Wpływ oligomerów procyanidolowych na aktywność antykoagulacyjną osocza

Background. Procyanidolic oligomers (PO) inhibit the degradation of subendothelial connective tissue by collagenase and elastase neutralization. Their efficacy in postphlebitic syndrome and venous insufficiency may suggest an additional systemic action mediated by endothelium. Therefore, the plasma anticoagulant response and the tissue plasma pathway inhibitor (TFPI) release induced by PO was assessed. Material and methods. Twenty-six patients, both surgical and medical, aged 29–86 years, who required antithrombotic prophylaxis for at least 5 days, were included in the study. The patients with higher thrombotic risk received either unfractionated heparin (UFH; 5000 IU bid, s.c., n = 8) or low molecular weight heparin (LMWH; 2850 IU AXa/0.3 mL o.d, s.c., n = 8). The patients with lower thrombotic risk received PO (150 mg bid, p.o., n = 10). In the control group there were age- and sex-matched healthy volunteers, to whom a placebo was administered. Blood samples were drawn before, on the 1, 4, 8 h, as well as on the days 2, 5 after administration of the study medication. Results. The TFPI concentration did not change significantly from the baseline value at any time, either in patients or in controls. Anti-Xa activity increased at 1 h until day 5 after administration of each study medication. Anti-IIa activity increased at 1 hour and remained elevated until day 5 under UFH and LMWH treatment, but only until day 2 in the PO group. The area under the curve of both anti-Xa and anti-IIa activity was similar in all three study groups but significantly larger as compared to the controls. Conclusions. Procyanidolic oligomers, like heparin and LMWH, induce anticoagulant response in plasma, but do not release TFPI into the blood.Wstęp. Oligomery procyanidolowe (PO) hamują degradację podśródbłonkowej tkanki łącznej poprzez neutralizację kolagenazy i elastazy. Skuteczność PO w zespole pozakrzepowym i niewydolności żylnej może sugerować ich dodatkowe działanie układowe, w którym pośredniczy śródbłonek. Było to przesłanką do oceny odpowiedzi antykoagulacyjnej osocza wywoływanej przez PO i uwalniania inhibitora drogi zewnątrzpochodnej (TFPI). Materiał i metody. Do badania włączono 26 chorych z oddziałów chirurgicznego i internistycznego w wieku 29–86 lat, u których konieczne było zastosowanie profilaktycznej terapii przeciwzakrzepowej przez co najmniej 5 dni. Chorzy z dużym ryzykiem zakrzepowym otrzymywali albo heparynę niefrakcjonowaną (UFH; 5000 jm. dwa razy dziennie podskórnie, n = 8), albo heparynę drobnocząsteczkową (LMWH; 2850 jm. AXa/0,3 ml raz dziennie podskórnie, n = 8). Pacjenci, u których ryzyko zakrzepowe było małe, otrzymywali PO (150 mg dwa razy dziennie doustnie, n = 10). Grupę kontrolną stanowili zdrowi ochotnicy zaklasyfikowani według wieku i płci, otrzymujący placebo. Krew do badań pobierano przed podaniem leku oraz w 1., 4. i 8. godzinie oraz w 2. i 5. dniu od podania leku. Wyniki. Stężenie TFPI nie zmieniało się w porównaniu z wartością wyjściową zarówno w grupach badanych, jak i kontrolnej. Aktywność anty-Xa zwiększała się od 1. godziny do 5. dnia po podaniu każdego leku. Aktywność anty-IIa była zwiększona od 1. godziny do 5. dnia po podaniu UFH i LMWH, ale tylko do 2. dnia po PO. Całkowita aktywność anty-Xa i anty-IIa, oceniana jako wielkość pola pod krzywą w badanym czasie, była podobna we wszystkich grupach badanych, ale znacząco wyższa w porównaniu z grupą kontrolną. Wnioski. Oligomery procyanidolowe, podobnie jak heparyna niefrakcjonowana i drobnocząsteczkowa, wywołują odpowiedź antykoagulacyjną w osoczu, ale nie powodują uwalniania TFPI do krwi

Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis following thrombocytopenia remission - a case report

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

Elevation of plasma fibrinogen in silent myocardial ischaemia

High plasma levels of fibrinogen and plasminogen activator inhibitor (PAI-1) are reported to be correlated with coronary heart disease. Therefore the level of fibrinogen concentration in plasma was examined and verified for the possible correlation with the previously explored PAI-1 antigen and PAI-1 activity in the pathogenesis of premature atherosclerosis (Grzywaczet al., 1998,Blood Coagul Fibrinol. 9, 245-249). Examination included only men, aged 33-46 years, who were in a stable condition for at least six months after the acute event. They were divided into two subgroups: group A (n = 14)  with and group B (n = 15) without ischaemic changes in 24 h Holter electrocardiogram. The number of involved vessels visible on the coronarography picture was similar in both groups. In the patients of group A the mean level of fibrinogen (3.92 vs 3.23 g/l, P < 0.05) was higher than in the controls (n = 15). No statistically differences were found between group B and control healthy subjects in any of the parameters measured. There were no correlation between fibrinogen concentration and PAI-1 antigen and activity levels, which were elevated in both groups of patients according to our previous study. Our results indicate that elevated levels of plasma fibrinogen and PAI-1 appeared in the group of patients with more severe disease, as revealed by silent myocardial ischaemia

Case reportMassive pulmonary embolism in a patient with ulcerative colitis and hyperhomocysteinemia &#8211; a case report

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&#8211;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 &#181;mol/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&#8594;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