Introduction: Even though thrombocytopenia following transcatheter aortic valve implantation (TAVI) has been described, further investigation of this phenomenon is needed. Aims: To determine which factors may explain the fall in platelet count that occurs after implantation of a TAVI device, including markers of platelet and blood coagulation activation. Material and methods: 32 patients without previous indications for dual antiplatelet therapy (mean age 78.5 +/- 7.9 years, 62% females) with severe aortic valve stenosis (mean gradient 54.6 +/- 16.9 mm Hg) who qualified for TAVI procedure (Edwards Sapien XT) were prospectively analyzed. Platelet counts were analyzed before the surgery, on the day of the procedure and for the three following postoperative days (POD 1 to 3). To assess platelet activation P-selectin (PS, serum) and platelet factor 4 (PF-4, CTAD plasma) were measured, whereas for the evaluation of coagulation activation prothrombin fragments 1 + 2 (F1 + 2, plasma) were assessed before the procedure, on POD-1 and POD-3 (ELISA). Results: During the postoperative period a significant platelet count drop, the most evident on POD-2, was observed followed by a platelet count raise. The platelet count drop correlated directly with the amount of iodinated contrast agent (r =3D 0.42, p =3D 0.016) and inversely with baseline mean platelet volume (r =3D -0.37, p =3D 0.046). Neither clinical nor perioperative parameters, except contrast medium, influenced platelet count decrease. No significant differences regarding the concentration of the evaluated markers in patients with and without thrombocytopenia were found. PF-4 and F1 + 2 significantly changed during the study (p < 0.05). Greater acute PF-4 decrease correlated with greater acute platelet count drop (r =3D 0.48, p =3D 0.043), and during the study slower PF-4 increase correlated with higher platelet count increase on POD-3 (r =3D -0.505, p =3D 0.032). Lower baseline PS correlated with lower baseline platelet count and higher platelet count increase on POD-3 (r =3D 0.45, p =3D 0.04 and =3D -0.55, p =3D 0.02, respectively). No significant correlations between F1 + 2 concentrations and platelet count changes have been found. Conclusions: Platelet reduction shortly after TAVI procedure is related to the amount of contrast agent applied during the procedure. Platelet activation and blood coagulation along with impaired baseline platelet renewal might be the mechanisms of thrombocytopenia following TAVI procedure. (C) 2017 Elsevier Ltd. All rights reserved.

OBJECTIVES: To investigate the role of endothelial cell mediators, E-selectin (ES), intercellular adhesion molecule-1 (ICAM-1), tissue factor (TF), and von Willebrand factor (vWF), in the early phase of severe acute pancreatitis (SAP) complicated with respiratory failure [pancreatitis-associated lung injury (PALI)].; PATIENTS AND METHODS: This study included 30 patients with SAP and 39 patients with PALI. Blood samples were taken from SAP and PALI patients on presenting to the hospital (day 1), and days 2, 3, 5, and 10. The relationship between blood concentrations of the studied endothelial mediators and lung function tests was analyzed.; RESULTS: PALI patients had significantly higher ES, ICAM-1, TF, and vWF blood levels than those with SAP as early as at admission and throughout the period studied. We found the highest concentration of ES on the second day, ICAM-1 and TF at admission, and vWF level on the fifth day. There were adverse correlations between ES, ICAM-1, TF, vWF concentrations, and the index of oxygenation--PaO2/FiO2 ratio (Rs=3D-0.385, Rs=3D-0.523, Rs=3D-0.505, Rs=3D-0.408, P<0.001, respectively). The most accurate prediction of PALI was provided by ICAM-1 and TF levels on the day of admission [areas under curve (AUCs): ES, 0.704; ICAM-1, 0.787; TF, 0.757; and vWF, 0.686].; CONCLUSION: Endothelium-related mediators ES, ICAM-1, TF, and vWF appear to participate in pancreatitis-associated lung injury. In SAP, the measurement of endothelial mediator levels (especially ICAM-1 and TF) may be used as an early prognostic indicator that would predict the development of respiratory failure and to monitor the severity of lung dysfunction.=20

The most common cause of isolated thrombocytopenia is primary immune thrombocytopenia (ITP). For patients failing initial corticosteroid-based treatment and with refractory ITP post-splenectomy, thrombopoietin receptor agonists are indicated. Two of this thrombopoiesis-stimulating agents have been approved for use in ITP - eltrombopag, formulated for oral administration, once a day and romiplostim, which is administered weekly as a subcutaneous injection. (C) 2013 Polskie Towarzystwo Hematologow i Transfuzjologow, Instytut Hematologii i Transfuzjologii. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.

Protein Z (PZ) deficiency may induce bleeding as well as thrombosis. The aim of our study was to estimate the concentration of PZ in patients with acute leukemia. Plasma levels of PZ were determined in 76 patients with newly diagnosed acute leukemia ([AML], n =3D 50; acute lymphoblastic leukemia [ALL], n =3D 26) and 62 healthy participants. In the patients, mean plasma concentrations of PZ were statistically lower than in healthy individuals: AML (1.24 =C2=B1 0.11 mug/mL vs 1.58 =C2=B1 0.05 mug/mL P =3D .01) and ALL (1.19 =C2=B1 0.16 mug/mL vs 1.58 =C2=B1 0.05 mug/mL P =3D .01). Levels of PZ below the fifth percentile (0.873 mug/mL) of normal value distribution in control participants were found in 30% of patients with AML and ALL and in 3% of controls (P < .0001). In this AML subgroup, we found statistically significant correlation between episodes of bleeding and PZ level (P =3D .01). There was no such correlation in ALL group. The results suggest that PZ can be a cofactor associated with an increased bleeding tendency in patients with AML.=20

The potential role of alterations in protein Z (PZ) concentrations in the pathogenesis of coagulation has been investigated in several studies which, however, yielded conflicting results. Protein Z deficiency may induce bleeding as well as prothrombotic tendencies and it might occur as an inherited disorder. The principal aim of the present study was to explore the concentration of protein Z and protein Z-dependent protease inhibitor (ZPI) in patients with haemophilia A. In haemophilia A patients mean plasma concentrations of PZ and ZPI were significantly higher than in healthy individuals: PZ (1.87 +/- 0.68 mu g/mL vs 1.49 +/- 0.54 mu g/mL) and ZPI (5.02 +/- 1.11 mu g/mL vs 4.22 +/- 0.55 mu g/mL), with p=0.02 and p=0.03, respectively. In the subgroup with severe haemophilia A, an in-depth analysis revealed a tendency to modulating effect of the PZ (r=-0.53; p=0.072) and a statistically significant one in the case of ZPI (rho=-0.79, p=0.002) on the bleeding rate. It simultaneously disclosed a statistically significant correlation between the number of bleeds to the joints (20.18 +/- 14.1), PZ (r=-0.72; p=0.04) and ZPI (rho=-0.88, p=0.001). With reference to this particular group of patients, the study also showed some other statistically meaningful correspondences: between PZ and ZPI (rho=0.65, p=0.02), PZ and FIX (r=-0.61, p=0.04), as well as ZPI and FVIII (rho=0.78, p=0.002). In conclusion, despite the fact that FVIII deficiency is undoubtedly the main mechanism of bleeding in haemophilia A patients, the activity of PZ/ZPI complex may play some modulating role in the matter. (C) 2012 Elsevier Ltd. All rights reserved.