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The unprecedented impact of the coronavirus disease 2019 (COVID-19) pandemic has resulted in global challenges to our health-care systems and our economic security. As such, there has been significant research into all aspects of the disease, including diagnostic biomarkers, associated risk factors, and strategies that might be used for its treatment and prevention. Toward this end, eosinopenia has been identified as one of many factors that might facilitate the diagnosis and prognosis of severe COVID-19. However, this finding is neither definitive nor pathognomonic for COVID-19. While eosinophil-associated conditions have been misdiagnosed as COVID-19 and others are among its reported complications, patients with pre-existing eosinophil-associated disorders (e.g., asthma, eosinophilic gastrointestinal disorders) do not appear to be at increased risk for severe disease; interestingly, several recent studies suggest that a diagnosis of asthma may be associated with some degree of protection. Finally, although vaccine-associated aberrant inflammatory responses, including eosinophil accumulation in the respiratory tract, were observed in preclinical immunization studies targeting the related SARS-CoV and MERS-CoV pathogens, no similar complications have been reported clinically in response to the widespread dissemination of either of the two encapsulated mRNA-based vaccines for COVID-19.

BackgroundIn cows with acute toxic mastitis (ATM), the leukogram aids in the assessment of the severity of disease. The goal of our study was to compare the leukogram of 158 cows with ATM (cases) and 168 clinically healthy cows (controls). We hypothesised that the leukograms of surviving and non-surviving cows differ and that there are variables of the leukogram with sufficient prognostic potential to be used in the decision to treat or not to treat a cow with ATM. The cows were examined clinically and underwent haematological and biochemical examination of blood and bacteriological culture of milk samples.ResultsAll cows with ATM had a poor appetite or anorexia, and 34 cows (21.5%) were recumbent. A single quarter was affected in 119 cows (75.3%), two quarters in 37 cows (23.4%) and three quarters in two cows (1.3%). Bacteriological culture showed Gram-negative pathogens in 100 cows (63.3%), Gram-positive in 15 (9.5%) and yeast in 4 (2.5%). The median total leukocyte count of cases was 4300 cells/µL (interquartile range = 2300–8200/µL), which was significantly lower than 8000 cells/µL (6525–9300/µL) in controls. Except for band neutrophils and metamyelocytes, the counts of all components of the leukogram were lower in cases compared with controls. Significantly more cows with ATM had leukopenia (60.1 vs. 4.1%) or leukocytosis (10.1 vs. 3.0%) than controls. Diseased cows had significantly lower segmented neutrophil counts than controls (860 vs. 2598 cells/µL), and 69.5 and 17.3%, respectively, had counts below the reference interval. Cases had increased band (77.3%) and metamyelocyte (25.0%) counts compared with controls (0.6 and 0%, respectively). In diseased cows, eosinopenia occurred in 66.4% (controls, 1.8%), monocytopenia in 40.6% (4.2%) and lymphopenia in 60.2% (1.8%). Twenty-one diseased cows (16.4%) had a regenerative and 57 (44.5%) had a degenerative left shift. The median neutrophil-to-lymphocyte ratio was 0.97 in diseased cows and 0.63 in controls. Toxic changes in neutrophils including cytoplasmic basophilia and vacuolisation were seen in 101 (91.8%) of 110 blood smears of diseased cows. The leukogram of the surviving and non-surviving cows did not differ significantly, and the hypothesis was rejected.ConclusionsATM results in severe changes in the leukogram particularly leukopenia, lymphopenia, and degenerative left shift. The hypothesis that the leukograms of surviving and non-surviving cows differ was rejected. The leukogram has not sufficient prognostic potential to be used in the decision to treat or not to treat a cow with ATM.

Background Data are lacking on the role of cellular components of hematological system as biomarkers for prognosis of sepsis. We planned to identify if these parameters measured at admission to ICU and at 72 hours can be useful as prognostic marker in septic critically ill patients. Materials and methods In this prospective observational study, 130 adult patients with sepsis were recruited. Various hematological study parameters (total, differential, and absolute leukocyte count, platelet count, platelet distribution width, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio) were noted at day 1 and day 3 of admission. Primary outcome was 28-day mortality, and secondary outcomes were duration of mechanical ventilation, vasopressor requirement, ICU length of stay, and requirement of renal replacement therapy. The variables were compared between two groups and using binary regression model and were evaluated as prognostic markers for 28-day mortality. Results Data from n = 129 were analyzed. At day-28, n = 58 (44.96%) patients survived. Baseline and demographic parameters were comparable between survivors and nonsurvivors. Admission Sequential Organ Failure Assessment score was more in nonsurvivors than survivors [8 (6–8) vs 6 (4–8); p = 0.002]. In nonsurvivors, monocyte, lymphocyte, basophil, eosinophil, and platelet count were significantly less at day 1 and lymphocyte, eosinophil, basophil and platelet count were significantly less at day 3. NLR and PLR at day 3 were significantly more in nonsurvivors. On logistic regression analysis, age, thrombocytopenia on day 1, and low eosinophil count on day 3 predicted 28-day mortality (p = 0.006, p = 0.02, and p = 0.04, respectively). Conclusion Thrombocytopenia on day 1 and eosinopenia on day 3 may predict 28-day mortality in sepsis. How to cite this article Sinha H, Maitra S, Anand RK, Aggarwal R, Rewari V, Subramaniam R, et al. Epidemiology and Prognostic Utility of Cellular Components of Hematological System in Sepsis. Indian J Crit Care Med 2021;25(6):660–667.

Rationale: Pulmonary vascular endotheliitis, perivascular inflammation, and immune activation are observed in COVID-19 patients. While the initial SARS-CoV-2 infection mainly infects lung epithelial cells, whether it also infects endothelial cells (ECs) and to what extent SARS-CoV-2-mediated pulmonary vascular endotheliitis is associated with immune activation remain to be determined. Methods: To address these questions, we studied SARS-CoV-2-infected K18-hACE2 (K18) mice, a severe COVID-19 mouse model, as well as lung samples from SARS-CoV-2-infected nonhuman primates (NHP) and patient deceased from COVID-19. We used immunostaining, RNAscope, and electron microscopy to analyze the organs collected from animals and patient. We conducted bulk and single cell (sc) RNA-seq analyses, and cytokine profiling of lungs or serum of the severe COVID-19 mice. Results: We show that SARS-CoV-2-infected K18 mice develop severe COVID-19, including progressive body weight loss and fatality at 7 days, severe lung interstitial inflammation, edema, hemorrhage, perivascular inflammation, systemic lymphocytopenia, and eosinopenia. Body weight loss in K18 mice correlated with the severity of pneumonia, but not with brain infection. We also observed endothelial activation and dysfunction in pulmonary vessels evidenced by the up-regulation of VCAM1 and ICAM1 and the downregulation of VE-cadherin. We detected SARS-CoV-2 in capillary ECs, activation and adhesion of platelets and immune cells to the vascular wall of the alveolar septa, and increased complement deposition in the lungs, in both COVID-19-murine and NHP models. We also revealed that pathways of coagulation, complement, K-ras signaling, and genes of ICAM1 and VCAM1 related to EC dysfunction and injury were upregulated, and were associated with massive immune activation in the lung and circulation. Conclusion: Together, our results indicate that SARS-CoV-2 causes endotheliitis via both infection and infection-mediated immune activation, which may contribute to the pathogenesis of severe COVID-19 disease.

