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Introduction. Anti-inflammatory, separate from anti-thrombotic activity of low molecular weight heparin, is still not well documented. Aim. We estimated the influence of enoxaparin on serum levels of tumor necrosis factor alpha, as the pro-inflammatory cytokine, and interleukin-12, as the heparin-binding, anti-inflammatory cytokine, in patients with exacerbations of chronic obstructive pulmonary disease. Material and methods. Seventy-three consecutive patients (48 males, 25 females) aged 56-75 years without thromboembolic history, were enrolled into the study. They were randomized to group who received enoxaparin in one daily dose 40 mg, or to group who did not receive it. Patients receiving oral anti-coagulants were excluded from the study. Using ELISA approach, we evaluated serum levels of tumor necrosis factor-alpha and interleukin-12 at the following periods: before the first dose of enoxaparin, after 7 days of treatment and 14 days of treatment. Serum level of the C-reactive protein was evaluated simultaneously. Results. In enoxaparin recipients statistically significant (p<0.01) decreasing of TNF-alpha serum levels (from 168.33 pg/ml in admission, to 85.67 pg/ml in the end of study) to compare enoxaparine non-recipients, was observed. Interleukin-12 serum levels were significantly higher in enoxaparine recipients both after 7 days (67.46 pg/ml) and 14 days (89.32 pg/ml) of the study (p<0.05). C-reactive proteins serum levels were significantly higher in enoxaparine non-recipients than recipients (p<0.05) in all study period. Conclusions. Enoxaparin in daily dose 40 mg, significantly depressed serum levels of TNF-alpha and promote serum levels of interleukin-12. Enoxaparin administration may be beneficial for the patients with COPD exacerbation during the first 14 days of treatment
The term “venous thromboembolism” encompasses two disease entities, i.e. deep vein thrombosis and its very serious complication – pulmonary embolism. In Poland, this disease affects almost 50 thousand people, nearly a half of whom develop pulmonary embolism which accounts for 10% of all hospital deaths. The incidence rate increases with age, and 70% of cases concern people above the age of 60. The treatment of complications caused by these symptoms is very expensive. It is estimated that the cost is nearly as high as in the treatment of neoplasms. Risk factors of thromboembolism include: age >40, family and personal history of venous thromboembolism, major surgeries (within lower extremities, pelvis and abdomen), malignant cancers and certain anticancer treatment regimens as well as pregnancy and postpartum period. The severity of symptoms mainly depends on disorders of blood outflow from the lower extremities and the extent of thrombotic lesions. The more extensive thrombosis is, the greater the blood stasis and the greater the vascular disorders. The most common symptoms include pain and edema. Thromboembolism is asymptomatic is nearly a half of patients. That is why a careful interview and risk factor estimation are so important. Non-invasive methods are used, such as: ultrasound assessment of venous flow, Doppler ultrasound, plethysmography (assessment of blood volume in the lower extremities), venography and D-dimer level assessment. Proper thromboprophylaxis is the most important element that increases the safety of patients and considerably decreases health care expenditure. This review presents indications for venous thromboembolism prophylaxis in accordance with the latest guidelines.
