23.604, 19.4154, and 9.3206 umol/l respectively. The mean concentration of homocysteine levels between every two groups was statistically significant differences (P<0.05) except for the CD and the CO group (P=0.957). In the CDO group, the males have higher mean concentrations than females (P<0.05). The means of homocysteine concentrations in the CDO group among different age groups were different (P <0.001). The serum homocysteine level in the CDO group has a strong positive correlation (R=0.748) with D-dimer and a strong negative correlation (R= - 0.788) with serum folate, while its correlation with serum vitamin B12 is moderate negative (-0.499) and its correlation with serum IL-6 is weakly positive (R=0.376). The AUC value for homocysteine in predicting COVID-19 in the CDO group was 0.843, while 0.714 for the CD group, and 0.728 for the CO group. The serum homocysteine concentration test for all study groups was compared to the serum IL-6 test and the sensitivity was equal to 95% and its specificity was 67.5%. Serum homocysteine has potential predictive power in COVID-19 patients, and the severity of COVID-19 infection and the type of comorbidity is associated with higher sensitivity and specificity of homocysteine serological tests.

ACE2 polymorphisms impact COVID-19 severity in obese patients

A strong association between obesity and COVID-19 complications and a lack of prognostic factors that explain the unpredictable severity among these patients still exist despite the various vaccination programs. The expression of angiotensin converting enzyme 2 (ACE2), the main receptor for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is enhanced in obese individuals. The occurrence of frequent genetic single nucleotide polymorphisms (SNPs) in ACE2 is suggested to increase COVID-19 severity. Accordingly, we hypothesize that obesity-associated ACE2 polymorphisms increase the severity of COVID-19. In this study, we profiled eight frequently reported ACE2 SNPs in a cohort of lean and obese COVID-19 patients (n = 82). We highlight the significant association of rs2285666, rs2048683, rs879922, and rs4240157 with increased severity in obese COVID-19 patients as compared to lean counterparts. These co-morbid-associated SNPs tend to positively correlate, hence proposing possible functional cooperation to ACE2 regulation. In obese COVID-19 patients, rs2285666, rs879922, and rs4240157 are significantly associated with increased blood nitrogen urea and creatinine levels. In conclusion, we highlight the contribution of ACE2 SNPs in enhancing COVID-19 severity in obese individuals. The results from this study provide a basis for further investigations required to shed light on the underlying mechanisms of COVID-19 associated SNPs in COVID-19 obese patients.

Association between Obesity and COVID-19 Outcomes in the Intensive Care Unit of RSUP Dr. M. Djamil Padang

Background: Obesity is one of the risk factors for severe clinical COVID-19. This is because these patients tend to have comorbidities such as metabolic disease and cardiovascular disease. Obesity may result in poor outcomes, such as prolonged hospital stays, higher incidence of ARDS and mortality. The purpose of this study was to determine the correlation between obesity and the outcome of confirmed COVID-19 patients.Methods: This was an analytical study with retrospective cohort design on COVID-19 patients treated in the intensive care unit (ICU)of RSUP Dr. M. Djamil Padang. Data were taken from patients’ medical records between November 2021 and February 2022. The correlation between obesity with length of stay and patient mortality was analyzed using Chi-square test. Odds ratio was also assessed.Results: This study obtained that the characteristics of obese COVID-19 patients were mainly women (54.20%). The most dominant age group was 60-69 years (31.3%). About83.3% of obese patients were found to be clinically critical. Inflammatory markers such as procalcitonin, ferritin, IL-6 and d-dimer were not significantly associated with obesity. Diabetes mellitus was significantly related to the outcome of COVID-19 patients with obesity and without obesity (0.009%). Obesity was not correlated with hospital length of stay of COVID-19 patients, but was significantly associated with length of stay in the ICU [OR 3.67 (95% CI, 1.09-12.35)]. Obesity was significantly associated with mortality [OR 2.84 (95% CI, 1.12-7.18)] and length of conversion for COVID-19 patients in the ICU [OR 30.00 (95% CI, 2.85-31, 61)]. The expansion of adipose tissue both subcutaneously and viscerally which could be observed in obese patients can increase the proinflammatory, prothrombotic, and vasoconstrictive state that might affect the clinical deterioration of COVID-19 patients. This condition also manifests as insulin resistance, hypertension, atherosclerosis, cardiovascular disease and immunocompromised conditions which can generate high mortality rate.Conclusion: Obesity was found to be significantly associated with mortality, conversion time and length of stay for COVID-19 patients in the ICU.

