Severe Cases Of Coronavirus Disease 2019 Research Articles

The influence of pre-existing hypertension on coronavirus disease 2019 patients.

Hypertension represents one of the most common pre-existing conditions and comorbidities in Coronavirus disease 2019 (COVID-19) patients. To explore whether hypertension serves as a risk factor for disease severity, a multi-centre, retrospective study was conducted in COVID-19 patients. A total of 498 consecutively hospitalised patients with lab-confirmed COVID-19 in China were enrolled in this cohort. Using logistic regression, we assessed the association between hypertension and the likelihood of severe illness with adjustment for confounders. We observed that more than 16% of the enrolled patients exhibited pre-existing hypertension on admission. More severe COVID-19 cases occurred in individuals with hypertension than those without hypertension (21% vs. 10%, P = 0.007). Hypertension associated with the increased risk of severe illness, which was not modified by other demographic factors, such as age, sex, hospital geological location and blood pressure levels on admission. More attention and treatment should be offered to patients with underlying hypertension, who usually are older, have more comorbidities and more susceptible to cardiac complications.

Profile of COVID-19 Patients at Zero Delay COVID-19 Ward, Tertiary Care Hospital in South India.

Introduction:Coronavirus disease 2019 (COVID-19) pandemic is a worldwide public health crisis. During huge surge in COVID-19 cases, most of the patient arrived at Rajiv Gandhi Government General Hospital, Chennai were severe due to late presentation and also available evidence demonstrating that the delay in treatment is directly associated with increased mortality or poor patient outcome. As an innovative concept of Zero Delay COVID-19 Ward were set up to provide the required critical care for all severe COVID-19 cases. The experience of setting up of such Zero Delay COVID-19 Ward and profile of admitted COVID-19 patients were described in this paper.Methods:A total of 4515 laboratory-confirmed COVID-19 patients admitted at Zero Delay COVID-19 Ward was analyzed retrospectively from 7th July to 31st December 2020.Results:At the time of admission the frequency of dyspnea were 85.6% among them 99.1% recovered from dyspnea after the oxygen therapy and other management at Zero Delay COVID-19 Ward. Of the 4515 COVID-19 individuals, about 1829 (40.5%) had comorbidity, 227 (5%) had died. Multivariable logistic regression analysis, COVID-19 death was more likely to be associated with comorbidity (OR: 18.687; 95% CI: 11.229-31.1) than other variables.Conclusions:Comorbidity is an independent high risk factor for mortality of COVID-19 patients. From our observation, it is strongly recommended that effective zero delay covid-19 ward model will help for the prevention of mortality in current/expected waves of COVID-19.

The risk factors for mortality of diabetic patients with severe COVID-19: A retrospective study of 167 severe COVID-19 cases in Wuhan.

Diabetes is one of the most common comorbidities in adult patients with coronavirus disease 2019 (COVID-19). This study aimed to analyze the mortality risk factors of diabetic patients with COVID-19. A total of 167 patients with severe COVID-19, including 55 diabetic patients and 112 nondiabetic patients at Tongji Hospital, Wuhan, China from January 28, 2020, to March 10, 2020, were collected. The laboratory, radiological, management information, and medical history was retrospectively reviewed. Potential mortality risk factors in diabetic patients with COVID-19 were evaluated by the proportional hazard Cox model. The clinical information of 167 patients with severe COVID-19 was analyzed. The median age was 65.0 years. Approximately 32.9% of patients had diabetes. In total patients, older age, diabetes, and lymphocyte count were associated with increased risk of death. In diabetic patients, increased mortality was associated with decreased lymphocyte count (≤0.45×10⁹/L, HR 0.196, 95% CI 0.049-0.781, P = 0.021), lactate dehydrogenase >600 U/L (HR 8.010, 95% CI 1.540-41.670, P = 0.013), hsCRP >90 mg/L (HR 4.551, 95% CI 1.472-14.070, P = 0.009) and interleukin-10 >10 U/mL (HR 5.362, 95% CI 1.239-23.199, P = 0.025). COVID-19 patients with diabetes had a poor prognosis, especially when they had two or more of the following abnormalities (χ2 = 58.62, P<0.001): lymphocyte count was ≤0.45×10⁹/L, lactate dehydrogenase was >600 U/L, hsCRP was >90 mg/L and IL-10 was >10 U/mL. For diabetic patients with COVID-19, more attention should be paid to the dynamic monitoring of cytokine levels, and the control of hyperglycemia.