Background: Biomarkers of resistance to H1-antihistamines (AH) and omalizumab in chronic spontaneous urticaria (CSU) are still a matter of debate. Objective: To identify clinical and laboratory attributes of the patient that may be predictive of AH and omalizumab resistance in CSU. Methods: We conducted a retrospective observational study by using the electronic patient record data base of patients with CSU and of sex- and age-matched controls. Patients with CSU were divided into three study groups: the CSU group, patients who responded to AHs; the antihistamine-resistant CSU (AH-CSU) group, patients refractory to a fourfold AH dose; and the control group, composed of a random sample of age- and sex-matched subjects, with a case-control ratio of 1:2. The patients in the AH-CSU group treated with omalizumab were compared according to the response or resistance to omalizumab. Results: A total of 106 subjects in the AH-CSU group, 483 in the CSU group, and 1198 in the control group were compared. Both AH-CSU (112.7 ± 43.1 kU/mL) and CSU (129.5 ± 52.4 kU/mL) groups were associated with higher plasma total IgE levels than control group (103.2 ± 49.5 kU/mL; p < 0.001). The AH-CSU group was characterized by a higher plasma high-sensitivity C-reactive protein level (6.4 ± 3.7 mg/L) than the CSU group (4.3 ± 1.4 mg/L; p < 0.001) and the control group (3.1 ± 1.8 mg/L; p < 0.001). The AH-CSU and CSU groups were characterized by a lower mean ± standard deviation basophil counts (0.18 ± 0.16 cells ×109/L and 0.19 ± 0.11 cells ×109/L, respectively) than the control group (0.22 ± 0.09 cells ×109/L; p < 0.001). The mean platelet volume was higher in the AH-CSU group (11.2 ± 0.3 fL) than in the CSU group (11.1 ± 0.4 fL; p = 0.002) and in the control group (10.3 ± 0.4 fL; p < 0.001). There were no significant differences in the mean levels of lymphocytes, monocytes, eosinophils, basophils, and platelets, and the rates of eosinopenia and basopenia between the patients in the AH-CSU group who responded to and those who were resistant to omalizumab. Conclusion: This study provided additional data of interest to examine the pathophysiologic role of low-grade inflammation and basopenia in patients with CSU and resistant to AHs and omalizumab.

Septic shock and acute respiratory distress syndrome (ARDS) are characterized by a dysregulated immune host response that may respond to steroid therapy. Eosinophils contribute to type 2 inflammation that often responds to steroid therapy; their role in immune dysregulation and outcomes in sepsis and ARDS is unclear.A systematic search of Cochrane Library, MEDLINE, and EMBASE was performed from inception to 9 September 2020. The search comprised the following terms: eosinophils, sepsis, septic shock, and ARDS. Two reviewers independently screened abstracts and texts and extracted data on disease severity and clinical outcomes.Thirty-nine studies were identified: 30 evaluated serum eosinophil count in sepsis, one evaluated eosinophil activity in sepsis, three assessed bronchoalveolar lavage (BAL) eosinophil count in ARDS, four assessed eosinophil activity in ARDS, and one assessed peripheral eosinophil count in ARDS. Eleven studies showed an association between eosinopenia and sepsis, and eight studies found persistent eosinopenia at48 hr of intensive care unit admission to predict mortality and readmission in septic patients. Three studies found BAL eosinophil count to be low in ARDS, although one found that levels rose in late-phase ARDS. Three studies found eosinophil activity markers in BAL to be high in ARDS and correlate with ARDS severity.Persistent peripheral eosinopenia is a marker of bacterial sepsis and is independently associated with poor outcomes. Bronchoalveolar lavage eosinophil counts are low in early-phase ARDS, but increase in late-phase ARDS, while elevated markers of eosinophil activity correlate with ARDS severity. Further studies understanding the mechanisms leading to eosinopenia in sepsis and increased eosinophil activity in ARDS are needed.RéSUMé: OBJECTIF: Le choc septique et le syndrome de détresse respiratoire aiguë (SDRA, ARDS en anglais) se caractérisent par une réponse immunitaire dérégulée chez l’hôte qui pourrait répondre à une corticothérapie. Les éosinophiles contribuent à l’inflammation de type 2, laquelle répond souvent à la corticothérapie; leur rôle dans la dérégulation immunitaire et les devenirs en cas de sepsis et de SDRA n’est pas clair.Une recherche systématique dans les bases de données Cochrane Library, MEDLINE et EMBASE a été réalisée de leur création au 9 septembre 2020. La recherche comprenait les termes suivants : éosinophiles, sepsis, choc septique et SDRA. Deux réviseurs ont examiné de manière indépendante les résumés et textes et ont extrait les données décrivant la gravité de la maladie et les devenirs cliniques.Trente-neuf études ont été identifiées : 30 études portaient sur le décompte d’éosinophiles sériques lors de sepsis, une étude examinait l’activité des éosinophiles dans un contexte de sepsis, trois ont évalué le décompte d’éosinophiles par lavage bronchoalvéolaire (LBA) dans les cas de SDRA, quatre ont examiné l’activité des éosinophiles dans le SDRA, et une a évalué le décompte d’éosinophiles périphériques dans les cas de SDRA. Onze études ont montré une association entre l’éosinopénie et le sepsis, et huit études ont remarqué qu’une éosinopédie persistante pour plus de 48 heures après l’admission à l’unité de soins intensifs était un prédicteur de mortalité et de réadmission chez les patients septiques. Trois études ont révélé que le nombre d’éosinophiles dans un LBA était faible en cas de SDRA, bien qu’une étude ait constaté que les taux augmentaient dans les SDRA de phase tardive. Trois études ont révélé que les marqueurs d’activité éosinophilique dans les LBA étaient élevés dans les cas de SDRA et étaient corrélés à la gravité du SDRA.L’éosinopénie périphérique persistante est un marqueur de sepsis bactérien et est indépendamment associée à de mauvais pronostics. Les décomptes d’éosinophiles dans les lavages bronchoalvéolaires sont bas dans les cas de SDRA en phase précoce, mais augmentent dans le SDRA en phase tardive, alors que des marqueurs élevés d’activité éosinophilique sont corrélés à la sévérité du SDRA. D’autres études visant à comprendre les mécanismes menant à l’éosinopénie dans le sepsis et à l’augmentation de l’activité éosinophilique dans le SDRA sont nécessaires.

Background: The confirmatory test for COVID-19 relies on the virus levels in the patients and sampling methods. Besides, there is no definitive description of the role of diagnostic lab parameters in the analysis of positive cases yet. Objective: To investigate the positive COVID-19 cases by screening out hematological biomarker for detection of disease severity and progression. Methods: Data of 110 confirmed COVID-19 cases at King Abdulaziz hospital were analyzed, 42 (38.2%) of the cases were treated in ICU. All variables’ means and variances were compared between two groups (non-severe patients and severe) using statistical analysis. Results: ICU and non-ICU positive cases rates were 38.2% and 61.8% respectively. Out of COVID-19 patients, 60% showed lymphopenia and neutrophilia (P < 0.025) and Eosinopenia (60.9%). Furthermore, low levels of MCH and hemoglobin were observed in 96.4% and 90%, respectively. At a significance level of 5%, statistical tests showed a statistically significant difference between groups under investigation in both the mean value and variance for lymphocyte, neutrophils, platelet, and WBCs variables. Conclusions: The analysed variables can be used for predicting patients with positive COVID-19 cases. Lymphocytes and neutrophils were much helpful in monitoring disease severity and infection progression. Moreover, these results encourage considering data as a useful, rapid, and easy way to arrive at a decision of disease severity. Keywords: CBC; Laboratory biomarker; COVID-19; Lymphopenia; Eosinopenia

Introduction Early diagnosis and identification of potential critical cases for timely treatment are crucial for COVID‐19 patients. The aim of this study was to analyze the diagnostic and prognostic implications of WBC and cell population data (CPD) abnormalities related to COVID‐19 at disease onset. Methods Baseline WBC counts and CPD data were analyzed in one hundred COVID‐19 patients presenting to emergency department and subsequently discharged (n = 49), admitted (n = 51) or deceased (n = 22), and in 47 healthy subjects. Results Lymphopenia and eosinopenia were observed in all COVID‐19 patients, with more intensity in the admitted and deceased groups, that also presented increased WBC and neutrophil counts. On CPD analysis, COVID‐19 was associated with increased volume of neutrophils, lymphocytes, and monocytes, whereas conductivity was decreased for neutrophils and increased for lymphocytes. The ROC curve analysis showed good performance for lymphocyte counts in predicting COVID‐19 diagnosis (AUC = 0.858), for neutrophil counts in predicting admission for COVID‐19 (AUC = 0.744) and for monocytes volume in predicting COVID‐19 diagnosis (AUC = 0.837). Conclusion WBC counts and CPD parameters at disease onset in COVID‐19 patients can improve diagnostic characterization and aid in the discrimination between severe and nonsevere presentations.