Challenge of New Norms: Obesity amid COVID-19 Pandemic

COVID-19 pandemic aggravated the global public health system, which is already overwhelmed by the increasing statistics of comorbidities and burden due to obesity. The number of individuals with obesity and obesity-associated diseases are rising in many regions that could attribute to the growing obesogenic environment and the lockdown implemented to curb COVID-19. This review focuses on the aspects of the obesity epidemic, chronic inflammatory effects of obesity, positive outcomes of obesity interventions and the worsening effects observed in obese COVID-19 patients. The chronic inflammatory effects of obesity are apparent by the increase of pro-inflammatory signals by immune cells in the adipose tissue and reactive species populations. The reduction of antioxidants exacerbates the effects of oxidative stress on genomic and tissue levels. The public must be made aware of the importance of practising a healthier lifestyle, even more now as we are fighting the COVID-19 pandemic.

Thrombosis Mechanisms in Obese and Ischemic Stroke COVID-19 Patients: A Literature Review

Highlight: The ongoing Coronavirus disease 2019 also affects multiorgan, including cardiovascular disease with several factors. Mechanism of thrombus in the patient that induces the subject such as obesity with increased BMI, thrombotic pathway modulator and pathophysiologist. An increase in acute CVD incidence, including ischemic stroke in COVID-19 patients, has been a new concern in the ongoing pandemic. ABSTRACT Coronavirus disease 2019 (COVID-19), despite being a respiratory infection, also causes neurological manifestations such as stroke due to thrombosis formation. Prior investigations have examined the correlation between COVID-19 and ischemic stroke, as well as COVID-19 and obesity. However, the mechanism of thrombosis in obese COVID-19 patients remains elusive. This review aims to examine the mechanism of thrombosis in COVID-19 patients with ischemic stroke and obesity. Chronic inflammation and impaired fibrinolysis are two major pathways responsible for thrombosis in people with obesity. Chronic inflammation activates prothrombic signaling pathways in vascular cells, resulting in procoagulant factors and adhesion molecules upregulation, anticoagulant proteins downregulation, platelet activation enhancement, and increased thrombin generation. SARS-CoV-2 enters human cells utilizing the angiotensin-converting enzyme 2 (ACE-2) receptors, which results in inflammation, which has been suggested as one of the factors contributing to thrombotic complications in COVID-19 patients. The infection also causes cytokine storm that induces atherosclerosis, plaque rupture, and superimposed thrombosis leading to brain damage. Together with endothelial injury, the cytokine storm might increase the expression of tissue factors and further promote a prothrombic state. In conclusion, the mechanisms of thrombosis in COVID-19 patients are related to direct infection of SARS-CoV-2 into the ACE-2 receptor and the cytokine storm that results in chronic inflammation and thrombosis formation. Obesity will further boost the inflammation process that leads to the formation of thrombosis and increase the risk of ischemic stroke among individuals with COVID-19 with obesity.

Mediators of Obesity Do Not Influence SARS-CoV-2 Infection or Activation of Primary Human Lung Microvascular Endothelial Cells In Vitro.