Evaluation of serum hepatic enzyme activities in different COVID-19 phenotypes.

Coronavirus disease 2019 (COVID-19) is a newly emerging infectious disease. Our understanding of the clinical characteristics of liver damage and the relationship with disease severity in COVID-19 is still limited. To investigate the serum hepatic enzyme activities in different phenotypes of COVID-19 patients, evaluate their relationship with the illness severity and analyze the correlation of glycyrrhizin treatment and abnormal liver enzyme activities, one hundred and forty-sevenpatients with COVID-19 were enrolledin a retrospective study that investigated hepatic dysfunction. Liver alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH), Y-glutamyl transferase (GGT), superoxide dismutase (SOD), and alkaline phosphatase (ALP) were analyzed in these patients. Patients with diammonium glycyrrhizinate (DG) treatment were further investigated. Of the 147 patients, 56 (38.1%) had abnormal ALT activity and 80 (54.4%) had abnormal AST activity. The peak of abnormal hepatic enzyme activities occurred at 3 to 6 days after on admission. Serum AST and LDH levels were elevated, while the SOD level was decreased in severe and critical patients, compared with mild cases. DG treatment may alleviate the abnormal liver enzyme activities in non-critical COVID-19 patients. Abnormal liver functions may be observed in patients with COVID-19, andwere associated with SARS-CoV-2-induced acute liver damage. Glycyrrhizin treatment may be an effective therapeutic approach for the outcome of abnormal hepatic enzyme activities in severe COVID-19 cases. Serum hepatic enzyme tests may reflect the illness severity and should be monitored.

Repurposing of Biologic and Targeted Synthetic Anti-Rheumatic Drugs in COVID-19 and Hyper-Inflammation: A Comprehensive Review of Available and Emerging Evidence at the Peak of the Pandemic.

Coronavirus disease 2019 (COVID-19) is a condition caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Severe cases of COVID-19 result in acute respiratory distress syndrome and death. A detrimental, hyper-inflammatory immune response with excess release of cytokines is the main driver of disease development and of tissue damage in these patients. Thus, repurposing of biologic agents and other pharmacological inhibitors of cytokines used for the treatment of various inflammatory conditions emerged as a logical therapeutic strategy to quench inflammation and improve the clinical outcome of COVID-19 patients. Evaluated agents include the interleukin one receptor blocker anakinra, monoclonal antibodies inhibiting IL-6 tocilizumab and sarilumab, monoclonal antibodies inhibiting granulocyte-monocyte colony stimulating factor and tumor necrosis factor, and Janus kinase inhibitors. In this review, we discuss the efficacy and safety of these therapeutic options based on direct personal experience and on published evidence from observational studies and randomized clinical trials.

Safety and efficacy of convalescent plasma therapy in severely and critically ill patients with COVID-19: a systematic review with meta-analysis.