BACKGROUND: The pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has made widespread impact recently. We aim to investigate the clinical characteristics of COVID-19 children with different severities and allergic status. METHODS: Data extracted from the electronic medical records, including demographics, clinical manifestations, comorbidities, laboratory and immunological results, and radiological images of 182 hospitalized COVID-19 children, were summarized and analyzed. RESULTS: The median age was 6 years, ranging from 3 days to 15 years, and there were more boys (male-female ratio about 2:1) within the studied 182 patients. Most of the children were infected by family members. Fever (43.4%) and dry cough (44.5%) were common symptoms, and gastrointestinal manifestations accounted for 11.0%, including diarrhea, abdominal discomfort, and vomiting. 71.4% had abnormal chest computed tomography (CT) scan images, and typical signs of pneumonia were ground-glass opacity and local patchy shadowing on admission. Laboratory results were mostly within normal ranges, and only a small ratio of lymphopenia (3.9%) and eosinopenia (29.5%) were observed. The majority (97.8%) of infected children were not severe, and 24 (13.2%) of them had asymptomatic infections. Compared to children without pneumonia (manifested as asymptomatic and acute upper respiratory infection), children with pneumonia were associated with higher percentages of the comorbidity history, symptoms of fever and cough, and increased levels of serum procalcitonin, alkaline phosphatase, and serum interleukins (IL)-2, IL-4, IL-6, IL-10, and TNF-α. There were no differences in treatments, duration of hospitalization, time from first positive to first negative nucleic acid testing, and outcomes between children with mild pneumonia and without pneumonia. All the hospitalized COVID-19 children had recovered except one death due to intussusception and sepsis. In 43 allergic children with COVID-19, allergic rhinitis (83.7%) was the major disease, followed by drug allergy, atopic dermatitis, food allergy, and asthma. Demographics and clinical features were not significantly different between allergic and nonallergic groups. Allergic patients showed less increase in acute phase reactants, procalcitonin, D-dimer, and aspartate aminotransferase levels compared with all patients. Immunological profiles including circulating T, B, and NK lymphocyte subsets, total immunoglobulin and complement levels, and serum cytokines did not show any difference in allergic and pneumonia groups. Neither eosinophil counts nor serum total immunoglobulin E (IgE) levels showed a significant correlation with other immunological measures, such as other immunoglobulins, complements, lymphocyte subset numbers, and serum cytokine levels. CONCLUSION: Pediatric COVID-19 patients tended to have a mild clinical course. Patients with pneumonia had higher proportion of fever and cough and increased inflammatory biomarkers than those without pneumonia. There was no difference between allergic and nonallergic COVID-19 children in disease incidence, clinical features, and laboratory and immunological findings. Allergy was not a risk factor for developing and severity of SARS-CoV-2 infection and hardly influenced the disease course of COVID-19 in children.

Highlights • Lymphopenia and eosinopenia might be predictors of disease severity in COVID-19. • Lymphopenia and eosinopenia might be predictors of disease progression in COVID-19. • Clinical classification-severe type is the dependently risk factor for alteration of PBICs. • PBICs might be a sentinel, and it deserves attention during COVID-19 management., Background The underlying changes of peripheral blood inflammatory cells (PBICs) in COVID-19 patients are little known. Moreover, the risk factors for the underlying changes of PBICs and their predicting role in severe COVID-19 patients remain uncertain. Material and Methods This retrospective study including two cohorts: the main cohort enrolling 45 patients of severe type serving as study group, and the secondary cohort enrolling 12 patients of no-severe type serving as control group. The PBICs analysis was based on blood routine and lymphocyte subsets. The inflammatory cell levels were compared among patients according to clinical classifications, disease-associated phases, as well as one-month outcomes. Results Compared with patients of non-severe type, the patients of severe type suffered from significantly decreased counts of lymphocytes, eosinophils, basophils, but increased counts of neutrophils. These PBICs alterations got improved in recovery phase, but persisted or got worse in aggravated phase. Compared with patients in discharged group, the patients in un-discharged/died group suffered from decreased counts of total T lymphocytes, CD4+T lymphocytes, CD8+T lymphocytes, as well as NK cells at 2 weeks after treatment. Clinical classification-critically severe was the independently risk factor for lymphopenia (OR=7.701, 95%CI:1.265-46.893, P=0.027), eosinopenia (OR=5.595, 95%CI:1.008-31.054, P=0.049) and worse one-month outcome (OR=8.984; 95%CI:1.021-79.061, P=0.048). Conclusion Lymphopenia and eosinopenia may serve as predictors of disease severity and disease progression in COVID-19 patients, and enhancing the cellular immunity may contribute to COVID-19 treatment. Thus, PBICs might become a sentinel of COVID-19, and it deserves attention during COVID-19 treatment.

SUMMARY OBJECTIVE The scientific community is constantly assessing the clinical and laboratory manifestations of COVID-19 in the organism. In view of the fragmentation of the large amount of information, knowledge gaps in relation to laboratory markers, and scarcity of papers in Portuguese, we propose a Literature review on laboratory changes observed in patients infected with SARS-CoV-2. METHODS Analysis of articles published between December 2019 and May 2020 on the PubMed and SciELO databases. The articles were identified, filtered, and evaluated based on the approach to the subject, language, and impact. Then, the articles were subjected to a thorough reading, in full, by 4 (four) independent researchers. RESULTS Leukopenia and lymphopenia were included in most studies, even in case definitions. Platelet count and platelet-lymphocyte ratio, at peak platelet, were associated with advanced age and longer hospital stay. Eosinopenia showed a sensitivity of 74.7% and specificity of 68.7% and, together with increased CRP, these are one of the future prospects for screening for disease. A high level of procalcitonin may indicate bacterial co-infection, leading to a worse prognosis. COVID-19 manifests itself with increased levels of many inflammatory markers such as IL-1, IL-2, IL-6, IL-7, IL-12, IP10, IFN-γ, MIP1A, MCP1, GSCF, TNF-α, and MCP1/CCL2, as well as LDH, ESR, D-dimer, CK, ALT, and AST. CONCLUSION There is a need for further studies on the new SARS-CoV-2. So far, there is no consensus regarding laboratory findings and their usefulness, whether as a prognostic marker, mortality, or disease severity. RESUMO OBJETIVO A comunidade científica avalia a todo momento, as manifestações clínicas e laboratoriais da COVID-19 no organismo e, em vista da fragmentação da grande quantidade de informações, lacunas de conhecimento em relação aos marcadores laboratoriais e escassez de trabalhos em português, propomos uma revisão de Literatura sobre alterações laboratoriais observadas em pacientes infectados por SARS-CoV-2. MÉTODOS Análise de artigos publicados entre dezembro de 2019 a maio de 2020 nas plataformas PubMed e SciELO. Os artigos foram identificados, filtrados e avaliados com base na abordagem ao assunto, idioma e impacto. Depois, os artigos foram submetidos a uma minuciosa leitura, na íntegra, por 4 (quatro) pesquisadores independentes. RESULTADOS A leucopenia e a linfopenia constaram na maioria dos trabalhos, presente até em definições de caso. A contagem de plaquetas e a razão plaquetas-linfócitos, no pico plaquetário, foram associados à idade avançada e maior tempo de hospitalização. A eosinopenia apresentou sensibilidade de 74,7% e especificidade de 68,7% e, juntamente com aumento da PCR, são uma das perspectivas futuras de triagem para doença. O alto nível de procalcitonina pode indicar uma co-infecção bacteriana, levando a pior prognóstico. A COVID-19 se manifesta com níveis aumentados de muitos marcadores inflamatórios como IL-1, IL-2, IL-6, IL-7, IL-12, IP10, IFN-γ, MIP1A, MCP1, GSCF, TNF-α e MCP1/CCL2, bem como LDH, VHS, dímero-D, CK, ALT e AST. CONCLUSÃO Há necessidade de estudos adicionais sobre o novo SARS-CoV-2. Até agora, não há unanimidade em relação aos achados laboratoriais e sua utilidade, seja como marcador prognóstico, de mortalidade, ou de severidade de doença.

