The aim of this study was to evaluate the long-term response to rituximab in patients with chronic and refractory immune thrombocytopenic purpura (ITP). Adults with ITP fail to respond to conventional therapies in almost 30% of cases, developing a refractory disease. Rituximab has been successfully used in these patients. We used rituximab at 375 mg/m², IV, weekly for a total of four doses in 18 adult patients. Complete remission (CR) was considered if the platelet count was >100 × 10⁹/l, partial remission (PR) if platelets were >50 × 10⁹/l, minimal response (MR) if the platelet count was >30 × 10⁹/l and <50 × 10⁹/l, and no response if platelet count remained unchanged. Response was classified as sustained (SR) when it was stable for a minimum of 6 months. Median age was 43.5 years (range, 17 to 70). Median platelet count at baseline was 12.5 × 10⁹/l (range, 3.0 to 26.3). CR was achieved in five patients (28%), PR in five (28%), MR in four (22%), and two patients were classified as therapeutic failures (11%). Two additional patients were lost to follow-up. The median time between rituximab therapy and response was 14 weeks (range, 4 to 32). SR was achieved in 12 patients (67%). There were no severe adverse events during rituximab therapy. During follow-up (median, 26 months; range, 12 to 59), no other immunosuppressive drugs were used. In conclusion, rituximab therapy is effective and safe in adult patients with chronic and refractory ITP. Overall response rate achieved is high, long term, and with no risk of adverse events.

SARS-CoV-2 contains certain molecules that are related to the presence of immunothrombosis. Here, we review the pathogen and damage-associated molecular patterns. We also study the imbalance of different molecules participating in immunothrombosis, such as tissue factor, factors of the contact system, histones, and the role of cells, such as endothelial cells, platelets, and neutrophil extracellular traps. Regarding the pathogenetic mechanism, we discuss clinical trials, case-control studies, comparative and translational studies, and observational studies of regulatory or inhibitory molecules, more specifically, extracellular DNA and RNA, histones, sensors for RNA and DNA, as well as heparin and heparinoids. Overall, it appears that a network of cells and molecules identified in this axis is simultaneously but differentially affecting patients at different stages of COVID-19, and this is characterized by endothelial damage, microthrombosis, and inflammation.

Background: Polymorphisms in the endothelial nitric oxide synthase (eNOS) and in the plasminogen activator inhibitor -1 (PAI-1) genes have been implicated in stroke pathogenesis but results are still controversial. The aim of this study was to examine the possible contribution of Glu298Asp in the eNOS and 4G/5G in the PAI-1polymorphisms with ischemic stroke in a young Mexican population. Materials and Methods: In a case-control study, conducted between January 2006 and June 2010, 204 patients ≤45 years of age with ischemic stroke and 204 controls matched by age and gender, were recruited. The Glu298Asp and 4G/5G polymorphisms were determined in all participants by polymerase chain reaction-restriction fragment length polymorphism. Results: There was a significant difference in the Glu298Asp genotype distribution (P=0.001) and allele frequency between the two groups (P=0.001). The 4G/5G genotype distribution (P=0.40) and the allele frequency was similar between groups; (P=0.13). There were independent factors for ischemic stroke: Asp carriage (GluAsp+AspAsp) (P=0.02); smoking (P=0.01); hypertension (P=0.03), and familial history of atherothrombotic disease (P=0.04). Conclusions: The Asp allele from the Gu298Asp gene represents an independent risk factor for ischemic stroke in a young Mexican population. In contrast, the 4G/5G was not associated with an increased risk for this disease in the same group of patients, as previously has been demonstrated in other populations. Les polymorphismes Glu298Asp et 4G/5G et le risque d’accident vasculaire cérébral ischémique chez des individus jeunes. Contexte: Des polymorphismes du gène de la synthase de l’oxyde nitrique endothélial (eNOS) et du gène de l’inhibiteur-1 de l’activateur du plasminogène (PAI-1) ont été impliqués dans la pathogenèse de l’accident vasculaire cérébral (AVC), mais les résultats de ces études demeurent controversés. Le but de cette étude était d’examiner la contribution possible du polymorphisme Glu298Asp du gène de l’eNOS et du polymorphisme 4G/5G du gène de PAI-1 à l’AVC dans une population mexicaine jeune. Méthode: Deux cent quatre patients atteints d’un AVC ischémique et 204 témoins appariés pour l’âge et le sexe ont été inclus dans une étude cas-témoin effectuée entre janvier 2006 et juin 2010. Les polymorphismes Glu298Asp et 4G/5G ont été identifiés chez tous les participants au moyen de la technique de réaction en chaîne par polymérase - polymorphismes de longueur des fragments amplifiés. Résultats: Nous avons noté une différence significative dans la distribution du génotype Glu298Asp (p = 0,001) et la fréquence allélique entre les deux groupes (p = 0,001). La distribution du génotype 4G/5G (p = 0,40) et la fréquence allélique étaient similaires dans les deux groupes (p = 0,13). Nous avons noté des facteurs indépendants de l’AVC ischémique : être porteur de GluAsp + AspAsp (p = 0,02), être fumeur (p = 0,01), hypertendu (p = 0,03) et avoir une histoire familiale de maladie athérothrombotique (p = 0,04). Conclusions: L’allèle Asp du gène Glu298Asp est un facteur de risque indépendant de l’AVC ischémique dans une population mexicaine jeune. Par contre, le polymorphisme 4G/5G n’est pas associé à un risque accru de cette pathologie dans ce groupe de patients, contrairement à ce qui a été démontré dans d’autres populations.

There are classical risk factors associated with arterial thrombosis (AT) or venous thromboembolic disease (VTD). However, less is known about these risk factors and AT or VTD episodes in patients with antiphospholipid syndrome (APS). Our aim was to elucidate whether APS-related thrombotic episodes are associated with the same risk factors as the non-APS population. We gathered demographics, medical history, complications, and causes of death associated with the risk factors for AT or VTD in patients with APS. We analyzed 677 thrombotic events in 386 patients. Type 2 diabetes mellitus and grade 3 obesity were associated with VTD instead of AT. There were no significant differences between the groups for almost all laboratory tests analyzed, although lupus anticoagulant was significantly higher in the VTD group. We suggest that thrombosis in APS is due to the APS itself and that the risks factors for AT or VTD do not have a main role. Our findings may have an ethnical background. Therefore, it may be difficult to elaborate predictive thrombotic clinical scores applicable to patients with different ethnical background.