Background: The rapidly evolving coronavirus disease 2019 (COVID-19) has resulted in more than 24 million infections and 821 thousand deaths. However, a vaccine or specific drug is absent up to this date and more attention has been focused on the use of convalescent plasma (CP). Several articles have described the CP treatment for patients with SARS-CoV-2 infection. But a comprehensive systematic review with meta-analysis about the safety and efficacy of CP transfusion in SARS-CoV-2-infected patients has not been published. We conducted this study for a better understanding of the therapeutic significance of CP for patients with COVID-19.Results: A fixed-effect model (I2=0.0%) was used on the 9 articles for quantitative analysis showing that the mortality of patients with COVID-19 treated with or without CP was statistically significant (RR=0.57 [0.44-0.74]). Subgroup analysis showed that the severely ill patients benefited more from CP than the critically ill patients. Our study concluded that clinical improvement in severe COVID-19 cases were obvious. Adverse events were few and the effect of convalescent plasma on reducing viral load was apparent.Conclusions: Convalescent plasma therapy appears safe for COVID-19, and plasma treated patients have marked reductions in their serum viral loads and most are virus negative after transfusion. Patients with severe COVID-19 benefit more from the convalescent plasma transfusion than critical patients, and patients treated in early stage are more likely to survive.Methods: We reviewed the scientific literature from four databases published from December 8, 2019 to August 20, 2020. Statistical analyses were performed with STATA (version 15.1; Stata Corporation, College Station, TX, USA). The frequency with 95% confidence intervals (CI) was assessed using fixed effect model in analyzing the overall mortality and p <0.05 was considered statistically significant.

SARS-CoV-2 and Viral Sepsis: Immune Dysfunction and Implications in Kidney Failure.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causal agent of coronavirus disease 2019 (COVID-19), first emerged in Wuhan, China. The clinical manifestations of patients infected with COVID-19 include fever, cough, and dyspnea, up to acute respiratory distress syndrome (ARDS) and acute cardiac injury. Thus, a lot of severe patients had to be admitted to intensive care units (ICU). The pathogenic mechanisms of SARS-CoV-2 infection are mediated by the binding of SARS-CoV-2 spikes to the human angiotensin-converting enzyme 2 (ACE-2) receptor. The overexpression of human ACE-2 is associated with the disease severity in SARS-CoV-2 infection, demonstrating that viral entry into cells is a pivotal step. Although the lung is the organ that is most commonly affected by SARS-CoV-2 infection, acute kidney injury (AKI), heart dysfunction and abdominal pain are the most commonly reported co-morbidities of COVID-19. The occurrence of AKI in COVID-19 patients might be explained by several mechanisms that include viral cytopathic effects in renal cells and the host hyperinflammatory response. In addition, kidney dysfunction could exacerbate the inflammatory response started in the lungs and might cause further renal impairment and multi-organ failure. Mounting recent evidence supports the involvement of cardiovascular complications and endothelial dysfunction in COVID-19 syndrome, in addition to respiratory disease. To date, there is no vaccine, and no specific antiviral medicine has been shown to be effective in preventing or treating COVID-19. The removal of pro-inflammatory cytokines and the shutdown of the cytokine storm could ameliorate the clinical outcome in severe COVID-19 cases. Therefore, several interventions that inhibit viral replication and the systemic inflammatory response could modulate the severity of the renal dysfunction and increase the probability of a favorable outcome.

Dynamic SARS-CoV-2-Specific Immunity in Critically Ill Patients With Hypertension.

BackgroundThe current outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses an unprecedented health crisis. The most common chronic illness among patients infected with SARS-CoV-2 is hypertension. Immune dysregulation plays an important role in SARS-CoV-2 infection and in the development of hypertension; however, the dynamic immunological characteristics of COVID-19 patients with hypertension remain largely unclear.MethodsIn total, 258 hypertensive patients infected with SARS-CoV-2 were included in this study. CD38+HLA-DR+ and CD38+PD-1+ CD8+ T cells, IFNγ+CD4+ and IFNγ+CD8+ T cells, the titers of IgG, IgM, and IgA against SARS-CoV-2 spike protein, and SARS-CoV-2 throat viral loads were measured weekly over 4 weeks after the onset of symptoms. Clinical outcomes were also monitored.FindingsCD4+ T lymphopenia was observed in 100% of the severe and critical cases. Compared with the surviving patients, the patients with fatal outcomes exhibited high and prolonged expression of CD38+HLA-DR+ and CD38+PD-1+ on CD8+ T cells, low expression of SARS-CoV-2-specific IFNγ+CD4+ and IFNγ+CD8+ T cells, low titers of IgG, IgM, and IgA against SARS-CoV-2 spike protein, and high SARS-CoV-2 viral load during the illness. In the surviving patients, the viral load was significantly inversely correlated with SARS-CoV-2-specific IFNγ+CD8+and IFNγ+CD4+ T cells, IgG, IgM, and IgA.InterpretationT lymphopenia is common in critical or severe COVID-19 cases with hypertension. Prolonged activation and exhaustion of CD8+ T cells were associated with severe disease. The delayed SARS-CoV-2-specific antibody responses may be insufficient for overcoming severe SARS-CoV-2 infection in the absence of SARS-CoV-2-specific cellular responses.

