Coagulation cascade and complement system in systemic lupus erythematosus

Liang, Yan; Xie, Shangbo; Wu, Changhao; Hu, Yuan; Zhang, Qin; Li, Si; Fan, Yin‐Guang; Leng, Rui‐Xue; Pan, Hai‐Feng; Xiong, Huabao; Ye, Dong‐Qing

doi:10.18632/oncotarget.23206

Cited by 26 publications

(26 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study D-dimer had good predictive value for 30-day all-cause mortality only in the subgroup of patients with persistent provoked PE. This result might be partly explained as active malignant disease, autoimmune diseases and other severe comorbidities predominate in this subgroup of patients and it is well-known that in these cohorts of patients D-dimer per se is the predictive factor for mortality [16][17][18].…”

Section: Discussionmentioning

confidence: 91%

Different predictive value for short-term all-cause mortality with commonly used biomarkers regarding the cause of pulmonary embolism

et al. 2021

View full text Add to dashboard Cite

Background/Aim. The evaluation of blood levels of cardiac troponin-I (cTnI), D-dimer, B-type natriuretic peptide (BNP) and C-reactive protein (CRP) at admission and during the treatment of pulmonary embolism (PE) are the part of routine diagnostic process and estimation of mortality risk. The aim of this study was to evaluate the predictive value of these biomarkers at admission for all-cause 30-day mortality in consecutive PE patients regarding whether they classified as spontaneous, transiently provoked and permanently provoked PE. Methods. This retrospective analysis is gained from the data of 590 PE patients from the Serbian University Multicenter Pulmonary Embolism Registry (SUPER). Patients had at least one of these biomarkers (BNP, CRP, cTnI and D-dimer) measurements during the first 24 hours from the admission. Results. ROC curve analyses demonstrated that BNP had the highest prognostic accuracy for 30-day mortality in patients (N=219) who had data for all examined biomarkers. BNP provided an AUC of 0.785 (p<0.001). Separately BNP had the highest c-statistic for all three groups of patients. CRP had modest predictive value for the 30-day all-cause mortality in the group with transient provoked PE. Troponin I had very modest predictive value for the 30-day all-cause mortality only in patients with spontaneous PE and D-dimer was very weak predictor of this end-point only in patients with persistent provoked PE. Conclusion. Patients with spontaneous, transient provoked and persistent provoked PE have significantly different profile of blood biomarkers level with different prognostic significance for early all-cause mortality.

show abstract

Section: Discussionmentioning

confidence: 91%

Different predictive value for short-term all-cause mortality with commonly used biomarkers regarding the cause of pulmonary embolism

et al. 2021

View full text Add to dashboard Cite

show abstract

“…REACTOME Reactions and Pathways analyses (18) revealed significant changes in gene expression involved in extracellular matrix (ECM) organisation, immune system activation through CD3, and cytokine/chemokine regulation that involved IL-10 signalling and trafficking in inflammation sites (12,19), with the majority of genes in the SLE-derived PB progenitors, being upregulated in comparison to Healthy-derived PB ( Figure 1B). Finally, KEGG pathways analysis (20) was indicative of DGE that involved the migratory and extramedullary increased potential (cytokine and cytokine-receptor interactions) as well as altered immune activation of circulating SLE progenitors when compared to their circulating Healthy progenitor counterparts ( Figure 1C).…”

Section: Human Sle Pb Hspcs Show An Enhanced Extramedullary Gene Exprmentioning

confidence: 99%

Patrolling human SLE haematopoietic progenitors demonstrate enhanced extramedullary colonisation; implications for peripheral tissue injury

Kokkinopoulos

Banos

Grigoriou

et al. 2021

Preprint

View full text Add to dashboard Cite

Systemic Lupus erythematosus (SLE) is an autoimmune disease where bone-marrow-derived haematopoietic cells have a key role in its pathogenesis with accumulating evidence suggesting an aberrant function of haematopoietic stem/progenitor cells (HSPCs). By employing next-generation sequencing, we compared the gene transcription signatures of CD34+ HSPCs deriving from either the bone marrow or HSPCs patrolling the bloodstream of healthy and individuals with SLE, seeking common transcriptional pathways that may have been modified between steady and disease states. Our findings indicate that circulating and bone marrow-derived HSPCs are distinct in steady and diseased states. Non-mobilised, SLE-derived circulating HSPCs demonstrated enhanced engrafting and altered differentiation capacities. Importantly, xenotransplantation of circulating HSPCs in humanised mice showed that human peripheral blood HSPCs possess the ability for extramedullary organ colonisation to the kidneys. SLE CD34+ HSPCs homing and engraftment at extramedullary sites such as the spleen and kidneys may participate in peripheral tissue injury.

show abstract

“…The link between the complement system activation and the development of thrombotic events may occur in different clinical conditions. Significant instances are represented by autoimmune disease [71], including systemic lupus erythematosus; they are also associated with thrombotic disturbances, especially in the presence of a PNH-like phenotype [72].…”

Section: Complement Activity and Thrombotic Risk: The Clinical Settingsmentioning

confidence: 99%

Thrombotic risk in paroxysmal nocturnal hemoglobinuria-like (PNH-like) phenotype

Carlisi

Mancuso

Caimi

et al. 2021

View full text Add to dashboard Cite

The complement system is an essential component of the innate immune defence that, if overly activated, may damage organs and tissues. For this reason, there is a fine complement regulatory system. The complement modulation system includes two proteins with important regulatory activity, CD55 or decay accelerating factor (DAF) and CD59 or membrane inhibitor of reactive lysis (MIRL). The paroxysmal nocturnal hemoglobinuria (PNH) is a clonal and non-neoplastic disease characterized by intravascular haemolysis, occurrence of thrombosis and bone marrow failure. In clinical practice, in opposition to PNH, a variety of pathological conditions have been observed with an acquired and non-genetic deficiency of the regulatory proteins CD55 and CD59. This abnormal, non-clonal, reduced expression of complement regulatory proteins configures what we may define as PNH-like phenotype. Similarly to PNH, even in the PNH-like phenotype diseases there has been a greater exposure to the mediated complement cellular lysis and, a likely increased risk of thromboembolic events. Therefore, the knowledge of the potential roles of the complement system becomes necessary for a deeper understanding of several pathological conditions and for an improved clinical management of the patients.

show abstract

Coagulation cascade and complement system in systemic lupus erythematosus

Cited by 26 publications

References 68 publications

Different predictive value for short-term all-cause mortality with commonly used biomarkers regarding the cause of pulmonary embolism

Different predictive value for short-term all-cause mortality with commonly used biomarkers regarding the cause of pulmonary embolism

Patrolling human SLE haematopoietic progenitors demonstrate enhanced extramedullary colonisation; implications for peripheral tissue injury

Thrombotic risk in paroxysmal nocturnal hemoglobinuria-like (PNH-like) phenotype

Contact Info

Product

Resources

About