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Submitted on November 29, 2001
From the Institute of Thrombosis and Hemostasis (O.S., U.S.), Laboratory of Vascular Surgery (I.R., R.V.), and the Branco and Eva Weiss Institute of Lipid and Atherosclerosis Research (D.H.), Sheba Medical Center, Tel-Hashomer, Israel; the Epidemiology Ultrasound Research Laboratory, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pa (K.S., K.S.T.); and the Department of Medicine, Mount Sinai Hospital, New York, NY (B.C.). * To whom correspondence should be addressed. E-mail: seligson{at}sheba.health.gov.il.
BackgroundPlatelets have been suggested to play a role in the early development of atherosclerosis. As one test of this hypothesis, we assessed whether patients with Glanzmann thrombasthenia who lack platelet glycoprotein Methods and ResultsSeven patients with Glanzmann thrombasthenia, 45 to 66 years of age, underwent bilateral carotid artery ultrasonography and screening for risk factors of atherosclerosis. Findings consistent with early atherosclerosis evaluated by measurement of intima-media thickness and presence of atherosclerotic plaques were observed in 6 of the 7 patients. Intima-media thickness values higher than the 75th and 90th percentiles of age- and sex-matched white control subjects of the Atherosclerosis Risk in Communities (ARIC) study were observed in 30 and 8 of 56 carotid artery measurements, respectively. Five of the 6 patients with signs consistent with early atherosclerosis lacked both ConclusionsGlanzmann thrombasthenia does not protect affected individuals from development of atherosclerosis.
Revised on December 21, 2001
Accepted on December 21, 2001
Patients With Glanzmann Thrombasthenia
Lacking Platelet Glycoprotein
O. Shpilberg MD, MPH,
IIbß3 (GPIIb/IIIa)
and
vß3 Receptors
Are Not Protected From Atherosclerosis
IIbß3 (GPIIb/IIIa) complexes or both
IIbß3 and the more ubiquitous
vß3 cell membrane complexes are protected from development of atherosclerosis.
IIbß3 and
vß3 complexes and 1 only lacked
IIbß3.
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