Classification of Severe and Critical Covid-19 Using Deep Learning and Radiomics.

The coronavirus disease 2019 (COVID-19) is rapidly spreading inside China and internationally. We aimed to construct a model integrating information from radiomics and deep learning (DL) features to discriminate critical cases from severe cases of COVID-19 using computed tomography (CT) images. We retrospectively enrolled 217 patients from three centers in China, including 82 patients with severe disease and 135 with critical disease. Patients were randomly divided into a training cohort (n = 174) and a test cohort (n = 43). We extracted 102 3-dimensional radiomic features from automatically segmented lung volume and selected the significant features. We also developed a 3-dimensional DL network based on center-cropped slices. Using multivariable logistic regression, we then created a merged model based on significant radiomic features and DL scores. We employed the area under the receiver operating characteristic curve (AUC) to evaluate the model's performance. We then conducted cross validation, stratified analysis, survival analysis, and decision curve analysis to evaluate the robustness of our method. The merged model can distinguish critical patients with AUCs of 0.909 (95% confidence interval [CI]: 0.859-0.952) and 0.861 (95% CI: 0.753-0.968) in the training and test cohorts, respectively. Stratified analysis indicated that our model was not affected by sex, age, or chronic disease. Moreover, the results of the merged model showed a strong correlation with patient outcomes. A model combining radiomic and DL features of the lung could help distinguish critical cases from severe cases of COVID-19.

Clinical characteristics and plasma antibody titer of patients with COVID-19 in Zhejiang, China.

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which first affected humans in China on December 31, 2019 (Shi et al., 2020). Coronaviruses generally cause mild, self-limiting upper respiratory tract infections in humans, such as the common cold, pneumonia, and gastroenteritis (To et al., 2013; Berry et al., 2015; Chan et al., 2015). According to the Report of the World Health Organization (WHO)-China Joint Mission on COVID-19 (WHO, 2020), the case fatality rate of COVID-19 increases with age, while the rate among males is higher than that among females (4.7% and 2.8%, respectively). Since an effective vaccine and specific anti-viral drugs are still under development, passive immunization using the convalescent plasma (CP) of recovered COVID-19 donors may offer a suitable therapeutic strategy for severely ill patients in the meantime. So far, several studies have shown therapeutic efficacy of CP transfusion in treating COVID-19 cases. A pilot study first reported that transfusion of CP with neutralizing antibody titers above 1:640 was well tolerated and could potentially improve clinical outcomes through neutralizing viremia in severe COVID-19 cases (Chen et al., 2020). Immunoglobulin G (IgG) and IgM are the most abundant and important antibodies in protecting the human body from viral attack (Arabi et al., 2015; Marano et al., 2016). Our study aimed to understand the aspects of plasma antibody titer levels in convalescent patients, as well as assessing the clinical characteristics of normal, severely ill, and critically ill patients, and thus provide a basis for guiding CP therapy. We also hoped to find indicators which could serve as a reference in predicting the progression of the disease.

Corticosteroid use in viral pneumonia: experience so far and the dexamethasone breakthrough in coronavirus disease-2019.