Clinical observations have shown that obesity is associated with the severe outcome of SARS-CoV-2 infection hallmarked by microvascular dysfunction in the lungs and other organs. Excess visceral fat and high systemic levels of adipose tissue (AT) derived mediators such as leptin and other adipokines have also been linked to endothelial dysfunction. Consequently, we hypothesized that AT-derived mediators may exacerbate microvascular dysfunction during of SARS-CoV-2 infection and tested this in a primary human lung microvascular endothelial (HLMVEC) cell model. Our results indicate that HLMVEC are not susceptible to SARS-CoV-2 infection since no expression of viral proteins and no newly produced virus was detected. In addition, exposure to the virus did not induce endothelial activation as evidenced by a lack of adhesion molecule, E-selectin, VCAM-1, ICAM-1, and inflammatory cytokine IL-6 induction. Incubation of endothelial cells with the pro-inflammatory AT-derived mediator, leptin, prior to virus inoculation, did not alter the expression of endothelial SARS-CoV-2 entry receptors and did not alter their susceptibility to infection. Furthermore, it did not induce inflammatory activation of endothelial cells. To verify if the lack of activated phenotype in the presence of adipokines was not leptin-specific, we exposed endothelial cells to plasma obtained from critically ill obese COVID-19 patients. Plasma exposure did not result in E-selectin, VCAM-1, ICAM-1, or IL-6 induction. Together our results strongly suggest that aberrant inflammatory endothelial responses are not mounted by direct SARS-CoV-2 infection of endothelial cells, even in the presence of leptin and other mediators of obesity. Instead, endothelial activation associated with COVID-19 is likely a result of inflammatory responses initiated by other cells. Further studies are required to investigate the mechanisms regulating endothelial behavior in COVID-19 and the mechanisms driving severe disease in obese individuals.

Obesity and Its Impact on Adverse In-Hospital Outcomes in Hospitalized Patients With COVID-19.

BackgroundAn increasing level of evidence suggests that obesity not only is a major risk factor for cardiovascular diseases (CVDs) but also has adverse outcomes during COVID-19 infection.MethodsWe used the German nationwide inpatient sample to analyze all hospitalized patients with confirmed COVID-19 diagnosis in Germany from January to December 2020 and stratified them for diagnosed obesity. Obesity was defined as body mass index ≥30 kg/m2 according to the WHO. The impact of obesity on in-hospital case fatality and adverse in-hospital events comprising major adverse cardiovascular and cerebrovascular events (MACCE), acute respiratory distress syndrome (ARDS), venous thromboembolism (VTE), and others was analyzed.ResultsWe analyzed data of 176,137 hospitalizations of patients with confirmed COVID-19 infection; among them, 9,383 (5.3%) had an additional obesity diagnosis. Although COVID-19 patients without obesity were older (72.0 [interquartile range (IQR) 56.0/82.0] vs. 66.0 [54.0/76.0] years, p < 0.001), the CVD profile was less favorable in obese COVID-19 patients (Charlson comorbidity index 4.44 ± 3.01 vs. 4.08 ± 2.92, p < 0.001). Obesity was independently associated with increased in-hospital case fatality (OR 1.203 [95% CI 1.131–1.279], p < 0.001) and MACCE (OR 1.168 [95% CI 1.101–1.239], p < 0.001), ARDS (OR 2.605 [95% CI 2.449–2.772], p < 0.001), and VTE (OR 1.780 [95% CI 1.605–1.973], p < 0.001) and also associated with increased necessity of treatment on intensive care unit (OR 2.201 [95% CI 2.097–2.310], p < 0.001), mechanical ventilation (OR 2.277 [95% CI 2.140–2.422], p < 0.001), and extracorporeal membrane oxygenation (OR 3.485 [95% CI 3.023–4.017], p < 0.001).ConclusionsObesity independently affected case fatality, MACCE, ARDS development, VTE, and other adverse in-hospital events in patients with COVID-19 infection. Obesity should be taken into account regarding COVID-19 prevention strategies, risk stratification, and adequate healthcare planning. Maintaining a healthy weight is important not only to prevent cardiometabolic diseases but also for better individual outcomes during COVID-19 infection.