The article studies the correlation of the content of peripheral blood and red bone marrow eosinophils with the level of secretion of fibroblast growth factor (FGF-21), insulin-like factor (IGF-1) and vasculoendothelial growth factor (VEGF-C) in blood serum during the formation of dermal collagen after local cold damage. Animals of the experimental group after the onset of narcotic sleep on the depilated skin of the back were simulated contact frostbite of the 3rd degree. On the 3rd, 7th, 14th and 21st day of the experiment, the concentrations of growth factors, % dermal collagen content, and also the content of eosinophils in peripheral blood and red bone marrow were determined in the blood serum. The research results showed that the development of eosinopenia after a local cold injury occurs due to the sequestration of eosinophils in the affected area. The presence of reactive changes after a local cold injury not only in peripheral blood, but also in the red bone marrow may indicate the participation of eosinophils in tissue repair processes after a local cold injury.

Introduction: An outbreak of coronavirus disease 2019 (COVID-19) occurred in Wuhan, Hubei Province, China. This study aimed to analyze the clinical and epidemiologic characteristics of patients with COVID-19 to better differentiate the suspected patients in Beijing, China. Methodology: This was a retrospective, single-center study. Clinical and epidemiologic data were collected from suspected patients with COVID-19 admitted to Beijing Ditan Hospital from January 29 to February 21, 2020. Results: One hundred and six patients (60 males and 46 females, median age 36 years) were enrolled. Thirty-six patients were ultimately laboratory confirmed. Fifty-three were excluded from the diagnosis of COVID-19. The remaining 17 patients were highly suspected, although their nucleic acid tests were repeatedly negative. The confirmed patients and highly suspected patients had a significantly higher proportion of epidemiologic history than the excluded patients (P < 0.001). There was no significant difference in clinical symptoms or the underlying diseases among the three groups. The confirmed patients had a higher frequency of lymphopenia and eosinopenia than the highly suspected and excluded patients. Chest computed tomography scans showed bilateral lung involvement, and ground-glass opacity was more likely observed in the confirmed patients. Conclusion: The clinical features of the confirmed patients with COVID-19 were insufficient for early diagnosis of COVID-19. The epidemiologic history was of great significance in the early diagnosis of COVID-19. More sensitive diagnostic methods are needed to aid the differential diagnosis of suspected patients with COVID-19.

Purpose We hypothesized that increased level of serum β2-microglobulin (β2M) is an independent factor associated with higher mortality in hospitalized patients with exacerbated chronic obstructive pulmonary disease (COPD). Patients and Methods We retrospectively analyzed 488 hospitalized patients with exacerbated COPD as the first diagnosis at Beijing Chao-Yang hospital, P. R. China between December 31st, 2012 and December 28th, 2017. Concentrations of serum β2M and other clinical indexes were measured or collected on admission, and all patients were followed up to 90 days. The relationship between β2M and 30- and 90-day all-cause mortality was explored by Cox regression analysis adjusted for age, C-reactive protein values, N-terminal pro-brain natriuretic peptide/100, respiratory failure [RF, defined as partial arterial oxygen pressure (PaO2)

Persistence of various symptoms in patients who have recovered from coronavirus disease 2019 (COVID-19) was recently defined as ‘long COVID’ or ‘post-COVID syndrome’ (PCS). This article reports a case of a 58-year-old woman who, although recovering from COVID-19, had novel and persistent symptoms including neurological complications that could not be explained by any cause other than PCS. In addition to a low inflammatory response, persistence of immunoglobulin G anticardiolipin autoantibody positivity and eosinopenia were found 1 year after acute COVID-19 infection, both of which have been defined previously as independent factors associated with the severity of COVID-19. The pathophysiological mechanism of PCS is unknown, but the possibility of persistence of the virus, especially in the nervous system, could be suggested with a post-infectious inflammatory or autoimmune reaction.

Background: Coronavirus-19 (COVID-19) pandemic is a worldwide public health problem that has been known in China since December 25, 2019. Phospholipids are structural components of the mammalian cytoskeleton and cell membranes. They suppress viral attachment to the plasma membrane and subsequent replication in lung cells. In the virus-infected lung, phospholipids are highly prone to oxidation by reactive oxygen species, leading to the production of oxidized phospholipids (OxPLs). Objective: This study was carried out to explain the correlation between the level of plasma phospholipids in patients with COVID-19 infection and the levels of cytokine storms to assess the severity of the disease. Methods: Plasma samples from 34 enrolled patients with mild, moderate, and severe COVID-19 infection were collected. Complete blood count (CBC), plasma levels of D-dimer, ferritin, C-reactive protein (CRP), cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), phospholipids, secretory phospholipase A2 (sPLA2)α2, and cytokine storms were estimated, and lung computed tomography (CT) imaging was detected. Results: The CBC picture showed the presence of leukopenia, lymphopenia, and eosinopenia in patients with COVID-19 infection. Furthermore, a significant increase was found in plasma levels of D-dimer, CRP, ferritin, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-13 as well as sPLA2α2 activity compared to normal persons. However, plasma levels of phospholipids decreased in patients with moderate and severe COVID-19 infection, as well as significantly decreased in levels of triacylglycerols and HDL-C in plasma from patients with severe infection only, compared to normal persons. Furthermore, a lung CT scan showed the presence of inflammation in a patient with mild, moderate, and severe COVID-19 infection. Conclusions: This study shows that there is a correlation between plasma phospholipid depletion and elevated cytokine storm in patients with COVID-19 infection. Depletion of plasma phospholipid levels in patients with COVID-19 infection is due to oxidative stress, induction of cytokine storm, and systemic inflammatory response after endothelial cell damage promote coagulation. According to current knowledge, patients with COVID-19 infection may need to administer surfactant replacement therapy and sPLA2 inhibitors to treat respiratory distress syndrome, which helps them to maintain the interconnected surfactant structures. [ FROM AUTHOR] Copyright of Bioinformatics & Biology Insights is the property of Sage Publications Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

Purpose Eosinopenia has been described in COVID-19. With this study, we aim to study the peripheral blood eosinophil counts in COVID-19 patients and to investigate whether there is an association between the peripheral blood eosinophil counts and disease severity of COVID-19. Methods We revised the electronical medical records of confirmed COVID-19 patients with polymerase chain reaction (PCR) assays in the Groene Hart Ziekenhuis, Gouda, The Netherlands. We divided patients in mild, moderate and severe groups based on clinical severity of COVID-19. Clinical severity was based on the therapy needed and the outcome of patients. We compared clinical characteristics, laboratory results and outcome between the three groups. Results Of the 230 patients included in this study, the mild, moderate and severe groups consisted of 16.5%, 45.7% and 37.8% of the included patients, respectively. The mean age was 68 years (IQR 57-78). 63% of patients were male. A significant decrease in the peripheral eosinophil counts was found corresponding to the increase of COVID-19 severity. In the mild, moderate and severe groups, the percentage of patients with eosinopenia was 73.7%, 86.7% and 94.3%, respectively (p value 0.002). Conclusion Eosinopenia is significantly more frequent present in patients with a severe COVID-19.

Background: Underestimation of leptospirosis cases is happening in many countries. The most common factor of underreporting is misdiagnosis. Considering the limitations of direct detection of pathogen and serological diagnosis for leptospirosis, clinical features and blood tests though non-specific are usually referred in making presumptive diagnosis to decide disease management. Methods: In this single-centre retrospective study, comparative analysis on clinical presentations and laboratory findings was performed between confirmed leptospirosis versus non-leptospirosis cases. Results: In multivariate logistic regression evidenced by a Hosmer-Lemeshow significance value of 0.979 and Nagelkerke R square of 0.426, the predictors of a leptospirosis case are hypocalcemia (calcium

Contains fulltext : 229398.pdf (Publisher’s version ) (Open Access) Acute infection is characterized by eosinopenia. However, the underlying mechanism(s) are poorly understood and it is unclear whether decreased mobilization/production of eosinophils in the bone marrow (BM) and/or increased homing to the tissues play a role. The objective of this study was to investigate the differentiation and activation status of eosinophils in the human BM and blood upon experimental human endotoxemia, a standardized, controlled, and reproducible model of acute systemic inflammation. A BM aspirate and venous blood was obtained from seven healthy volunteers before, 4 h after, and 1 week after intravenous challenge with 2 ng/kg endotoxin. Early progenitors (CD34+/IL-5Rα+), eosinophil promyelocytes, myelocytes, metamyelocytes, and mature eosinophils were identified and quantified in the bone marrow and blood samples using flowcytometry based on specific eosinophil markers (CD193 and IL-5Rα). Activation status was assessed using antibodies against known markers on eosinophils: Alpha-4 (CD49d), CCR3 (CD193), CR1 (CD35), CEACAM-8 (CD66b), CBRM 1/5 (activation epitope of MAC-1), and by plasma cytokine analysis. Four hours after endotoxin administration, numbers of mature eosinophils in the blood and in the BM markedly declined compared with baseline, whereas numbers of all eosinophil progenitors did not change. The remaining eosinophils did not show signs of activation or degranulation despite significantly increased circulating levels of eotaxin-1. Furthermore, the expression of CD49d and CD193 on eosinophils was lower compared to baseline, but normalized after 7 days. Together these data imply that circulatory eosinopenia after an innate immune challenge is mediated by CD49d-mediated homing of eosinophils to the tissues.

