SPECIALTY AND TITLE

Associate Professor, Department of Medicine, Department of Biochemistry, and Biomedical Sciences

Co-director, Michael G. DeGroote Centre for Transfusion Research

HOSPITAL AFFILIATIONS

N/A

UNIVERSITY AFFILIATIONS

McMaster University

AREA OF RESEARCH

Dr. Ishac Nazy’s research strives to understand disease mechanisms to improve and/or develop diagnostic tools and therapeutic approaches, which improve the health and everyday lives of those affected by immune-mediated platelet disorders. This involves disorders with increased clotting such as heparin-induced thrombocytopenia (HIT) and thrombotic thrombocytopenic purpura (TTP) as well as those involving bleeding such as immune thrombocytopenia (ITP). Recently, a new syndrome known as vaccine-induced immune thrombotic thrombocytopenia (VITT) characterized by the onset of low blood platelets and blood clotting due to adenoviral vector-based COVID-19 vaccines has emerged and is currently his primary focus.

MAJOR CONTRIBUTIONS TO SCIENCE AND/OR HEALTH CARE DELIVERY

Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction that results in thrombocytopenia and thrombotic complications due to antibodies that bind platelet factor 4 (PF4) and heparin. Using alanine scanning mutagenesis, Dr. Nazy characterized possible binding sites of pathogenic HIT antibodies on PF4. He also published a case report in The New England Journal of Medicine (NEJM) detailing the diagnosis of the first three patients in Canada with vaccine-induced thrombotic thrombocytopenia (VITT). This study also demonstrated the impact of intravenous immune globulin (IVIG) plus anticoagulation therapy for managing this new condition. In addition, his McMaster Platelet Immunology Laboratory became the Canadian diagnostic center for VITT testing after developing the platelet activating PF4-serotonin release assay (PF4-SRA), the gold standard confirmatory test for VITT. Furthermore, in his recent Nature publication his research group identified the VITT antibody binding site on PF4 was restricted to the heparin binding site normally seen in HIT.