Respiratory and nonrespiratory COVID-19 complications in patients with obesity: recent developments.

This narrative review summarizes recent reports to provide an updated understanding of the multiorgan effects of SARS-CoV-2 infection in obese individuals. A PubMed search of 528 primary articles was performed, with inclusion based on novelty, relevance and redundancy. Obesity confers an increased risk for hospitalization, intensive care unit admission, severe pneumonia, intubation and acute kidney injury in COVID-19 patients. Obesity is also associated with higher levels of inflammatory and thrombotic markers. However, the associations between obesity and mortality or cardiac injury in COVID-19 patients remain unclear. Obesity is a risk factor for several respiratory and nonrespiratory COVID-19 complications. Future work is needed to further explore these relationships and optimize the management of obese COVID-19 patients.

Ketogenic Diet for Obese COVID-19 Patients: Is Respiratory Disease a Contraindication? A Narrative Review of the Literature on Ketogenic Diet and Respiratory Function.

Morbid obese people are more likely to contract SARS-CoV-2 infection and its most severe complications, as need for mechanical ventilation. Ketogenic Diet (KD) is able to induce a fast weight loss preserving lean mass and is particularly interesting as a preventive measure in obese patients. Moreover, KD has anti-inflammatory and immune-modulating properties, which may help in preventing the cytokine storm in infected patients. Respiratory failure is actually considered a contraindication for VLCKD, a very-low calorie form of KD, but in the literature there are some data reporting beneficial effects on respiratory parameters from ketogenic and low-carbohydrate high-fat diets. KD may be helpful in reducing ventilatory requirements in respiratory patients, so it should be considered in specifically addressed clinical trials as an adjuvant therapy for obese patients infected with SARS-CoV-2.

The majority of SARS-CoV-2-specific antibodies in COVID-19 patients with obesity are autoimmune and not neutralizing

Background/objectivesObesity decreases the secretion of SARS-CoV-2-specific IgG antibodies in the blood of COVID-19 patients. How obesity impacts the quality of the antibodies secreted, however, is not understood. Therefore, the objective of this study is to evaluate the presence of neutralizing versus autoimmune antibodies in COVID-19 patients with obesity.Subjects/methodsThirty serum samples from individuals who tested positive for SARS-CoV-2 infection by RT-PCR were collected from inpatient and outpatient settings. Of these, 15 were lean (BMI < 25) and 15 were obese (BMI ≥ 30). Control serum samples were from 30 uninfected individuals, age-, gender-, and BMI-matched, recruited before the current pandemic. Neutralizing and autoimmune antibodies were measured by ELISA. IgG autoimmune antibodies were specific for malondialdehyde (MDA), a marker of oxidative stress and lipid peroxidation, and for adipocyte-derived protein antigens (AD), markers of virus-induced cell death in the obese adipose tissue.ResultsSARS-CoV-2 infection induces neutralizing antibodies in all lean but only in few obese COVID-19 patients. SARS-CoV-2 infection also induces anti-MDA and anti-AD autoimmune antibodies more in lean than in obese patients as compared to uninfected controls. Serum levels of these autoimmune antibodies, however, are always higher in obese versus lean COVID-19 patients. Moreover, because the autoimmune antibodies found in serum samples of COVID-19 patients have been correlated with serum levels of C-reactive protein (CRP), a general marker of inflammation, we also evaluated the association of anti-MDA and anti-AD antibodies with serum CRP and found a positive association between CRP and autoimmune antibodies.ConclusionsOur results highlight the importance of evaluating the quality of the antibody response in COVID-19 patients with obesity, particularly the presence of autoimmune antibodies, and identify biomarkers of self-tolerance breakdown. This is crucial to protect this vulnerable population at higher risk of responding poorly to infection with SARS-CoV-2 than lean controls.