BACKGROUND: Scrub typhus, an acute febrile illness, is one of the emerging and re-emerging infectious diseases in India. This study was undertaken to assess the clinicohematological, treatment, and outcome profile of the patients diagnosed with scrub typhus at the clinical microbiology department of a tertiary care teaching hospital in Coastal Karnataka, India. MATERIALS AND METHODS: This was a retrospective study conducted with patients diagnosed as scrub typhus between January 2014 and December 2017. The demographic, clinical, laboratory, treatment, and outcome profile of these patients were noted and analyzed by Student's t-test. A P < 0.5 was considered statistically significant. RESULTS: A total of 146 patients were included in the study. The males were more infected than females, and people in the age group of 51–60 years were affected the most. Fever (139, 95.2%) was the most common symptom. Eschar was seen in only 52 (34.89%) patients. Anemia, leukocytosis, neutrophilia, lymphocytopenia, eosinophilia, monocytosis, thrombocytopenia, and raised erythrocyte sedimentation rate were statistically significant in scrub patients. The hepatic and renal indicators were also deranged. All patients were treated with doxycycline, and platelet was transfused in 7 (4.8%) patients. Among the seven dead patients, there were significant eosinopenia and deranged renal parameters compared to the survived patients. CONCLUSION: In endemic area, when a middle-aged individual presents with fever and leukocytosis with thrombocytopenia with or without eschar, scrub typhus should be considered as a differential diagnosis and empirical therapy started.

Background: Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are common and often fatal; however, accurate prognosis of patients hospitalized with an exacerbation is difficult. The Dyspnea, Eosinopenia, Consolidation, Acidemia, and Atrial Fibrillation (DECAF) score uses indices routinely available at the time of hospital admission and can accurately predict the inhospital mortality and outcomes in patients hospitalized with AECOPD. Methodology: A cross-sectional study was conducted in Jawaharlal Nehru Medical College, Belagavi, from January 2016 to June 2018. Consecutive patients hospitalized with an exacerbation of chronic obstructive pulmonary disease were included. DECAF indices and inhospital death rates were recorded. The prognostic value of DECAF was assessed by comparing the total score with the inhospital mortality. Statistical analysis was done using SPSS version 20. Results: Two hundred and twenty-eight patients were recruited. The mean (standard deviation) age was 61.09 ± 10.6 years; 73.68% were male and 48 patients (21.05%) died in hospital. One hundred and twelve patients were identified as low risk (DECAF: 0–1) with 6 (5.4%) patients dying in the hospital and 56 patients were identified as high risk (DECAF: 3–6) with an inhospital mortality of 60.1%. Length of stay for scores of 0–1, 2, and ≥3 was 6.42, 7.47, and 9.64 days, respectively, with P < 0.05. The receiver operating characteristic curve analysis showed P < 0.001, thereby proving that the DECAF is a significant predictor of mortality in AECOPD. Conclusion: This study proved that with an increase in the DECAF score, the mortality among patients in AECOPD increased. The DECAF score helps clinicians predict prognosis accurately by identifying low-risk patients potentially suitable for home-based care or early hospital discharge and high-risk patients requiring escalated palliation with high-level care to improve their outcome.

Aims: This retrospective study aimed to evaluate the impact of eosinopenia on 28-day mortality in Staphylococcus aureus bloodstream infection (SABSI). Methods: A retrospective study was designed to evaluate the impact of eosinopenia on 28-day mortality in SABSI. Results: Patients who were ≥16 years old with SABSI at Sun Yat-Sen Memorial Hospital between January 1st 2014 and December 31st 2018 were included. The overall 28-day mortality of all patients was 14.3% (44 out of 307). Patients with eosinopenia in the onset of SABSI had a significantly higher 28-day mortality than those without eosinopenia (22.4% vs 6.5%; P

Zusammenfassung. Typhus ist zwar ein relativ seltenes Krankheitsbild in unseren Breitengraden, zählt aber zu den häufigsten Gründen für Fieber beim Reiserückkehrer aus tropischen Gebieten, insbesondere bei Patienten aus Süd(ost)asien und Subsahara-Afrika. Zu den typischen klinischen Manifestationen beim Typhus gehören i) Puls-Temperatur-Dissoziation, ii) Eosinopenie, iii) Entfieberung über mehrere Tage und iv) verschiedene Systemmanifestationen (z.B. Hepatitis). Der Goldstandard für die Diagnostik sind positive Blutkulturen. Die empirische antibiotische Therapie hängt stark vom Reiseland ab, da die Resistenzlage in den Endemiegebieten unterschiedlich ist. Die beste Prävention besteht in der Verwendung von hygienisch einwandfreiem Wasser und Vermeidung von rohen Speisen. Eine Typhusimpfung liefert ebenfalls einen gewissen Schutz.

Introduction . Eosinopenia has been previously investigated as a marker to differentiate infectious from non-infectious diagnoses and as a prognostic marker. Most previous studies were conducted in intensive care unit patients. Our study focuses on the value of eosinopenia in patients admitted to the Internal Medicine department. Methods . We retrospectively analyzed 271 consecutive patients with infection and 31 patients presenting with fever or inflammatory syndrome and a non-infectious diagnosis. We evaluated and compared the following markers for differentiating infectious from non-infectious diagnoses: eosinophil count [EC], CRP, WBC and neutrophil-to-lymphocyte count ratio [NLCR]. We also evaluated the value of eosinopenia as a monitoring parameter in patients with infections. Results . Eosinopenia at admission was found in 71% of patients with infection compared to 32% in the non-infection group. EC and NLCR were moderate markers for discriminating infection from non-infection, with an area under the receiver operating characteristic curve of 0.789 and 0.718 respectively. Significant eosinopenia (≤ 10/µL) had a high specificity (90%) for diagnosing infections. High EC at admission (> 400/µL) was rare in the infection group (1.5%), but not uncommon in the non-infection group (25.8%). Persistent eosinopenia was noted in non-survivors, compared to the rapid normalization of EC in survivors. Conclusions . Among patients presenting with fever and/or high inflammatory markers a low EC is supportive of infection, while a high EC may suggest non-infectious diagnoses. The persistence/ resolution of eosinopenia may be a useful monitoring parameter to predict response to therapy.

IntroductionSARS-CoV-2 nucleocapsid antigen (N-Ag) can be detected in the blood of patients with Covid-19. In this study, we used a highly sensitive and specific nucleocapsid-Ag assay to explore the presence of N-Ag in urine during the course of Covid-19, and explore its relationship with the severity of the disease.Material and MethodsUrine and blood samples were collected from 82 patients with a SARS-CoV-2 infection proven by PCR and included in the COVIDotheque. We explored the presence of N-Ag in urine and blood using the AAZ N-Ag test, studied the kinetics of the marker according to the time since the onset of symptoms and evaluated the association between N-Ag levels, clinical severity and inflammation.ResultsIn the first and second weeks of Covid-19, hospitalized patients tested positive for urinary N-Ag (81.25% and 71.79%, respectively) and blood N-Ag (93.75% and 94.87%, respectively). N-Ag levels in urine and blood were moderately correlated with the number of days after the onset of symptoms (r=-0.43, pConclusionOur study demonstrate that N-Ag is present in the urine of patients hospitalized in the early phase of Covid-19. As a direct marker of SARS-CoV-2, urinary N-Ag reflects the dissemination of viral compounds in the body. Urine N-Ag is a promising marker to predict adverse evolution of SARS-CoV-2 infections.