Dexamethasone was shown to decrease the mortality in coronavirus disease-2019 (COVID-19) recently. Use of corticosteroids was harmful in other coronavirus infections previously. WHO recommended against routine use of corticosteroids in COVID-19. In view of these, we reviewed the evidence about the use of corticosteroids in virus-induced acute respiratory distress syndrome (ARDS). Corticosteroids are beneficial in ARDS regardless of etiology. However, they increased the mortality rate in influenza-associated ARDS. In SARS and the Middle East respiratory syndrome, corticosteroids increased the mortality, delayed the viral clearance and increased the length of hospital stay. In the case of COVID-19, the available evidence from retrospective and observational studies is inconclusive about the corticosteroid use. Low-dose therapies appear to be effective. Evidence from a randomized control study found dexamethasone is effective in decreasing mortality in severe COVID-19 cases. More studies are needed to validate the benefit of corticosteroids in COVID-19.

High Prevalence of SARS-CoV-2 Genetic Variation and D614G Mutation in Pediatric Patients With COVID-19.

BackgroundThe full spectrum of the disease phenotype and viral genotype of coronavirus disease 2019 (COVID-19) have yet to be thoroughly explored in children. Here, we analyze the relationships between viral genetic variants and clinical characteristics in children.MethodsWhole-genome sequencing was performed on respiratory specimens collected for all SARS-CoV-2-positive children (n = 141) between March 13 and June 16, 2020. Viral genetic variations across the SARS-CoV-2 genome were identified and investigated to evaluate genomic correlates of disease severity.ResultsHigher viral load was detected in symptomatic patients (P = .0007) and in children <5 years old (P = .0004). Genomic analysis revealed a mean pairwise difference of 10.8 single nucleotide variants (SNVs), and the majority (55.4%) of SNVs led to an amino acid change in the viral proteins. The D614G mutation in the spike protein was present in 99.3% of the isolates. The calculated viral mutational rate of 22.2 substitutions/year contrasts the 13.5 substitutions/year observed in California isolates without the D614G mutation. Phylogenetic clade 20C was associated with severe cases of COVID-19 (odds ratio, 6.95; P = .0467). Epidemiological investigation revealed major representation of 3 of 5 major Nextstrain clades (20A, 20B, and 20C) consistent with multiple introductions of SARS-CoV-2 in Southern California.ConclusionsGenomic evaluation demonstrated greater than expected genetic diversity, presence of the D614G mutation, increased mutation rate, and evidence of multiple introductions of SARS-CoV-2 into Southern California. Our findings suggest a possible association of phylogenetic clade 20C with severe disease, but small sample size precludes a definitive conclusion. Our study warrants larger and multi-institutional genomic evaluation and has implications for infection control practices.

Evaluating the effects of Intravenous Immunoglobulin (IVIg) on the management of severe COVID-19 cases: A randomized controlled trial

BackgroundThe newly discovered coronavirus has turned into coronavirus disease 2019 (COVID-19) pandemic and it rages at an unprecedented rate. Considering the findings of previous studies on the use of Intravenous Immunoglobulin (IVIg) for treating severe H1N1 infection and the satisfying results for reducing viral load and mortality, this study aimed to investigate the potential usefulness of IVIg for the management of severe cases. MethodsIn this randomized controlled trial, 84 patients were included: 52 in the IVIg group and 32 in the control group. The intervention group received IVIg at a dose of 400 mg/kg, IV, daily for three days. Both groups received hydroxychloroquine, lopinavir/ritonavir and supportive care. The demographic data, mortality rate, the need for mechanical ventilation, length of stay in hospital and in Intensive Care Unit (ICU), and imaging findings were recorded and compared in terms of the mentioned factors. ResultsThe mean time from admission to IVIg initiation was 3.84 ± 3.35 days. There was no significant difference between the two groups in terms of mortality rate (P-value = 0.8) and the need for mechanical ventilation (P-value = 0.39). The length of hospital stay was significantly lower for the control group than that of the intervention group (P-value = 0.003). There was a significant positive relationship between the time from hospital admission to IVIg initiation and the length of stay in the hospital and ICU among the survivors (P-value < 0.001 and =0.01, respectively). ConclusionsOur findings did not support the use of IVIg in combination with hydroxychloroquine and lopinavir/ritonavir in treatment of severe COVID-19 cases.