Fetuin-A Deficiency but Not Pentraxin 3, FGF-21, or Irisin, Predisposes to More Serious COVID-19 Course.

Analysis of liver biopsy specimens showed that SARS-CoV-2 might have led to liver damage. This study aimed to evaluate the role of selected hepatokines and myokines in the development and progression of COVID-19. Seventy patients with laboratory-confirmed COVID-19 and 20 healthy volunteers were enrolled in the study. Irisin, pentraxin 3, fetuin-A, and FGF-21 serum concentrations and biochemical parameters were assessed using an immunoenzymatic method with commercially available enzyme immunoassay (EIA) or enzyme-linked immunosorbent assay (ELISA) kits. Serum fetuin-A concentrations were significantly decreased in COVID-19 patients compared to healthy volunteers. The serum concentration of FGF-21 was significantly increased in obese COVID-19 patients compared to overweight ones. Moreover, the FGF-21 level was higher in COVID-19 patients diagnosed with metabolic syndrome than in patients without metabolic syndrome. PTX3 concentration was higher in COVID-19 patients with higher HOMA-IR values than those with lower HOMA-IR values. COVID-19 patients with HOMA-IR ≤ 3 and >3 had significantly lower fetuin-A levels than the control group. Irisin concentration was significantly decreased in the HOMA-IR ≤ 3 COVID-19 subgroup when comparing with the control group. Lower levels of fetuin-A observed in COVID-19 patients despite higher HOMA-IR, CRP, and ferritin levels, pneumonia, patients requiring ICU care suggests that fetuin-A deficiency predisposes to more severe COVID-19 course. Upregulated pentraxin 3 may be used as a potential predictor of COVID-19 severity.

Impact of High Serum Levels of MMP-7, MMP-9, TGF-β and PDGF Macrophage Activation Markers on Severity of COVID-19 in Obese-Diabetic Patients.

ObjectiveThe aim of this study was to identify an association between the severity of COVID-19 in obese-diabetic patients and altered serum levels of MMP-7, MMP-9, TGF-β, and PDGF macrophage activation markers.MethodologyThe study included 70 COVID-19 patients, divided into two groups: Group 1 included: Obese COVID-19 patients with type 2 diabetes mellitus (T2D, n=22 patients) and group 2 included; non-obese, non-diabetic COVID-19 patients as an age- and sex-matched control group (n=48 patients). Serum levels of the tested biomarkers were measured by ELISA at admission and after one weak follow-up.ResultsThere was a significant reduction in the serum levels of LBP in obese-diabetic COVID-19 patients versus the control group (8.34±3.94 vs 20.78±7.61) (p 0.0001). Significant elevation of MMP-7, MMP-9, PDGF and TGF-β was detected in obese diabetic COVID-19 patients compared to the non-obese non-diabetic group: 1044.7±519.6 vs 405.6±164.1, 483.05±46.5 vs 173.31±76.26, 154.5±62.78 vs 39.77±21.52, and 603.05±258.82 vs 180.29±97.17, respectively. The serum levels of macrophage activation markers in obese-diabetic patients one week after admission revealed that patients with acute respiratory distress syndrome (ARDS) had significantly higher serum levels of MMP-7 and MMP-9 than non-ARDS patients (p 0.02 and p 0.01 respectively).ConclusionMacrophages were mainly polarized towards the M2 phenotype in obese-diabetic COVID-19 patients with significant upregulation of the pro-fibrotic markers MMP-7, MMP-9, PDGF, and TGF-β. Thus, high levels of MMP-7 and MMP-9 are associated with ARDS in severe COVID-19 disease among obese-diabetic patients.

Daily Energy Requirements and Substrate Utilization in Hyper- and Hypometabolism of Obese COVID-19 Patients Measured by Indirect Calorimetry: Two Case Reports

Daily Energy Requirements and Substrate Utilization in Hyper- and Hypometabolism of Obese COVID-19 Patients Measured by Indirect Calorimetry: Two Case Reports

Gene signatures of autopsy lungs from obese patients with COVID-19.

