Advances in the pathophysiology and treatment of heparin-induced thrombocytopenia.

PURPOSE OF REVIEW: To review the recent developments in understanding the pathophysiology of heparin-induced thrombocytopenia (HIT) and in applying this knowledge to the treatment of patients with suspected and proven HIT. RECENT FINDINGS: HIT pathophysiology is dynamic and complex. HIT pathophysiology is initiated by four essential components--heparin (Hep), platelet factor 4 (PF4), IgG antibodies against the Hep-PF4 complex, and platelet FcγRIIa. HIT is propagated by activated platelets, monocytes, endothelial cells, and coagulation proteins. Insights into the unique HIT antibody response continue to emerge, but without consensus as to the relative roles of B cells, T cells, and antigen-presenting cells. Platelet activation via FcγRIIa, the sine qua non of HIT, has become much better appreciated. Therapy remains challenging for several reasons. Suspected HIT is more frequent than proven HIT, because of the widespread use of Hep and the inadequacies of current diagnostic tests and scoring systems. In proven HIT, approved treatments reduce but do not eliminate thrombosis, and have substantial bleeding risk. Rational novel therapeutic strategies, directed at the initiating steps in HIT pathophysiology and with potential combinations staged over time, are in various phases of development. SUMMARY: Progress continues in understanding the breadth of molecular and cellular players in HIT. Translation to improved diagnosis and treatment is needed

Author Correction: Convalescent plasma for hospitalized patients with COVID-19: an open-label, randomized controlled trial (Nature Medicine, (2021), 27, 11, (2012-2024), 10.1038/s41591-021-01488-2)

In the version of this Article initially published, there was an omission in the member list for the CONCOR-1 Study Group. Valérie Arsenault (Héma-Québec, Montreal, Quebec, Canada) has now been included in the CONCOR-1 Study Group in the online version of the article

Additive effects of blood donor smoking and gamma irradiation on outcome measures of red blood cell transfusion

BACKGROUND: Recent publications have reported conflicting results regarding the role of blood donor tobacco use on hemoglobin levels in patients following red blood cell (RBC) transfusion. We examined associations and interactions between donor, component, and recipient factors to better understand the impact of donor smoking on transfusion outcomes. STUDY DESIGN AND METHODS: We linked blood donor and component manufacturing data, including self-reported cigarette smoking, with a cohort of patients transfused RBCs between 2013 and 2016. Using multivariable regression, we examined hemoglobin increments and subsequent transfusion requirements following single-unit RBC transfusion episodes, adjusting for donor, component, and recipient factors. RESULTS: We linked data on 4,038 transfusion recipients who received one or more single-unit RBC transfusions (n=5,086 units) to donor demographic and component manufacturing characteristics. Among RBC units from smokers (n=326), hemoglobin increments were reduced following transfusion of gamma irradiated units (0.76 g/dL; p=0.033) but not unirradiated units (1.04 g/dL; p=0.54) compared to those from non-smokers (1.01 g/dL; n=4,760). In parallel with changes in hemoglobin levels, donor smoking was associated with the receipt of additional RBC transfusions for irradiated (OR 2.49; p=0.01) but not unirradiated RBC units (OR 1.10; p=0.52). CONCLUSION: Donor smoking was associated with reduced hemoglobin increments and the need for additional transfusions in recipients of gamma irradiated RBC units. Additional research is needed to better understand interactions between donor, component, and recipient factors on efficacy measures of RBC transfusion