Neuropathobiology of COVID-19: The Role for Glia.

SARS-CoV-2, which causes the Coronavirus Disease 2019 (COVID-19) pandemic, has a brain neurotropism through binding to the receptor angiotensin-converting enzyme 2 expressed by neurones and glial cells, including astrocytes and microglia. Systemic infection which accompanies severe cases of COVID-19 also triggers substantial increase in circulating levels of chemokines and interleukins that compromise the blood-brain barrier, enter the brain parenchyma and affect its defensive systems, astrocytes and microglia. Brain areas devoid of a blood-brain barrier such as the circumventricular organs are particularly vulnerable to circulating inflammatory mediators. The performance of astrocytes and microglia, as well as of immune cells required for brain health, is considered critical in defining the neurological damage and neurological outcome of COVID-19. In this review, we discuss the neurotropism of SARS-CoV-2, the implication of neuroinflammation, adaptive and innate immunity, autoimmunity, as well as astrocytic and microglial immune and homeostatic functions in the neurological and psychiatric aspects of COVID-19. The consequences of SARS-CoV-2 infection during ageing, in the presence of systemic comorbidities, and for the exposed pregnant mother and foetus are also covered.

Analysis of Chest CT Results of Coronavirus Disease 2019 (COVID-19) Patients at First Follow-Up.

Objective To investigate the dissipation and outcomes of pulmonary lesions at the first follow-up of patients who recovered from moderate and severe cases of COVID-19. Methods From January 21 to March 3, 2020, a total of 136 patients with COVID-19 were admitted to our hospital. According to inclusion and exclusion criteria, 52 patients who recovered from COVID-19 were included in this study, including 33 moderate cases and 19 severe cases. Three senior radiologists independently and retrospectively analyzed the chest CT imaging data of 52 patients at the last time of admission and the first follow-up after discharge, including primary manifestations, concomitant manifestations, and degree of residual lesion dissipation. Results At the first follow-up after discharge, 16 patients with COVID-19 recovered to normal chest CT appearance, while 36 patients still had residual pulmonary lesions, mainly including 33 cases of ground-glass opacity, 5 cases of consolidation, and 19 cases of fibrous strip shadow. The proportion of residual pulmonary lesions in severe cases (17/19) was statistically higher than in moderate cases (19/33) (χ2 = 5.759, P < 0.05). At the first follow-up, residual pulmonary lesions were dissipated to varying degrees in 47 cases, and lesions remained unchanged in 5 cases. There were no cases of increased numbers of lesions, enlargement of lesions, or appearance of new lesions. The dissipation of residual pulmonary lesions in moderate patients was statistically better than in severe patients (Z = −2.538, P < 0.05). Conclusion Clinically cured patients with COVID-19 had faster dissipation of residual pulmonary lesions after discharge, while moderate patients had better dissipation than severe patients. However, at the first follow-up, most patients still had residual pulmonary lesions, which were primarily ground-glass opacity and fibrous strip shadow. The proportion of residual pulmonary lesions was higher in severe cases of COVID-19, which required further follow-up.

Mesenchymal stem cells as living anti-inflammatory therapy for COVID-19 related acute respiratory distress syndrome.