Background & aimsObesity is associated with low grade systemic inflammation and insulin resistance. Although metabolic and immunological changes may contribute to the increased risk for COVID-19 mortality in obese, little is known about the impact of obesity in the lungs of patients with COVID-19.MethodsWe analyzed gene expression profiles of autopsy lungs of a cohort of 14 COVID-19 patients and 4 control individuals. Patients were divided into 3 groups according to their comorbidities: hypertension, type 2 diabetes (T2D) and obesity. We then identified the molecular alterations associated with these comorbidities in COVID-19 patients.ResultsPatients with only hypertension showed higher levels of inflammatory genes and B-cell related genes when compared to those with T2D and obesity. However, the levels of IFN-gamma, IL22, and CD274 (a ligand that binds to receptor PD1) were higher in COVID-19 patients with T2D and obesity. Several metabolic- and immune-associated genes such as G6PD, LCK and IL10 were significantly induced in the lungs of the obese group.ConclusionOur findings suggest that SARS-CoV-2 infection in the lungs may exacerbate the immune response and chronic condition in obese COVID-19 patients.

The J-Shaped Relationship Between Body Mass Index and Mortality in Patients With Covid-19: A Systematic Review and Dose-Response Meta-Analysis

Introduction: Several studies have linked obesity to more severe illness and higher mortality in COVID-19 patients. However, the relationship between being underweight and COVID-19 mortality remains inconclusive. Previous dose-response meta-analyses did not enroll or specifically analyze the underweight population. Herein, we conducted a systematic review and dose-response meta-analysis to investigate the relationship between body mass index (BMI) and mortality in both obese and underweight patients with COVID-19. Methods: We searched PubMed, Embase, Cochrane Library, Scopus, and Web of Science databases from inception until August 12, 2020 using the keywords “COVID-19,” “body mass index,” “obesity,” “overweight”, and “underweight.” Three reviewers independently assessed the relevant articles, including the title, abstract, and full text, to identify eligible studies. We performed a two-stage random-effects dose-response meta-analysis, including only studies with at least three quantitative classifications for BMI. The nonlinear trend was evaluated using a restricted cubic splines model with three-knots at the 10th, 50th, and 90th percentiles. A sensitivity analysis was conducted by pooling only those studies which specifically evaluated underweight patients (BMI<18.5 kg/m2). Results: Thirteen studies comprising 25,828 patients were included in the analysis. In the linear model, the mortality of patients with COVID-19 increased by 1.5% for each 1-kg/m2 increase in BMI (pooled relative risk [RR] =1.015, 95% confidence interval [CI] =1.004−1.027). However, a significant non-linear relationship between BMI and mortality was observed (Wald test: Pnon-linearity<0.001). We demonstrated a J-shaped curve, indicating that both underweight and obese patients had a higher mortality than those with normal weight. Interestingly, overweight patients (BMI, 25−30 kg/m2) seemed to have the lowest mortality risk. Using a BMI of 15 kg/m2 as the reference, the RRs of mortality decreased with BMI, and this trend continued until BMI of approximately 28 kg/m2 (RR=0.743, 95% CI=0.576−0.959). The relationship between BMI and mortality was then reversed, and an upward trend was observed when BMI exceeded 30 kg/m2; the RRs (95% CI) at BMIs 30, 35, 40, and 45 kg/m2 were 0.745 (0.570−0.974), 0.841 (0.643−1.100), 1.082 (0.850−1.377), and 1.457 (1.129−1.879), respectively. Conclusion: This study is the first dose-response meta-analysis that showed both underweight and obese COVID-19 patients are at higher risk of increased mortality. A J-curve relationship was demonstrated between BMI and COVID-19 mortality.