Korean J Clin Pathol.
2001 Dec;21(6):431-436.
Measurement of Thrombus Precursor Protein in the Diseases Associated with Thrombosis and Changes after Heparin Therapy
- Affiliations
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- 1Department of Clinical Pathology, School of Medicine, Kyungpook National University, Daegu, Korea.
Abstract
- BACKGROUND
The relationship between thrombosis and atherosclerosis has long been recognized. It is important to diagnose them earlier and utilize thrombolytic agents earlier in the clinical diseases associated with thrombosis and atherosclerosis. So we measured the thrombus precursor protein (TpP) in these diseases and intended to investigate the changes after heparin therapy.
METHODS
TpP concentration was measured in 17 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (UA), 2 patients with aortic dissection (AD), 10 patients with other chest pain, and 9 patients with cerebral infarction and 18 healthy controls. We divided AMI into two groups, early presenters (n=10) who presented to the emergency room (ER) within 6 hours and late presenters (n=7) who presented to the ER after 6 hours of the onset of chest pain. Among the patients, in 24 patients treated with unfractionated heparin, the level of TpP was measured from plasma at 8 hours after therapy. We used the microtiter plate ELISA procedure.
RESULTS
TpP was significantly increased in AD (mean+/-SD; 51.21+/-8.08 microgram/mL), AMI (12.07+/-9.62 microgram/mL), early AMI (11.39+/-9.25 microgram/mL), late AMI (13.05+/-10.78 microgram/mL), cerebral infarction (7.34+/-4.67 microgram/mL), and UA (7.05+/-4.72 microgram/mL) compared with healthy controls (3.03+/-1.48 g/ mL). Abnormal concentrations of TpP were observed in 2 of 2 patients (100%) with AD, 12 of 17 patients (70.6%) with AMI, 8 of 10 patients (80.0%) with early AMI, 4 of 7 patients (57.1%) with late AMI, 5 of 9 patients (55.6%) with cerebral infarction, 3 of 7 patients (42.9%) with UA, and 2 of 10 patients (20.0%) with other chest pain. Among the 24 patients following heparin therapy, the level of TpP did not show significant decrease after heparin therapy in the group of UA and AMI with increased TpP above the upper limit of normal (n=14).
CONCLUSTIONS: TpP appears to be a sensitive marker of the clinical diseases associated with thrombosis and atherosclerosis. But, TpP measurement does not allow for the accurate monitoring in the treatment with unfractionated heparin.