[Non-bacterial thrombotic endocarditis on the bicuspid aortic valve in a 25-year-old male with lupus anticoagulant]. / Niebakteryjne zakrzepowe zapalenie wsierdzia na dwuplatkowej zastawce aortalnej u 25-letniego mezczyzny z antykoagulantem toczniowym.

Non-bacterial thrombotic endocarditis (NBTE) is characterized by presence of sterile vegetations that develop from fibrin and platelets on heart valves. The main conditions predisposing to NBTE are malignancy, autoimmune diseases and other hypercoagulable states. The authors describe a case of a 25-year-old male, in whom NBTE was diagnosed on the bicuspid aortic valve. The presence of significant aortic regurgitation and dental caries were initially suggestive of infective endocarditis; although, serial blood culture were negative and procalcytonin concentration was within normal ranges. Empiric antibiotic therapy did not result in diminishing of vegetations, similarly to the anticoagulation treatment initiated when strongly positive lupus anticoagulant was detected in laboratory findings. Aortic valve replacement was necessary. Bacteriologic examination of the excised valve was negative. Widespread fibrin masses at different stages of organization on the leaflets confirmed NBTE in histopathologic assessment. Lupus anticoagulant was probably secondary to thyroid autoimmune disease.

Non-thermal plasma-driven synthesis of Eu3+:Y2O3 nanosized phosphors.

The synthesis of nanosized phosphors by using the non-thermal plasma-driven method is presented. The method allows to control the average grain size of nanocrystals. The synthesis of Eu3+-doped Y2O3 nanocrystalline phosphors at water solution of nitrates is described. The average sizes of nanocrystals were controlled by sintering temperature. Their structure, morphology, and luminescent properties were investigated.

Resistance to acetylsalicylic acid in patients after ischemic stroke.

INTRODUCTION: Acetylsalicylic acid (ASA) due to its antiplatelet action is used in ischemic stroke therapy. The platelet response to ASA shows an interindividual variation. Decreased platelet sensitivity to ASA is termed as resistance to ASA. OBJECTIVES: The aim of the study was to assess the prevalence of resistance to ASA in stroke patients and discover dependence between resistance to ASA and stroke recurrence and certain genetic and environmental factors. PATIENTS AND METHODS: 59 patients aged 22-83 years (mean age: 53) who had ischemic stroke within the period of 1 month to 10 years prior to the study were analyzed. 51 patients received ASA in a daily dose of 75 mg, and 8 in a higher dose. ASA had been taken since the stroke episode. Resistance was analyzed using the PFA-100 and optical aggregometer, with adenosine diphosphate, collagen and arachidonic acid as platelet agonists. RESULTS: Resistance to ASA in patients after stroke is observed with frequency ranging from 9% in arachidonic acid-induced aggregometry to 65% in the PFA-100. There were correlations between platelet aggregation in response to various agonists (r = 0.37-0.77, p < or = 0.005), and between collagen-induced aggregation and the PFA-100 (r = -0.33, p = 0.016). Platelet aggregation induced by arachidonic acid (r = 0.39, p = 0.029) correlated with the stroke recurrence (n = 12). ASA resistance detected in aggregometry in response to collagen was more common in patients with 807CT genotype for Ia glycoprotein (p = 0.05), and in patients with diabetes (p = 0.039). CONCLUSIONS: In patients after ischemic stroke resistance to ASA is commonly observed. In patients with diabetes or C807Tglycoprotein Ia gene CT polymorphisms this phenomenon is more frequently detected.

[Massive pulmonary embolism in a patient with ulcerative colitis and hyperhomocysteinaemia -- a case report]. / Masywna zatorowosc plucna w przebiegu wrzodziejacego zapalenia jelita grubego i hiperhomocysteinemii.

We describe a case of a 37-year-old man with active ulcerative colitis complicated by proximal deep vein thrombosis of the left lower limb and subsequent massive pulmonary embolism requiring mechanical ventilation and catecholamine infusion. In spiral CT a large thrombus obturating left pulmonary artery as well as bilateral embolic material in lobar and segmental branches were visible. Haemodynamic status improved after infusion of rtPA. Haemoglobin decrease (7.0-5.6 mmol/L) was corrected with erythrocyte mass transfusion. During subsequent therapy with intravenous full dose of unfractionated heparin and further long-term treatment with subcutaneous enoxaparin (1.5 mg/kg and after 3 months 1.0 mg/kg daily) haemoglobin value was relatively stable. Underlying disease was treated with 5-ASA (mesalazine) and steroids. Due to hyperhomocysteinaemia (16.0 micromol/L) coexisting with a low plasma folic acid (2.1 ng/ml) and cyanocobalamin (137 pg/ml) levels, supplementation with these vitamins was prescribed. The screening tests for familial thrombophilia (including 677C-->T MTHFR mutation) were negative. The authors discuss the pathogenesis of increased thromboembolic risk in inflammatory bowel disease and therapeutic dilemmas connected with treatment of such complications.

[Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis following thrombocytopenia remission--a case report]. / Gleboka maloplytkowosc po zastosowaniu abciximabu w ostrym zawale serca. Zakrzepica w stencie po ustapieniu trombocytopenii.

Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis. This article presents a case of a 62-years-old man with acute anterior myocardial infarction, treated with PCI and stent implantation, in whom profound acute thrombocytopenia was observed after abciximab administration. Nadir platelet count was 6 G/L (before treatment: 250 G/L). Pseudothrombocytopenia was excluded. The remaining antiplatelet drugs (heparin, ASA, clopidogrel) were discontinued. There were no symptoms of bleeding, but next morning (platelet count: 14 G/L) a gross hematoma at femoral puncture site was observed. The patient received 5 U transfusion of platelets. On the 4th day, when the platelet count reached 64 G/L, he was started again on ASA (150 mg) and clopidogrel (75 mg). On the 7th day (platelet count: 138 G/L) he developed anterior ischemia and stent reocclusion was diagnosed. After p.o. clopidogrel (300 mg), balloon PCI with i.c. heparin was performed and ischemia symptoms subsided. The platelet value before the patient's discharge, on subsequent therapy with ASA and clopidogrel, increased to 300 G/L. A review of current literature on this topic is provided.

[Recurrent hemoptysis following thienopyridines and amiodarone administration. therapeutic dilemma]. / Nawracajace krwioplucie podczas leczenia tienopirydynami i amiodaronem. Dylemat terapeutyczny.

The authors describe a case of a 74-year-old man with advanced coronary heart disease in whom pulmonary hemorrhagic complications during therapy with ticlopidine and subsequently with clopidogrel and amiodarone were observed. Fever and massive hemoptysis following five days of ticlopidine treatment, before elective coronary angiography, were noticed. Transient interstitial X-ray changes of the right lung were visible. Three months later a new episode on the third day of clopidogrel administration was manifested. He was after PCI, performed because of ACS complicated with ventricular fibrillation. Two days following clopidogrel discontinuation hemoptysis remitted but after ten days occurred again (this time with bilateral X-ray changes). Amiodarone, given after VF, was stopped. Spectacular improvement with steroid treatment was observed. Indobufen (reversible COX- 1 inhibitor) as an antiplatelet therapy was availed. The authors discuss therapeutic dilemma concerning the patient with coexisting different diseases.

Plasma markers of hypercoagulability in patients with serious infections and risk of septic shock.

Hyperthrombinogenesis due to bacterial septicemia may aggravate the risk of irreversible septic shock. In 22 patients with septicemia complicating urinary or alimentary infections, daily assessment of hemostasis was performed throughout 1 week. Standard screening of hemostasis revealed significantly increased mean values of prothrombin time, fibrinogen, and fibrinogen degradation product (FDP) concentration. However, platelet counts, activated partial thromboplastin times (APTT), thrombin times, ethanol gelation tests, and antithrombin activity remained within the normal range. By contrast, except for insignificant changes in protein C activity and activated factor VII content, specific markers of plasma hypercoagulability, that is, thrombin-antithrombin (TAT) complexes, prothrombin activating factor F 1+2, activated factor XII (XIIa), and dimer D were all markedly increased. Pathologic levels of TAT and Xlla were found in 82% and 73% of all plasma samples, respectively. The augmentation of TAT correlated with prolongation of thrombin time and increases in F 1+2 levels. The increase in XIIa correlated with thrombocytopenia, prolongation of APTT, exhaustion of antithrombin, and accumulation of F 1+2 and FDP in the plasma. Moreover, a significant increase in XIIa, stronger positivity of the ethanol gelation test, a greater increase in FDP, and a more pronounced decrease in protein C activity were observed in 8 patients with fatal septic shock. This study suggests the usefulness of TAT and XIIa measurements in the early recognition of plasma hypercoagulation in serious infections.