Coronavirus disease 2019 (COVID-19), a pandemic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is growing at an exponential rate worldwide. Manifestations of this disease are heterogeneous; however, advanced cases often exhibit various acute respiratory distress syndrome-like symptoms, systemic inflammatory reactions, coagulopathy, and organ involvements. A common theme in advanced COVID-19 is unrestrained immune activation, classically referred to as a “cytokine storm”, as well as deficiencies in immune regulatory mechanisms such as T regulatory cells. While mesenchymal stem cells (MSCs) themselves are objects of cytokine regulation, they can secrete cytokines to modulate immune cells by inducing anti-inflammatory regulatory Treg cells, macrophages and neutrophils; and by reducing the activation of T and B cells, dendritic and nature killer cells. Consequently, they have therapeutic potential for treating severe cases of COVID-19. Here we discuss the unique ability of MSCs, to act as a “living anti-inflammatory”, which can “rebalance” the cytokine/immune responses to restore equilibrium. We also discuss current MSC trials and present different concepts for optimization of MSC therapy in patients with COVID-19 acute respiratory distress syndrome.

Management of bacteriological specimens of patients suffering from coronavirus disease 2019 (COVID-19)

Management of bacteriological specimens of patients suffering from coronavirus disease 2019 (COVID-19)

Investigation of hematological parameters related to the severity of COVID-19 disease in Mashhad, Iran

Introduction:Human coronavirus disease 2019 (COVID-19) is an emerging respiratory disease that has become pandemic worldwide. The patients have a range of mild to severe symptoms, such as pneumonia, acute respiratory distress syndrome, arrhythmia, shock, and other organs involvement. Clinical and hematological evidence can serve as a prognostic factor to detect severe cases of COVID-19. Objectives: The present study aimed to evaluate hematological parameters related to the severity of the disease in COVID-19 patients in Mashhad, Eastern Iran. Patients and Methods: All the individuals with positive real-time reverse transcription-polymerase chain reaction test results and the patients with clinical symptoms whose computed tomography scan results were matched with the diagnosis of viral pneumonia were included in the study. The hematological examinations and complete blood count of the patients were performed by the healthcare personnel through collecting blood samples at the time of admission and discharge from the hospital. Results: In total, 189 COVID-19 patients were included in the study, 47.6% and 58.73% of whom were over 60 years old and male, respectively. Investigation of the hematological parameters revealed that the number of white blood cells, mean value of corpuscular volume, number of platelets, and lymph count had significantly increased at the time of discharge (P&lt;0.01). On the other hand, red blood cells, hemoglobin, hematocrit, mean corpuscular hemoglobin, mean corpuscular hemoglobin, and red cell distribution width values were significantly higher at the time of admission in comparison to discharge (P&lt;0.01). Furthermore, it was found that male gender had a significant relationship with the development of lymphopenia in the patients (P=0.021). Conclusion: It can be concluded that hematological parameters and inflammatory biomarkers in COVID-19 patients could potentially act as the independent factors and affect the prognosis of the disease.

Evidence of potent humoral immune activity in COVID-19-infected kidney transplant recipients.

Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID‐19) infection and 36 matched, transplanted controls without COVID‐19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4+ and CD8+ T cells in the COVID‐19 subjects. We also showed fewer anergic and senescent CD8+ T cells in COVID‐19 individuals, but no differences in exhausted CD8+ T cells, nor in any of these CD4+ T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID‐19 patients. Sixteen of 18 COVID‐19 subjects tested for anti‐SARS‐CoV‐2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID‐19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID‐19 infection can mount SARS‐CoV‐2‐reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID‐19 may not be required.

COVID-19-related Cerebrovascular Disease and Vasculitis

Cerebrovascular disease and vasculitis-related diseases have been reported as systemic complications of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A proposed underlying mechanism is that SARS-CoV-2 infects vascular endothelial cells via the angiotensin-converting enzyme 2 (ACE2) and causes inflammation. Cerebrovascular disease and vasculitis are often observed in severe COVID-19 cases, and they may be associated with critical systemic conditions, such as the cytokine storm and thrombotic tendencies. Several other mechanisms have been proposed, and diverse pathological conditions may be associated with COVID-19-related cerebrovascular disease and vasculitis. Clarifying the pathophysiology and establishing a better therapeutic regimen will facilitate favorable outcomes.