Nazwa „żylna choroba zakrzepowo-zatorowa” (venous thromboembolism) zawiera w sobie dwie jednostki chorobowe, a mianowicie zakrzepicę żył głębokich oraz bardzo poważne jej następstwo, jakim jest zator tętnicy płucnej. W Polsce choroba ta dotyka blisko 50 tys. osób, z czego prawie u połowy wystąpi zator tętnicy płucnej, który powoduje 10% wszystkich zgonów w szpitalu. Liczba zachorowań zwiększa się z wiekiem, a 70% dotyczy osób >60. roku życia. Leczenie powikłań spowodowanych przez ten zespół objawów jest niezwykle kosztowne – szacuje się, że wydatki są zbliżone nawet do kosztów leczenia chorób nowotworowych. Do czynników ryzyka żylnej choroby zakrzepowo-zatorowej należą: wiek >40 lat, żylna choroba zakrzepowozatorowa w wywiadzie rodzinnym, przebyta choroba zakrzepowo-zatorowa, duże zabiegi operacyjne (w zakresie kończyn dolnych, miednicy i jamy brzusznej), nowotwory złośliwe i niektóre schematy leczenia przeciwnowotworowego, ciąża i połóg. Ciężkość objawów zależy głównie od stopnia zaburzenia odpływu krwi z kończyn dolnych, a także rozległości zmian zakrzepowych. Im rozleglejsza zakrzepica, tym większy zastój krwi i większe zaburzenia naczyniowe. Najczęstszymi objawami są ból oraz obrzęk. Niemal u połowa pacjentów żylna choroba zakrzepowo-zatorowa przebiega bez objawów, dlatego tak ważny jest dokładny wywiad oraz oszacowanie czynników ryzyka. Stosuje się metody nieinwazyjne, takie jak: ultradźwiękowa ocena przepływu krwi w żyłach, ultrasonografia dopplerowska, pletyzmografia – ocena objętości krwi w kończynach dolnych, flebografia oraz ocena stężenia D-dimerów. Prawidłowa profilaktyka stanowi najważniejszy element zwiększający bezpieczeństwo chorych, a także zdecydowanie zmniejszający koszty opieki zdrowotnej. W opracowaniu przedstawiono wskazania do profilaktyki żylnej choroby zakrzepowo-zatorowej według najnowszych wytycznych.
Acute pulmonary embolism (APE) is one of the main causes of cardiovascular deaths and anticoagulant treatment plays a key role in preventing recurrent episodes, chronic thromboembolic pulmonary hypertension (CTEPH), and deaths. The aim of this study is to assess the real-life trends and to determine factors associated with the choice of anticoagulation therapy in patients with APE. This is a single center prospective open study. We followed 178 consecutive patients admitted to the tertiary clinical center with APE proven with computed tomography (CT) scan within period of 24 months. A total number of 178 patients with APE were enrolled in the study. 48.9% of subjects were hospitalized in cardiology department. As a prolonged anticoagulant therapy 35.7% of study cohort received direct oral anticoagulants (DOACs), 35.1% LMWH, and 29.2% vitamin K antagonists (VKA), respectively. No statistically significant differences were found between the departments regarding frequency of prescribing anticoagulants (p=0.15). The multivariable analysis showed that oral anti-coagulants (OACs) were less likely to be prescribed than LMWH in patients with malignancy, history of major bleeding, serious medical condition and altered mental status. OACs were preferred over LMWH in symptoms of deep vein thrombosis (DVT). VKA were significantly less likely to be chosen than DOACs in patients with history of orthopaedics procedure. After six months anticoagulation therapy was discontinued in 24.3% of patients. Concluding, the form of anticoagulant therapy was associated with the presence of chronic diseases. LMWH was prescribed in high bleeding risk patients more frequently.
 Colon anastomosis is therapeutically challenging because multiple, usually undetectable factors influence a spectrum of repair mechanisms. We hypothesized that low molecular weight heparins, routinely administered perioperatively, may differentially affect gene expression related to colon healing. Twenty pairs of untreated and enoxaparin-treated rats underwent left-side hemicolectomy with a primary end-to-end anastomosis. Normal colon and anastomotic bowel segments were resected on day 0 and on days 1, 3, 5, and 7 after surgery, respectively. Serial anastomosis transverse cross-sections were evaluated microscopically and by microarray (Rat Genome 230 2.0, Affymetrix). Differentially expressed probe sets were annotated with Gene Ontology. We also examined the influence of enoxaparin on fibroblast proliferation and viability in vitro. Among the 5476 probe sets, we identified differential expression at each healing time point, yielding 79 subcategories. Most indicated genes were involved in wound healing, including multicellular organismal development, locomotory behavior, immune response, cell adhesion, inflammatory response, cell-cell signaling, blood vessel development, and tissue remodeling. Although we found no intensity differences in histological features of healing between enoxaparin-treated and control rats, treatment did induce significant expression changes during early healing. Of these changes, 83 probe sets exhibited at least twofold changes and represented different functional annotations, including inflammatory response, regulation of transcription, regulation of apoptosis, and angiogenesis. Fibroblast culture confirmed an anti-viability effect of enoxaparin. Enoxaparin affects colon wound-related gene expression profiles, but further studies will resolve whether heparin treatment is a risk factor after intestinal surgery, at least in some patients.
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