Borja G Cosio,1,2 Hanaa Shafiek,1,3 Nuria Toledo-Pons,1,2 Amanda Iglesias,1,2 Margalida Barcelo,1 Cristina Represas-Represas,4 Lorena Comeche,5 Pablo Catalan,6 Alberto Fernandez-Villar,4 Jose Luis Lopez- Campos,7 Jose Echave-Sustaeta,5 Juan Jose Soler-Cataluna8 1Respiratory Medicine, Hospital Universitario Son Espases-IdISBa, Palma de Mallorca, Spain; 2CIBERES-IDISBa, Palma de Mallorca, Spain; 3Chest Diseases Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt; 4Respiratory Medicine, Hospital Alvaro Cunqueiro, Vigo, Spain; 5Respiratory Medicine, Hospital Universitario Quironsalud Madrid, Madrid, Spain; 6Respiratory Medicine, Hospital General de Castellón, Castellón, Spain; 7Respiratory Medicine, Hospital Virgen del Rocio-CIBERES, Sevilla, Spain; 8Respiratory medicine, Hospital Arnau de Vilanova-CIBERES, Valencia, SpainCorrespondence: Borja G CosioHospital Universitario Son Espases, Ctra de Valldemossa 79, Palma de Mallorca, 07010, SpainTel +34 871 20 6714Email borja.cosio@ssib.esPurpose: Exacerbations of COPD (ECOPD) are a frequent cause of hospitalization that seemed to ameliorate during the COVID outbreak. We aimed to evaluate the clinical characteristics of COPD-related hospital admissions and mortality in relation to the presence of COVID-19.Patients and Methods: We conducted a case–control study of patients admitted in four teaching hospitals throughout Spain between March 15 and April 30, 2020. Hospital admissions of respiratory cause with and without PCR-proven SARS-CoV-2 infection in patients with COPD were evaluated. Baseline and episode-related clinical characteristics were analyzed. Logistic regression analysis was performed to evaluate the risk for mortality.Results: During the study period, 2101 patients were admitted for respiratory worsening, 1200 (57.1%) with COVID-19. A total of 228 (10.8%) were admitted due to COPD worsening, of whom 52 (22.8%) tested positive for COVID-19. COPD patients with COVID-19, when compared to those without COVID-19, were more frequently males with better lung function (FEV1 postbronchodilator 71% vs 46% respectively, p< 0.001) and had higher mortality (44.9% vs 13.6% respectively, p< 0.001) despite similar age, comorbidities, total days of hospitalization and admission to intensive care unit. COVID-19 and eosinopenia were the strongest risk factors for mortality in the multivariate analysis in the overall COPD population. Inhaled corticosteroid use was not associated to mortality.Conclusion: Hospitalizations for ECOPD without COVID-19 were more frequent than COPD with COVID-19 during the first outbreak, but the latter were associated with higher mortality and low eosinophil counts that warrant further analysis.Keywords: COPD exacerbation, mortality, inhaled corticosteroids, hospitalization

Introduction As the Coronavirus disease 2019 (COVID‐19) pandemic is still ongoing with patients overwhelming healthcare facilities, we aimed to investigate the ability of white blood cell count (WBC) and their subsets, high fluorescence lymphocyte cells (HFLC), immature granulocyte count (IG), and C‐reactive protein (CRP) to aid diagnosis of COVID‐19 during the triage process and as indicators of disease progression to serious and critical condition. Methods We collected clinical and laboratory data of patients, suspected COVID‐19 cases, admitted at the emergency department of University General Hospital of Ioannina (Ioannina, Greece). We selected 197 negative and 368 positive cases, confirmed by polymerase chain reaction test for severe acute respiratory syndrome coronavirus 2. COVID‐19 cases were classified into mild, serious, and critical disease. Receiver operating characteristic curve and binary logistic regression analysis were utilized for assessing the diagnosing ability of biomarkers. Results WBC, neutrophil count (NEUT), and HFLC can discriminate efficiently negative cases from mild and serious COVID‐19, whereas eosinopenia and basopenia are early indicators of the disease. The combined WBC‐HFLC marker is the best diagnostic marker for both mild (sensitivity: 90.6% and specificity: 64.1%) and serious (sensitivity: 90.3% and specificity: 73.4%) disease. CRP and Lymphocyte count are early indicators of progression to serious disease whereas WBC, NEUT, IG, and neutrophil‐to‐lymphocyte ratio are the best indicators of critical disease. Conclusion Lymphopenia is not useful in screening patients with COVID‐19. HFLC is a good diagnostic marker for mild and serious disease either as a single marker or combined with WBC whereas IG is a good indicator of progression to critical disease.

Knowledge about the immune responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, particularly regarding the function of eosinophils, has been steadily emerging recently. There exists controversy regarding the implications of eosinophils in the coronavirus disease 2019 (COVID-19)’s pathology. We report a retrospective cohort study including the comparison of leukocyte counts in COVID-19 patients, considering the outcomes of recovery (n = 59) and death (n = 60). Among the different types of leukocytes, the eosinophil counts were those that showed the greatest difference between recovered and deceased patients. Eosinopenia (eosinophil count &lt, 0.01 × 109/L) was more frequently observed in deceased than recovered patients (p = 0.0012). The eosinophil counts more rapidly increased and showed a greater proportion over the course of the disease in the recovered than deceased patients. Furthermore, the estimated survival rate was greater in patients without eosinopenia than in patients with eosinopenia (p = 0.0070) during hospitalization. Importantly, recovered but not deceased patients showed high negative correlations of the eosinophils with the neutrophil-to-lymphocyte ratio (NLR) and neutrophil counts at Day 9 of the onset of clinical symptoms (p ≤ 0.0220). Our analysis suggests that eosinopenia may be associated with unfavorable disease outcomes and that the eosinophils have a beneficial function in COVID-19 patients, probably contributing by controlling the exacerbated inflammation induced by neutrophils.

Introduction: Severe asthma and chronic rhinosinusitis (CRS), with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP), are heterogeneous diseases characterized by different mechanistic pathways (endotypes) and variable clinical presentations (phenotypes).Areas covered: This review provides the clinician with an overview of the prevalence and clinical impact of severe chronic upper and lower airways disease and suggests a novel therapeutic approach with biological agents with possible biomarkers. To select relevant literature for inclusion in this review, we conducted a literature search using the PubMed database, using terms 'severe airways disease' AND 'endotype' AND 'treatment.' The literature review was performed for publication years 2010-2020, restricting the articles to humans and English language publications.Expert opinion: The coronavirus disease (COVID-19) pandemic has brought forth many challenges for patients with severe airway disease and healthcare practitioners involved in care. These patients could have an increased risk of developing severe SARS-CoV-2 disease, although treatment with biologics is not associated with a worse prognosis. Eosinopenia on hospital admission plays a key role as a diagnostic and prognostic biomarker.

Background Type-4 abomasal ulcers (U4) are perforated ulcers causing diffuse peritonitis. This retrospective study describes the clinical, laboratory and ultrasonographic findings in 38 calves with U4. The medical records of 38 calves aged three days to 20 weeks with U4 were scrutinised. Results The most common clinical findings were poor general health (95%), reduced skin elasticity (95%), rumen atony (91%), abdominal guarding (76%) and positive percussion auscultation and/or swinging auscultation on the right side of the abdomen (75%). The most frequent laboratory findings were increased numbers of segmented neutrophils (87%), eosinopenia (87%), acidosis (84%), azotaemia (79%) and hyponatraemia (79%). The most frequent abdominal ultrasonographic findings were intestinal atony (68%), fluid (67%) and fibrin deposits (58%) in the abdomen. Thirty-five calves were euthanased and three calves died spontaneously. All calves underwent pathological examination. Diffuse peritonitis caused by a transmural abomasal ulcer was the principal diagnosis in all calves. Conclusions Perforated abomasal ulcers cause severe illness, and a thorough clinical examination combined with ultrasonographic abdominal examination should lead to a tentative diagnosis.

