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INTRODUCTION The risk of stroke in patients with atrial fibrillation (AF) seems to be independent of the presence or duration of arrhythmia at a given moment. However, there is no single approved measurable parameter that would allow to predict the risk of stroke in patients with newly diagnosed AF. OBJECTIVES We aimed to determine the levels of von Willebrand factor (vWF) and high-sensitivity C-reactive protein (hs-CRP) as well as to measure the intima-media thickness (IMT) in patients in the first hours of an AF episode and compare these markers with predicted risk of stroke. PATIENTS AND METHODS The study group consisted of 60 consecutive adult patients with symptomatic AF lasting less than 48 hours. In all patients, vWF and hs-CRP levels as well as IMT were measured and compared with the calculated CHA2DS2-VASc score. RESULTS We found a significant difference in the levels of the measured markers (vWF, 110.3% [range, 92.3%-124.2%] vs 170.2% [range, 111.1%-219.5%], P

Systemic lupus erythematosus (SLE) is an autoimmune disease, whose main pathomechanism is attributed to the disturbed apoptotic process and dysfunction of the immune cells, leading to the accumulation of undegraded cellular matrix. This paper presents molecules such as complement components, pentraxins, and collectins, which are involved in the opsonization and removal of cellular material, and shows how deficiencies in these processes may contribute to SLE development and progression. Many reports indicate the specific role of the pentraxins (C-reactive protein, serum amyloid P, pentraxin 3), which, due to enhancing the phagocytosis of damaged cells and inducing the classical pathway of complement activation, participate in masking antigens from the immune system. The influence of CRP on inhibition of development and progression of kidney disease and decreasing the immune activity markers was demonstrated on the basis of research in experimental, mouse models of SLE. The decreased pentraxin response described in systemic lupus erythematosus patients, despite the presence of high levels of interleukin-6 and other markers of disease activity, is still unclear. Anti-mCRP antibodies bind CRP to form immune complexes, which are deposited in glomeruli and may initiate or exacerbate inflammation. In the literature, the correlation between raised levels of anti-CRP antibodies and clinical and immunological activity of lupus nephritis was proved. It shows their importance as a factor determining the severity of the disease and response to treatment. Novel studies suggest that the low CRP response in SLE is due to interferon-α inhibition of gene expression and CRP synthesis. This suggests that therapeutic targets in systemic lupus erythematosus should also be based on inhibiting the synthesis of interferon-α .

Introduction:There is a growing body of data concerning significant interactions between markers of inflammation and cardiovascular diseases such as hypertension accompanied by elevated levels of plasma C-reactive protein (CRP). Therefore CRP is thought to be an independent risk factor of cardiovascular diseases.Material/Methods:The aim of this study was to evaluate the effects of antihypertensive therapy (perindopril, bisoprolol and combined therapy) on plasma CRP concentration in 67 subjects with mild or moderate hypertension who have been treatment-naive and otherwise healthy.Results:The results show a correlation between CRP level and blood pressure values. BP reduction was associated with a decrease in CRP concentration. The CRP-lowering effect of perindopril and bisoprolol was comparable and the degree of reduction might reflect their similar influence on blood pressure. Combined treatment influenced the CRP level to a greater extent than both monotherapies.Conclusions:Plasma CRP level was lowered by antihypertensive therapy independently of the drug applied. The CRP level did not normalize completely in moderate hypertensive patients.