Venous thromboembolism (VTE) is a common complication in patients with hepatocellular carcinoma (HCC). Its pathomechanism is associated with non-malignant origin in chronic liver disease as well as malignant disease. However, this high incidence is likely to correlate with other factors. Patients with HCC and VTE have a shorter survival time than patients without VTE. Factor VIII is an important procoagulant protein that binds with high affinity to von Willebrand factor. Factor VIII increased to more than 150% may cause an approximately 6-fold higher risk of venous thrombosis compared to patients with normal factor VIII. Its level rises with increasing age, during inflammation, and in pregnancy. Cancer patients with higher FVIII activity had a statistically higher proportion of VTE (14%) compared to patients with normal values (4%). Selectins are membrane glycoproteins that are involved in cell adhesion. P-selectin is considered to be a risk factor for VTE in cancer patients. The level of soluble P-selectin at the time of cancer diagnosis may identify patients at risk of VTE. In our study, we identified P-selectin and factor VIII as risk factors for thromboembolic disease in HCC patients. We defined patients as benefiting from thromboprophylaxis in terms of delaying VTE. We examined 30 patients with HCC and compared the results to a healthy population. We determined etiology of liver cirrhosis, the presence of VTE, basic laboratory parameters, genetic examinations as well as examinations for other thrombophilic conditions such as protein C, antithrombin, soluble P-selectin, P-selectin expression, factor VIII and PAI-1 activity. Patients with HCC and VTE had higher factor VIII levels of 2,325 (1,65 - 2,77) than patients with HCC without VTE, who had values of 1,6413 (0,77 - 2,70). The healthy control group had average factor VIII levels of 1,1970 IU / ml (0,86 – 1,89) - SD of 0,25331. The level of soluble P-selectin in HCC patients was significantly higher than in the healthy control group (p = 0,0003). The number of patients with thromboembolic disease was 33.3%. The average levels of soluble P-selectin were 59.8 ng/ml (26-180), suggesting high risk. However, patients who did not have VTE also had elevated levels of soluble P-selectin: 20 patients (66.6%) with 54.72 ng/ml. Above the cut off level of 53.1 ng/ml, 17 of the 30 HCC patients were present. Of these, 4 patients (23%) outperformed VTE. Mean expression of membrane P-selectin in HCC patients versus healthy control was 14.724% (5.31 - 39.40%) of SD 8.28363 vs. 2.933% (1.1 - 6.5%). The best predictive parameters of the risk of VTE in HCC patients are factor VIII and P-selectin in plasma as well as CD62 expression by flow cytometry. Based on our results, we consider FVIII and P-selectin as predictive biomarkers of VTE. If investigated at the time of diagnosis, they could predict the risk of developing VTE in the future. Thromboprophylaxis should be considered individually, especially in patients with other associated risk factors for VTE.

OBJECTIVE:Bring a comprehensive overview of the available knowledge about thrombophilia in pregnat women.DESIGN:Overview study.SETTING:Departmentof Haematology and Transfusion Medicine, National Centre for Haemostasis and Thrombosis, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia.METHODS:Analysis of literary sources.CONCLUSION:Anticoagulation may provide benefit for women both as prophylaxis and as treatment for venous thrombosis during pregnancy. The use of anticoagulants in women with inherited thrombophilia and history of miscarriage remains controversial. In contrast, pregnant women with acquired thrombophilia should be anticoagulated.

