Ankaferd Blood Stopper® (ABS), a standardized mixture of the plants Thymus vulgaris, Glycyrrhiza glabra, Vitis vinifera, Alpinia officinarum, and Urtica dioica has been used as a haemostatic agent. However, the essential ‘mechanism of action’ of ABS is currently unknown. The aim of this study is to search the essential mechanism underlying the haemostatic actions of ABS. In our study, ABS induced a very rapid (less than 1 second) formation of a protein network within the plasma and serum. Individual clotting factors namely factor V, factor VII, factor VIII, factor IX, factor X, factor XI, factor XIII are not affected during the consecutive measurements. Plasma fibrinogen activity and antigen decreased from 302 mg/dl to 10 mg/dl, and fibrinogen antigen decreased from 299 mg/dl to 30 mg/dl, in parallel to the prolongation of thrombin time (TT). Biochemical tests also revealed that total protein, albumin, and globulin levels significantly decreased with the interactions of ABS. Red blood cells come together to form vital erythrocyte mass blocks in the presence of ABS. Vital physiological red blood cell aggregation after the exposure to Ankaferd Bloood Stopper in less than one second is depicted in Figure 1. The network of ABS could cover the entire physiological haemostatic process without unequally disturbing individual clotting factors. The basic mechanism of action for ABS appears to be the formation of an encapsulated protein network representing focal points as a niche for vital erythrocyte aggregation. ABS is a novel effective haemostatic agent that has the therapeutic potential for the management of hemorrhage in medical practice. Clinical trials with that promising medicine can provide the development of a new drug particularly active in pathological haemostasis.
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Systemic lupus erythematosus (SLE) patients are at increased risk of thrombosis and cardiovascular diseases. Aspirin is an effective treatment option for these patients. The aim of this study was to investigate the presence of aspirin resistance in SLE patients. We studied aspirin resistance in 33 SLE patients and nine healthy controls by using a Multiplate® impedance aggregometer (Dynabyte GmbH, Munich, Germany). Twenty-six SLE patients were on regular aspirin treatment. Aspirin resistance was found in five (19.2%) out of 26 patients who were on aspirin treatment. When the tests were repeated by adding acetylsalicylic acid in the medium, all of these patients became responsive to the aspirin. SLE disease activity, body mass index, smoking status, and the presence of anticardiolipin antibodies or positive lupus anticoagulant test results were no different in patients with or without aspirin resistance. (p>0.05 for all). Our results suggest that there may be a considerable number of SLE patients with aspirin resistance.
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