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Sanja Petrusevska Marinkovic, Irena Kondova Topuzovska, Zvonko Milenkovic and Biserka Kaeva
The aim of this study was to identify the participations of the serum coagulations and fibrinolysis factors that contribute to the differential diagnosis of the patients with community-acquired pneumonia (CAP) without effusion, uncomplicated parapneumonic effusion (UCPPE) and complicated parapneumonic effusion (CPPE).
The coagulations system is fundamental for the maintenance of homeostasis, and contributes to the inflammatory process responsible for CAP and the parapneumonic effusion. The factors of coagulations and fibrinolysis participate in the cellular proliferation and migration as in the synthesis of the inflammatory mediators.
We evaluated the laboratory profile of coagulations and fibrinolysis in the serum of 148 patients with CAP without effusion, 50 with UCPPE and 44 with CPPE. We determined the test of the coagulation cascade which measures the time elapsed from the activation of the coagulation cascade at different points to the fibrin generation. As a consequence, there is an activation of the fibrinolytic system with the increased D-dimer levels measured in the plasma in the three groups.
The patients were with mean age ± SD (53,82 ± 17,5) min – max 18–93 years. A significantly higher number of thrombocytes was in the group with CPPE with median 412 × 109/L (rank 323–513 × 109/L). The extended activation of the prothrombin time (aPTT) was significantly higher in the same group of patients with median of 32 sec. (rank 30–35 sec). The mean D-dimer plasma level was 3266,5 ± 1292,3 ng/ml in patients with CPPE, in CAP without effusion 1646,6 ± 1204 ng/ml and in UCPPE 1422,9 ± 970 ng/ml.
The coagulations system and the fibrinolysis play important role in the development and pathophysiology of CAP and the parapneumonic effusions.
Vladimir Pushevski, Petar Dejanov, Vesna Gerasimovska, Gordana Petrushevska, Angel Oncevski, Aleksandar Sikole, Zivko Popov and Ninoslav Ivanovski
Background: Hemodialysis as an efficient therapy for advanced CKD is the most used treatment modality all over the world. Even though primary AVF is widely accepted as a best permanent vascular access in hemodialysis patients, up to 60% of all fistulas fail to mature. The pathogenesis of early fistula failure is not very well understood. Many general and local factors are involved: patient′s age, sex, primary renal disease, small vessel′s diameter, presence of accessory veins, prior venipunctures, surgical skill, genetics, etc. Histological investigations have confirmed the neointimal venous hyperplasia as a major pathological finding in stenotic lesions of AVF failure, due to local inflammation, oxidative stress and migration and proliferation of myofibroblasts, fibroblasts and endothelial cells.
Materials and methods: A total of 89 patients with stadium 4-5 of CKD are involved in the study. A typical radio-cephalic AVF is created in all patients. Part of the fistula vein was taken for histological, immunohistochemical (Vimentin, TGF β and KI67) and morphometric analysis. Appriopriate statistical method was applied.
Results: Up to 80% of the patients showed some degree of endothelial changes at the time of creation of AVF, among them 19 pts with substantial intimal hyperplasia, 51 with medial hypertrophy and 19 pts with normal histology. Almost two thirds of the patients did not have expression of TGFβ. More than 95% had some expression of Vimentin. None of the patients had expression of the marker KI 67.
Conclusion: Medial hypertrophy is predominant preexisting pathohistological lesion prior the AVF creation, despite the presence of neointimal hyperplasia. The absence of TGFβ expression in majority of our patients could suggest that inflammation and oxidative stress are developing later, after vascular access surgery. The dominant cells within the stenosis in the veins are myofibroblasts. Their increased presence maybe a reason why some patients are prone to developing venous endothelial changes as a results of exaggerated vascular endothelial response to the effect of uremia, hypertension and other insults.
Poverty is a complex phenomenon involving various dimensions of not only the lack of goods and services. Being poor means being sick and not being able to see a doctor; all that it means to be unemployed and do not have a secure future; the poor rate it mean to be illiterate, not being able to attend school or abandon eaten; poverty rate means lack of many services and tools for everyday life. It 'hard to give a final definition of poverty because it varies from one period to another and from one country to another. Furthermore, poverty can be measured and evaluated in different ways. The evaluation of poverty based on a multidimensional definition of poverty and deprivation in income or consumption, seen from the flows, but also the non-monetary context poverty defined on my inadequacy of a series of welfare measures that have no income, as in education, health, empowerment, access to basic services and infrastructure.
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Viktor Kamnar, Anastasika Poposka, Nenad Atanasov and Milena Bogojevska
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