A malfunction of the innate immune response in COVID-19 is associated with eosinopenia, particularly in more severe cases. This study tested the hypothesis that this eosinopenia is COVID-19 specific and is associated with systemic activation of eosinophils. Blood of 15 healthy controls and 75 adult patients with suspected COVID-19 at the ER were included before PCR testing and analyzed by point-of-care automated flow cytometry (CD10, CD11b, CD16, and CD62L) in the absence or presence of a formyl peptide (fNLF). Forty-five SARS-CoV-2 PCR positive patients were grouped based on disease severity. PCR negative patients with proven bacterial (n = 20) or other viral (n = 10) infections were used as disease controls. Eosinophils were identified with the use of the FlowSOM algorithm. Low blood eosinophil numbers (&lt, 100 cells/μL, p &lt, 0.005) were found both in patients with COVID-19 and with other infectious diseases, albeit less pronounced. Two discrete eosinophil populations were identified in healthy controls both before and after activation with fNLF based on the expression of CD11b. Before activation, the CD11bbright population consisted of 5.4% (CI95% = 3.8, 13.4) of total eosinophils. After activation, this population of CD11bbright cells comprised nearly half the population (42.21%, CI95% = 35.9, 54.1). Eosinophils in COVID-19 had a similar percentage of CD11bbright cells before activation (7.6%, CI95% = 4.5, 13.6), but were clearly refractory to activation with fNLF as a much lower percentage of cells end up in the CD11bbright fraction after activation (23.7%, CI95% = 18.5, 27.6, 0.001). Low eosinophil numbers in COVID-19 are associated with refractoriness in responsiveness to fNLF. This might be caused by migration of fully functional cells to the tissue.

Background: This study aimed to seek for an association between absolute eosinopenia (eosinophils count < 10 /mm3) and mortality in an older adults suffering from COVID-19 hospitalized in a specific geriatric ward. Methods: This observational retrospective study was conducted in a French geriatric ward from March 17 to April 18, 2020. All 118 patients hospitalized for COVID-19 over 70 yo in acute stay care were enrolled. Patients with a treatment or a pathology which could interfere with eosinophil count were excluded. Results: No statistical difference was found between surviving or deceased patient regarding age (mean age (SD): 87 years (7)) and sex (34% of males). Differences for the most frequent acute events were statically different: Quick Sepsis-related Organ Failure Assessment (qSOFA) score was ≥ 2 at admission for 23% in the survivor group vs. 23 (72%) in the deceased (p < .001); acute kidney injury concerned 17% of the survivors vs. 69% of the decease (p< .001). Eosinopenia < 10/mm3 was significantly associated with mortality (OR (CI95%)) = 3.5 (1.2-11.4) after adjustment on age, gender, and activity of daily living. Conclusion: Absolute eosinopenia was associated with in hospital mortality in older adults. This result, if confirmed in other study, may help to predict the outcome of a SARS-COV-2 infection on geriatric patients and calls for immunologist to explore more globally the impact of inflammaging on the SARS-CoV-2 infection.

A significant surge in cases of multisystem inflammatory syndrome in children (MIS-C, also called Pediatric Inflammatory Multisystem Syndrome - PIMS) has been observed amidst the COVID-19 pandemic. MIS-C shares many clinical features with Kawasaki disease (KD), although clinical course and outcomes are divergent. We analyzed whole blood RNA sequences, serum cytokines, and formalin fixed heart tissues from these patients using a computational toolbox of two gene signatures, i.e., the 166-gene viral pandemic (ViP) signature, and its 20-gene severe (s)ViP subset that were developed in the context of SARS-CoV-2 infection and a 13-transcript signature previously demonstrated to be diagnostic for KD. Our analyses revealed that KD and MIS-C are on the same continuum of the host immune response as COVID-19. While both the pediatric syndromes converge upon anIL15/IL15RA-centric cytokine storm, suggestive of shared proximal pathways of immunopathogenesis, they diverge in other laboratory parameters and cardiac phenotypes. The ViP signatures also revealed unique targetable cytokine pathways in MIS-C, place MIS-C farther along in the spectrum in severity compared to KD and pinpoint key clinical (reduced cardiac function) and laboratory (thrombocytopenia and eosinopenia) parameters that can be useful to monitor severity.

Standard blood laboratory parameters may have diagnostic potential, if polymerase-chain-reaction (PCR) tests are not available on time. We evaluated standard blood laboratory parameters of 655 COVID-19 patients suspected to be infected with SARS-CoV-2, who underwent PCR testing in one of five hospitals in Vienna, Austria. We compared laboratory parameters, clinical characteristics, and outcomes between positive and negative PCR-tested patients and evaluated the ability of those parameters to distinguish between groups. Of the 590 patients (20–100 years, 276 females and 314 males), 208 were PCR-positive. Positive compared to negative PCR-tested patients had significantly lower levels of leukocytes, neutrophils, basophils, eosinophils, lymphocytes, neutrophil-to-lymphocyte ratio, monocytes, and thrombocytes; while significantly higher levels were detected with erythrocytes, hemoglobin, hematocrit, C-reactive-protein, ferritin, activated-partial-thromboplastin-time, alanine-aminotransferase, aspartate-aminotransferase, lipase, creatine-kinase, and lactate-dehydrogenase. From all blood parameters, eosinophils, ferritin, leukocytes, and erythrocytes showed the highest ability to distinguish between COVID-19 positive and negative patients (area-under-curve, AUC: 72.3–79.4%). The AUC of our model was 0.915 (95% confidence intervals, 0.876–0.955). Leukopenia, eosinopenia, elevated erythrocytes, and hemoglobin were among the strongest markers regarding accuracy, sensitivity, specificity, positive and negative predictive value, positive and negative likelihood ratio, and post-test probabilities. Our findings suggest that especially leukopenia, eosinopenia, and elevated hemoglobin are helpful to distinguish between COVID-19 positive and negative tested patients.

Background: Studies on the role of eosinophils in coronavirus disease 2019 (COVID-19) are scarce, though available findings suggest a possible association with disease severity. Our study analyzes the relationship between eosinophils and COVID-19, with a focus on disease severity and patients with underlying chronic respiratory diseases. Methods: We performed a retrospective analysis of 3,018 subjects attended at two public hospitals in Madrid (Spain) with PCR-confirmed SARS-CoV-2 infection from January 31 to April 17, 2020. Patients with eosinophil counts less than 0.02 × 109/L were considered to have eosinopenia. Individuals with chronic respiratory diseases (n = 384) were classified according to their particular underlying condition, i.e., asthma, chronic pulmonary obstructive disease, or obstructive sleep apnea. Results: Of the 3018 patients enrolled, 479 were excluded because of lack of information at the time of admission. Of 2539 subjects assessed, 1,396 patients presented an eosinophil count performed on admission, revealing eosinopenia in 376 cases (26.93%). Eosinopenia on admission was associated with a higher risk of intensive care unit (ICU) or respiratory intensive care unit (RICU) admission (OR:2.21; 95% CI:1.42–3.45; p < 0.001) but no increased risk of mortality (p > 0.05). Conclusion: Eosinopenia on admission conferred a higher risk of severe disease (requiring ICU/RICU care), but was not associated with increased mortality. In patients with chronic respiratory diseases who develop COVID-19, age seems to be the main risk factor for progression to severe disease or death.

Introduction:COVID-19 is a viral zoonosis caused by the coronavirus strain SARS-CoV-2. Due to the rapid spread ofthis emerging infectious disease, the WHO has qualified it as an international pandemic. The objective of our study is to describe the haematological characteristics of patients with COVID-19 hospitalised at the CHU of Oran in Algeria.Patients and methods:This is a prospective study carried out between July 1st and October 15th, 2020, which included patients hospitalised and/or followed up in COVID-19 units of the CHU Oran in Algeria. The blood count was done on a Mindray BC - 6800 machine.Results:Our study included 68 patients of which 67.2% were male and 32.8% female (sex ratio M/F = 2) with a median age of 65 years. Check-ups revealed anaemia in 38.2% of patients. Hyperleukocytosis (62.2%), hyperneutrophilia (72.1%), lymphopenia (66.2%) , Eosinopenia (58.8%), monocytopenia (08.8%), monocytosis (20.6%), thrombocytosis (14.7%), high PMV (Mean Platelet Volume) in 27.9% of cases and high PPI (Platelet Distribution Index) in all patients. It is also noted that 85% of patients over 50 years of agehave an NLR ≥ 3.13.Conclusion:Some parameters such as lymphopenia and eosinopenia have an important diagnosticvalue, while other parameters such as NLR (Neutrophils-to-lymphocyte ratio), MLR (Monocyte -to-lymphocyte ratio) and PLR (Platelet-to-lymphocyte ratio) offer a very valuable prognostic value.

