Early prediction of COVID-19 outcome using artificial intelligence techniques and only five laboratory indices

We aimed to develop a prediction model for intensive care unit (ICU) hospitalization of Coronavirus disease-19 (COVID-19) patients using artificial neural networks (ANN). We assessed 25 laboratory parameters at first from 248 consecutive adult COVID-19 patients for database creation, training, and development of ANN models. We developed a new alpha-index to assess association of each parameter with outcome. We used 166 records for training of computational simulations (training), 41 for documentation of computational simulations (validation), and 41 for reliability check of computational simulations (testing). The first five laboratory indices ranked by importance were Neutrophil-to-lymphocyte ratio, Lactate Dehydrogenase, Fibrinogen, Albumin, and D-Dimers. The best ANN based on these indices achieved accuracy 95.97%, precision 90.63%, sensitivity 93.55%. and F1-score 92.06%, verified in the validation cohort. Our preliminary findings reveal for the first time an ANN to predict ICU hospitalization accurately and early, using only 5 easily accessible laboratory indices

Genetic prediction of ICU hospitalization and mortality in COVID-19 patients using artificial neural networks

There is an unmet need of models for early prediction of morbidity and mortality of Coronavirus disease-19 (COVID-19). We aimed to a) identify complement-related genetic variants associated with the clinical outcomes of ICU hospitalization and death, b) develop an artificial neural network (ANN) predicting these outcomes and c) validate whether complement-related variants are associated with an impaired complement phenotype. We prospectively recruited consecutive adult patients of Caucasian origin, hospitalized due to COVID-19. Through targeted next-generation sequencing, we identified variants in complement factor H/CFH, CFB, CFH-related, CFD, CD55, C3, C5, CFI, CD46, thrombomodulin/THBD, and A Disintegrin and Metalloproteinase with Thrombospondin motifs (ADAMTS13). Among 381 variants in 133 patients, we identified 5 critical variants associated with severe COVID-19: rs2547438 (C3), rs2250656 (C3), rs1042580 (THBD), rs800292 (CFH) and rs414628 (CFHR1). Using age, gender and presence or absence of each variant, we developed an ANN predicting morbidity and mortality in 89.47% of the examined population. Furthermore, THBD and C3a levels were significantly increased in severe COVID-19 patients and those harbouring relevant variants. Thus, we reveal for the first time an ANN accurately predicting ICU hospitalization and death in COVID-19 patients, based on genetic variants in complement genes, age and gender. Importantly, we confirm that genetic dysregulation is associated with impaired complement phenotype

Uncovering the multifaceted roles played by neutrophils in allogeneic hematopoietic stem cell transplantation

Allogeneic hematopoietic stem cell transplantation (alloHSCT) is a life-saving procedure used for the treatment of selected hematological malignancies, inborn errors of metabolism, and bone marrow failures. The role of neutrophils in alloHSCT has been traditionally evaluated only in the context of their ability to act as a first line of defense against infection. However, recent evidence has highlighted neutrophils as key effectors of innate and adaptive immune responses through a wide array of newly discovered functions. Accordingly, neutrophils are emerging as highly versatile cells that are able to acquire different, often opposite, functional capacities depending on the microenvironment and their differentiation status. Herein, we review the current knowledge on the multiple functions that neutrophils exhibit through the different stages of alloHSCT, from the hematopoietic stem cell (HSC) mobilization in the donor to the immunological reconstitution that occurs in the recipient following HSC infusion. We also discuss the influence exerted on neutrophils by the immunosuppressive drugs delivered in the course of alloHSCT as part of graft-versus-host disease (GVHD) prophylaxis. Finally, the potential involvement of neutrophils in alloHSCT-related complications, such as transplant-associated thrombotic microangiopathy (TA-TMA), acute and chronic GVHD, and cytomegalovirus (CMV) reactivation, is also discussed. Based on the data reviewed herein, the role played by neutrophils in alloHSCT is far greater than a simple antimicrobial role. However, much remains to be investigated in terms of the potential functions that neutrophils might exert during a highly complex procedure such as alloHSCT

Editorial : Women in science - hematology 2021

202309 bcvcVersion of RecordOthersASH Global Research Award; Health and Medical Research Fund Commissioned Research on COVID-19; National Heart, Lung, and Blood Institute grantPublishe

