Mechanism Driving Blood-Clotting Disorder Identified
Researchers at McMaster University have identified the molecular mechanism that causes heparin-induced thrombocytopenia (HIT), a dangerous immune reaction to blood thinners. By using advanced NMR spectroscopy, the team discovered a 'molecular switch' in the PF4 protein that triggers the disorder.
Why it matters
This discovery could lead to better diagnostic tools and preventative treatments for a rare but life-threatening side effect of common medical care.
Although heparin, a commonly used blood thinner, typically reduces clotting, a rare but potentially life-threatening immune reaction called heparin-induced thrombocytopenia (HIT) is possible. A team of researchers from McMaster University have combined their varied expertise in chemistry, structural biology, and transfusion medicine to uncover the mechanism driving this contradictory medical outcome in some patients.
Prior research has identified platelet factor 4 (PF4) as a protein of interest in HIT. PF4 is a protein produced in the body with a role in blood clotting. However, in some patients treated with heparin, PF4 changes shape, resulting in irregular proteins that are targeted by antibodies, triggering an immune response resulting in HIT. Though rate, the blood clots developed through HIT can be life-threatening, potentially leading to stroke, heart attack, limb loss, or death.
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