Background: Viral infections cause alteration in the total number of lymphocytes and their subset distribution. We aimed to study peripheral blood lymphocyte subsets in COVID-19 patients and to correlate these subsets with clinical and laboratory data, which may help in clarifying the pathogenesis to develop novel diagnostic and prognostic biomarkers for COVID-19.Methods: Twenty-six reverse-transcription polymerase chain reaction (RT-PCR) confirmed COVID-19 patients were subjected to medical history-taking and a thorough clinical examination. Laboratory tests included complete blood count, D dimer, ferritin, and C-reactive protein (CRP). Chest CT was used to diagnose COVID-19 pneumonia. Lymphocyte subsets were compared with those in 20 healthy controls using flow cytometry.Results: Leucopenia, relative neutrophilia, lymphopenia, eosinopenia together with marked elevation in neutrophil/lymphocyte ratio were observed in our COVID-19 patients. A marked reduction was observed in T cells, including both CD4 and CD8 cells, natural killer (NK), and natural killer T cells (NKT). Double-positive T (DPT) cells, double-negative T (DNT) cells, and B cells were elevated in the patients relative to the other lymphocyte subsets.Conclusion: Immune-inflammatory parameters are of utmost importance in understanding the pathogenesis and in the provisional diagnosis of COVID-19. Yet, due care must be taken during their interpretation because of the vast discrepancies observed between studies even in the same locality. Further studies are needed to clarify the role of B cells, DPT, and DNT cells in the pathogenesis and control of COVID-19.

Highlights • Lymphopenia and eosinopenia are associated with the severe form of COVID-19. • Increased levels of D-dimer, procalcitonin, and C reactive protein are prognostic biomarkers predicting coagulopathy. • Corticosteroids resulted the best therapy for the immune dysregulation in severe form of COVID-19. • Anticoagulative therapy is associated with reduced in-hospital mortality for COVID-19., Clinical symptoms of COVID-19 include fever, cough, and fatigue which may progress to acute respiratory distress syndrome (ARDS). The main hematological laboratory findings associated with the severe form of disease are represented by lymphopenia and eosinopenia which mostly occur in the elderly population characterized by cardiovascular comorbidities and immunosenescence. Besides, increased levels of D-dimer, procalcitonin, and C reactive protein (CRP) seem to be powerful prognostic biomarkers helping to predict the onset of coagulopathy. The host immune response to SARS-CoV-2 can lead to an aberrant inflammatory response or “cytokine storm” which contributes to the severity of illness. At immunological level, patients affected by a severe form of COVID-19 show poor clinical trajectories characterized by differential “immunotypes” for which T cell response seems to play a critical role in understanding pathogenic mechanisms of disease. Also, patients with mild to severe COVID-19 displayed macrophage activation syndrome (MAS), very low human leukocyte antigen D related (HLA-DR) expression with a parallel reduction of CD04+ lymphocytes, CD19 lymphocytes, and natural killer (NK) cells. Corticosteroids resulted the best therapy for the immune dysregulation whereas repurposing of tocilizumab (IL-6 receptor antagonist) appears to have mixed results in patients with COVID-19. Besides, anticoagulative therapy was associated with reduced in-hospital mortality and need of intubation among COVID-19 patients. Furthermore, the beneficial use of intravenous immunoglobulin (IVIG) and passive immunotherapy with convalescent plasma needs to be validated in large controlled clinical trials. In this review, we summarize the main hematological parameters with a prognostic value in COVID-19 and the basis of immunological reactivity during COVID-19, with a focus on ongoing clinical trials evaluating immune targets as possible therapeutic strategies.

Visceral leishmaniasis (VL), also known as kala-azar (black fever in Hindi), is a disease primarily caused by Leishmania donovani. The most important clinical manifestation of visceral leishmaniasis is fever. Nonspecific laboratory findings of visceral leishmaniasis include anemia, neutropenia, eosinopenia, and thrombocytopenia. Definitive diagnosis of visceral leishmaniasis requires the demonstration of either parasite by smear or tissue by culture (usually bone marrow or spleen). Myasthenia gravis is an autoimmune disease caused by antibodies to acetylcholine receptors in the post-junctional membrane of the neuromuscular junction. It typically presents with fatigable muscle weakness without any sensory or brain involvement. It is usually treated with corticosteroids and immunosuppressants like azathioprine. Here we encountered a confirmed case of myasthenia gravis on azathioprine with pancytopenia. While working up to evaluate pancytopenia, bone marrow examination revealed presence of Donovan bodies and the patient showed good response to liposomal amphotericin-B. In retrospect, a case of myasthenia gravis, who presented with pancytopenia presumably drug-induced, was found to have visceral leishmaniasis.

Autoimmune chronic spontaneous urticaria (aiCSU) comes with high disease activity and poor response to treatment. Recently, elevated levels of IgG anti-thyroid peroxidase (aTPO) and low levels of total IgE were reported to be common in aiCSU.To investigate how high aTPO and low IgE individually and combined are linked to features of aiCSU, including treatment responses.We analyzed records of patients with CSU from 2 independent cohorts (n = 1120) for demographic, clinical, and laboratory parameters and treatment responses. Total IgE and aTPO were measured, and 4 markers of aiCSU were analyzed: autologous serum skin test, basophil activation test (BAT), and blood eosinophil and basophil counts. Cutoff values were greater than or equal to 34 kU/L (high aTPO) and less than 40 IU/mL (low total IgE).One of 10 patients with CSU had both high aTPO and low IgE (aTPO↑IgE↓, 11%, n = 123). aTPO↑IgE↓ was linked to higher age at CSU onset, being female, angioedema, and shorter CSU duration. aTPO↑IgE↓ was associated with markers of aiCSU, that is, BAT and autologous serum skin test positivity, basopenia, and eosinopenia (P.01 for all). Almost half the patients with aTPO↑IgE↓ (44%, 19 of 43) had a positive BAT result, the best single marker for aiCSU, versus 12% (43 of 344) of patients without aTPO↑IgE↓ (P.001). Relative risk of showing BAT positivity for a patient with aTPO↑IgE↓ is 3.636 (95% CI, 2.382-5.551). Patients with aTPO↑IgE↓ showed low response rates to antihistamine treatment as compared with patients without aTPO↑IgE↓ (30% vs 47%; P = .01).Our findings suggest that aTPO↑IgE↓ is a useful diagnostic marker for aiCSU in everyday clinical practice.

Background The outbreak of COVID-19 has resulted in serious concerns in China and abroad. To investigate clinical features of confirmed and suspected patients with COVID-19 in west China, and to examine differences between severe versus non-severe patients. Methods Patients admitted for COVID-19 between January 21 and February 11 from fifteen hospitals in Sichuan Province, China were included. Experienced clinicians trained with methods abstracted data from medical records using pre-defined, pilot-tested forms. Clinical characteristics between severe and non-severe patients were compared. Results Of the 169 patients included, 147 were laboratory-confirmed, 22 were suspected. For confirmed cases, the most common symptoms from onset to admission were cough (70·7%), fever (70·5%) and sputum (33·3%), and the most common chest CT patterns were patchy or stripes shadowing (78·0%); throughout the course of disease, 19·0% had no fever, and 12·4% had no radiologic abnormality; twelve (8·2%) received mechanical ventilation, four (2·7%) were transferred to ICU, and no death occurred. Compared to non-severe cases, severe ones were more likely to have underlying comorbidities (62·5% vs 26·2%, P = 0·001), to present with cough (92·0% vs 66·4%, P = 0·02), sputum (60·0% vs 27·9%, P = 0·004) and shortness of breath (40·0% vs 8·2%, P P = 0·003) and eosinopenia (84·2% vs 57·0%, P = 0·046). Conclusions The symptoms of patients in west China were relatively mild, and an appreciable proportion of infected cases had no fever, warranting special attention.