The vicious cycle of intradialytic hypotension, inflammation and myocardial Stunning: Overview of pathophysiological aspects

Intradialytic hypotension (IDH) represents a well-known and intractable complication in hemodialysis patients. Despite the innovations in hemodialysis techniques, its tenacious presence indicates the complexity of underlying pathophysiological mechanisms. The need of an integrated approach in understanding its pathogenesis is thought to be imperative as it may prevent devastating consequences through the implementation of more successful avoidance tactics. It is well established that IDH has been associated with impaired myocardial function and peripheral vascular resistance, attributed to either the hemodialysis procedure per se or patients' unique features. This review aims to describe traditional risk factors of IDH and focus on non- traditional but crucial factors of hemodynamic instability related to endothelial dysfunction. In particular, chronic subclinical inflammation may be considered the missing link in the vicious cycle of IDH, ischemia and myocardial stunning. Repeated episodes of enteric ischemia during hemodialysis represent an additional source of chronic systemic inflammation that induces the phenomenon of bacterial or endotoxin translocation through the impaired enteric epithelial cell barrier. Thus, increased endothelial dysfunction and oxidative stress result in decreased left ventricular pumping function and finally permanent systolic dysfunction through genetic adaptations. In total, these pathophysiological mechanisms preserve the vicious cycle of IDH

B12 deficiency in chronic kidney disease: Early recognition matters

[No abstract available

Role of the lectin pathway of complement in hematopoietic stem cell transplantation-associated endothelial injury and thrombotic microangiopathy

Hematopoietic stem cell transplantation-associated thrombotic microangiopathy (HSCT-TMA) is a life-threatening syndrome that occurs in adult and pediatric patients after hematopoietic stem cell transplantation. Nonspecific symptoms, heterogeneity within study populations, and variability among current diagnostic criteria contribute to misdiagnosis and underdiagnosis of this syndrome. Hematopoietic stem cell transplantation and associated risk factors precipitate endothelial injury, leading to HSCT-TMA and other endothelial injury syndromes such as hepatic veno-occlusive disease/sinusoidal obstruction syndrome, idiopathic pneumonia syndrome, diffuse alveolar hemorrhage, capillary leak syndrome, and graft-versus-host disease. Endothelial injury can trigger activation of the complement system, promoting inflammation and the development of endothelial injury syndromes, ultimately leading to organ damage and failure. In particular, the lectin pathway of complement is activated by damage-associated molecular patterns (DAMPs) on the surface of injured endothelial cells. Pattern-recognition molecules such as mannose-binding lectin (MBL), collectins, and ficolins-collectively termed lectins-bind to DAMPs on injured host cells, forming activation complexes with MBL-associated serine proteases 1, 2, and 3 (MASP-1, MASP-2, and MASP-3). Activation of the lectin pathway may also trigger the coagulation cascade via MASP-2 cleavage of prothrombin to thrombin. Together, activation of complement and the coagulation cascade lead to a procoagulant state that may result in development of HSCT-TMA. Several complement inhibitors targeting various complement pathways are in clinical trials for the treatment of HSCT-TMA. In this article, we review the role of the complement system in HSCT-TMA pathogenesis, with a focus on the lectin pathway.Nephrolog

Seroepidemiology of Chlamydia Pneumoniae in Northern Greece

The prevalence of IgG and IgA antibodies to Chlamydia pneumoniae was evaluated in a group of an apparently healthy population in northern Greece. Serum samples were obtained over a period of one year (June 2006 to May 2007) from 530 individuals (300 males and 230 females, aged from 1 month to 90 years). The sera were tested for specific antibodies to C. pneumoniae by two commercial methods, an ELISA and a micro-IF assay based on the principles of MIF. The prevalence of IgG and IgA antibodies to C. pneumoniae was 53.2% and 45.9%, respectively, and was found to be unrelated to gender, even in the elderly >61 years old. The IgG antibody prevalence was low in children under 5 years old (7.7%), sharply increased by the age of 20 (40%) and continued to increase, gradually, to reach 80.1% in the elderly. IgA antibodies also increased with similar kinetics to IgG, although at a lower level (3.8–66.1%). Our results show that infection with C. pneumoniae is common in northern Greece. The high prevalence of IgA specific antibodies reported in the present study is due to primary infection at a young age, while in the elderly is probably due to infection or reinfection, although the option of persistence cannot be excluded