Background/aim COVID-19 (Coronavirus disease of 2019) is an infectious disease outbreak later on declared as a pandemic, caused by the SARS-CoV-2 (severe acute respiratory syndrome coronavirus-2). It spreads very rapidly and can result in severe acute respiratory failure. The clinical studies have shown that advanced age and chronic diseases increase the risk of infection. However, influence of the blood groups on COVID-19 infection and its outcome remains to be confirmed. The aim of this study is to investigate whether there exists a relationship between the blood groups of the patients and risk of SARS-CoV-2 infection and the clinical outcomes in COVID-19 patients. Material and method 186 patients with PCR confirmed diagnosis of COVID-19 were included in this study. Age, sex, blood groups, comorbidities, need for intubation and intensive care unit follow up and mortalities of the patients were analyzed retrospectively. 1881 healthy individuals, who presented to the Hacettepe University Blood Bank served as the controls. Results The most frequently detected blood group was blood group A (57%) amongst the COVID-19 patients. This was followed by blood group O (24.8%). The blood group types did not affect the clinical outcomes. The blood group A was statistically significantly more frequent among those infected with COVID-19 compared to controls (57% vs. 38%, P < 0.001; OR: 2.1). On the other hand, the frequency of blood group O was significantly lower in the COVID-19 patients, compared to the control group (24.8% vs. 37.2%, P: 0.001; OR: 1.8). Conclusions The results of the present study suggest that while the blood group A might have a role in increased susceptibility to the COVID-19 infection, the blood group O might be somewhat protective. However, once infected, blood group type does not seem to influence clinical outcome.
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. Figure Figure
Objective: Ankaferd ® Blood Stopper (ABS) is an herbal extract that has historically been used as a hemostatic agent in traditional Turkish medicine. ABS is comprised of a standardized herbal mixture of T. vulgaris, G. glabra, V. vinifera, A. officinarum, and U. dioica. ABS's basic mechanism of action is the formation of an encapsulated protein web, which represents the focal point for vital erythrocyte masses. The hemostatic effects of ABS have been observed in vitro and in vivo. ABS was registered as a hemostatic agent for external hemorrhages and dental bleeding following phase I randomized, double-blind crossover placebo-controlled clinical research, and safety and efficacy reports. In terms of the potential use of ABS, transcription factors may be novel factors that play a role in the hemostatic and other pleiotropic effects of ABS. Materials and Methods: Hence, the present study aimed to investigate the effects of ABS on endothelium, and possible transcription factor changes in HUVEC (human umbilical vein endothelial cells) and the erythrocyte membrane profile. ABS (5 μL and 50 μL) was administered to HUVEC (in 75 cm 2 ; ~75% fullness) for 5 min and 15 min. Results: ABS caused significant increases in the level of activation of the following transcription factors; AP2, AR, CRE/ATF1, CREB, E2F1-5, E2F6, EGR, GATA, HNF-1, ISRE, Myc-Max, NF-1, NFkB, p53, PPAR, SMAD 2/3, SP1, TRE/AP1, and YY1. Following erythrocyte membrane isolation, protein complexes were undissolved, but denatured. The protein complex formed was resistant to heat and detergent. Trypsin and sonication were used in order to break this complex; the complex dissolved and erythrocyte membrane proteins were released in SDS-PAGE. Conclusion: ABS established a very fast and solid protein web, and increased the level of transcription factor activation. Therefore the cellular effects of ABS could be related to different intracellular biological pathways. (Turk J Hematol 2011; 28: 276-85)
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