1993 Fiscal Year Final Research Report Summary
Development of a new method for detection of hypercoagulable state of whole blood
| Project/Area Number |
04454546
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | Kobe University |
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Principal Investigator |
OKUNOMIYA Akiko Kobe University School of Allied Medical Sciences Associated Professor, 医療技術短期大学部, 助教授 (10107948)
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| Co-Investigator(Kenkyū-buntansha) |
FUNAHARA Yoshinori Kobe University School of Medicine Associated Professor, 医学部, 助教授 (90030840)
ISHIKAWA Hitoshi Kobe University School of Allied Medical Sciences Professor, 医療技術短期大学部, 教授 (30107958)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Blood coagulation / Erythrocyte / Platelet / Thalassemia / Rheumatoid Arthritis / Thrombin |
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| Research Abstract |
For the purpose of developing a technique that is accurate and sensitive enough to detect hypercoagulable state in blood, the following method was proposed : After the whole blood was incubated at 37 C, the intrinsic coagulation pathway was activated by ellagic acid and CaC12 in the presence of MD805, and at the fixed time, thrombin activity in the mixture was measureed by using S-2238 as substrate. The amount of thrombin formed depended on the amount of freeze-thawed platelets, ghosts of erythrocytes or calcium ionophore-treated blood cells.
By applying the method to the whole blood from 19 beta-thalassemia/HbE cases, we could tentatively divide the results into three groups : Group A(4 post-splenectomized cases) showing very high activities at 90 minutes after the blood collection, Group B (4 post-splenectomized and 2 non-splenectomized) showing higher activeties than those of volunteers and Group C (2 post-splenectomized treated with aspirin and 7 non-splenectomized) showing lower activities. This suggested that the abnormal erythrocytes that appeared after splentomy may play some role in the increase of the thrombin-forming activity in the whole blood.
On the basis of these results, a clinical trial started in 1994 to improve the symtoms of 11 beta-thalassemia/HbE patients with the treatment of the drug (Dirazep) acting on menbranes of blood cells such as platelets and red blood cells. Results so far obtained suggested that the treatment was efficacious for inhibiting the decrease of Hb, decreasing the thrombin-forming activity in whole blood and improving the performance status. These results suggested the usefulness of our method detecting the thrombin-forming activity in the whole blood for the pathophysiological and clinical research of diseases involving blood cells abnormalities, such as beta-thalassemia/HbE.
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