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Cocaine-Induced Erythrocytosis and Increase in von Willebrand Factor
Evidence for Drug-Related Blood Doping and Prothrombotic Effects
Arthur J. Siegel, MD;
Michelle B. Sholar, BA;
Jack H. Mendelson, MD;
Scott E. Lukas, PhD;
Marc J. Kaufman, PhD;
Perry F. Renshaw, MD, PhD;
Jane C. McDonald, RP;
Kent B. Lewandrowski, MD;
Fred S. Apple, PhD;
James J. Stec, BS;
Izabella Lipinska, PhD;
Geoffrey H. Tofler, MD;
Paul M. Ridker, MD
Arch Intern Med. 1999;159:1925-1929.
Background Mechanisms that mediate cocaine-induced cardiovascular events following vasoconstriction are incompletely understood.
Objective To examine the effects of cocaine in moderate doses on hematologic and hemostatic parameters that influence blood viscosity and thrombotic potential.
Methods Changes in hemoglobin concentration, hematocrit, and red blood cell counts were measured in human subjects who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for long-term cocaine abuse, before and sequentially after moderate intranasal and intravenous doses of cocaine. Hemostatic parameters, including von Willebrand factor, fibrinolytic activity, fibrinogen, plasminogen activator inhibitor antigen, and tissue-type plasminogen activator antigen, were sequentially measured after intravenous cocaine or saline placebo with cardiac troponin subunits T and I.
Results Hemoglobin level (P=.002), hematocrit (P=.01), and red blood cell counts (P=.04) significantly increased from 4% to 6% over baseline from 10 to 30 minutes after intranasal (n=14) and intravenous (n=7) cocaine administration in doses of 0.9 mg/kg and 0.4 mg/kg, respectively, with no change in white blood cell or platelet counts. There was a significant increase (P=.03) in von Willebrand factor from 30 to 240 minutes, peaking at 40% over baseline following intravenous cocaine administration in a dose of 0.4 mg/kg (n=12), with no change after 0.2 mg/kg (n=3) or placebo (n=6). Other hemostatic factors, creatinine, blood urea nitrogen, and cardiac troponin subunits T and I showed no changes.
Conclusions Cocaine induced a transient erythrocytosis that may increase blood viscosity while maintaining tissue oxygenation during vasoconstriction. An increase in von Willebrand factor without a compensatory change in endogenous fibrinolysis may trigger platelet adhesion, aggregation, and intravascular thrombosis.
From the Department of Medicine (Dr Siegel), Alcohol and Drug Abuse Research Center (Ms Sholar and Drs Mendelson and Lukas), Brain Imaging Center (Drs Kaufman and Renshaw), and Pharmacy Department (Ms McDonald), McLean Hospital, Belmont, Mass; Department of Clinical Laboratory, Massachusetts General Hospital, Boston (Dr Lewandrowski); Department of Laboratories, Hennepin County Medical Center and University of Minnesota School of Medicine, Minneapolis (Dr Apple); Institute for the Prevention of Cardiovascular Disease, Beth Israel-Deaconess Medical Center, Boston (Mr Stec and Dr Lipinska); Royal North Shore Hospital, Sydney, Australia (Dr Tofler); Department of Cardiology, Brigham and Women's Hospital, Boston (Dr Ridker); and Harvard Medical School, Boston (Drs Siegel, Mendelson, Lukas, Kaufman, Renshaw, Lewandrowski, and Ridker).
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