BACKGROUNDS:Translational medicine is a medical field encompassing basic research and development of new diagnostic and therapeutic strategies for clinical practice. The present scientific paper focuses on our previous experience in the field of chemoresistance testing in patients with oncological diseases.MATERIAL AND METHODS:Since 2005, we sampled 71 patients with a leukaemia (AML, ALL and CML) and 92 patients with a solid tumour (lung and gastrointestinal tract cancer). Malignant cell in vitro drug resistance testing was carried out using cytotoxic methyl-thiazol tetrazolium (MTT) assay.RESULTS:Based on the LC50 (lethal concentration of a drug killing 50% of cell population), we found that patients with acute myeloblastic leukaemia exhibit a greater degree of resistance than patients with acute lymphoblastic leukaemia. In patients with bronchogenic carcinomas, primary resistance to cisplatin was identified in 28% of tested samples, paclitaxel 36%, vincristine 50%, etoposide 56%, vinorelbine 57%, topotecan 62%, gemcitabine 77% and dacarbazine 86%.CONCLUSION:In vitro tests with gastrointestinal tract cancers also suggested high effectiveness of cisplatin (with the exception of gastric carcinoma) that was comparable with 5-fluorouracil. Even though the MTT assay has some limitations (insufficient number of vital cells, possible contamination by non-malignant cells, etc.), this in vitro method proved very effective in testing malignant cell resistance to clinically used cytostatics.

Burley tobacco (Nicotiana tabacum L.) is an important raw material in the production of Chinese-style blended cigarettes. However, the high levels of tobacco-specific nitrosamines (TSNA) have devalued the industrial use of burley tobacco and limited its sustainable use. The objective of this paper was to investigate the effects of acetylsalicylic acid (ASA) application on accumulation of TSNA, its precursors and quality of air-cured burley tobacco (Nicotiana tabacum L. cv. DaBai 1). Field experiments were conducted to determine the contents of TSNA and the precursors and the sensory quality of burley tobacco under 0, 0.1, 0.3 mM of ASA in 2014 and 2015 at Dazhou, Sichuan Province, China. The results showed that TSNA, nitrate, nitrite and alkaloids levels were significantly reduced by the application of ASA, of which the total TSNA were significantly lower by 10.40–24.75%, and two of the strong animal carcinogens in tobacco products, i.e. N-nitrosonornicotine (NNN) and 4-(methylnitrosamino) -1- (3- pyridyl) -1- butanone (NNK) were reduced by 9.01–24.23% and 11.43–26.86%, respectively. Year had significant effects on TSNA and the TSNA contents in 2014 were higher than in 2015. Interestingly, the sensory quality of burley tobacco remained or was even better after application of ASA. In conclusion, this study revealed that ASA application was able to reduce the levels of TSNA and its precursors in sustaining burley tobacco industry potentially.

Currently, recombinant activated factor VII (rFVIIa) (NovoSeven) is indicated for the treatment of spontaneous and surgical bleeding in congenital haemophilia A and B patients with inhibitors to factors VIII (FVIII) and IX (FIX) >5 Bethesda units (BU) worldwide, and in patients with acquired haemophilia, congenital FVII deficiency and Glanzmann's thrombasthenia in Europe. Until April 2003, almost three-quarters of a milion doses of rFVIIa have been administered proving its efficacy and excellent safety record. According to results from initial clinical trials and a large number of case reports, the rFVIIa may be effective not only in treating haemophilia patients but also in treatment of bleeding in patients on oral anticoagulation or heparin, patients with liver diseases, von Willebrand disease (vWD), thrombocytopenia, various platelet defects, congenital or acquired deficiency of FVII, and in subjects without any pre-existing coagulopathy with diffuse life-threatening bleeding triggered by surgery or trauma. This review will briefly summarize rFVIIa mode of action in haemostasis, the current clinical experience with rFVIIa and focus on the alternative use of rFVIIa in patients at the high risk of bleeding in both spontaneous cases and clinical trials reports.

Localised and following systemic inflammatory reaction accompanying progression of infection causes generation of anti-inflammatory cytokines. They activate leucocytes, endothelium, coagulation and fibrinolysis. Sepsis is usually accompanied by already decompensated disseminated intravascular coagulation which significantly affects mortality of patients with this disease. The main cause of hypercoagulation state during sepsis seems to be inhibition of fibrinolysis as a result of overproduction of plasminogen activator inhibitor-1 in later stages of the disease. Some microorganisms have specific properties which affect individual components of hemostasis and thus increase their virulence. Because natural inhibitors of coagulation have not only anticoagulation but also strong anti-inflammatory effect, they seem to be an optimum remedy for fluorid coagulopathy during sepsis. Moreover, their use usually does not increase risk of bleeding.