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Nonsteroidal antiinflammatory drugs (NSAIDs) contain conventional nonselective drugs and selective inhibitors cyclooxygenase-2 (ICOX-2). NSAIDs frequently cause adverse effects tied with cyclooxygenases (COX, COXs) inhibition and prostaglandins (PG, PGs) synthesis, which exerts different physiological effects and are involved in the patophysiology of osteoarthritis. NSAIDs don't inhibit leucotriens (LT LTs) generation. Nonselective drugs cause detrimental results in the gastrointestinal tract. Selective COX-2 inhibitors exert thrombotic cardiovascular events and other negative effects in cardiovascular system. NSAIDs can intensify symptoms of OA and accelerate its progress. Analgetic and antiinflammatory properties possess also licofelone, a competitive inhibitor of cyclooxygenases and 5-lipooxygenase (5-LOX), which presents well gastrointestinal tract tolerability in contrast to NSAIDs. Licofelone decreases the production of proinflammatory leucotrienes and prostaglandins. Moreover inhibition of 5-lipooxygenase activity can delay of cartilago degradation.

For more than 30 years statins have been successfully used in patients with hypercholesterolemia and cardiovascular diseases. Recently, there is a growing body of evidence, that statins exert effects by much exceeding the effect of cholesterol level decrease. Inhibition of earlier stages of cholesterol biosynthesis pathway (not influencing the very cholesterol level) results in blocking the intermediate metabolite synthesis; isoprenoids (farnesyl phosphate and geranyl phosphate), which play a regulatory function in cells. Statins have antiatherosclerotic, antiinflammatory, antioxidant, immunomodulatory and antithrombotic effects. It applies equally to diseases of chronic inflammation type, as to those, where bone metabolism is disturbed. It is well known that statins decrease bone fracture risk; through bone formation intensification, and inhibition of bone tissue resorption. Slowing down the atherosclerosis progression is a very important effect, considering that in rheumatoid arthritis (RA) and in systemic lupus erythematosus (SLE) we are dealing with premature and rapid progression of atherosclerotic lesions. In this paper statins pathways of action in rheumatic diseases (including pleiotropic effects), and their potential use in rheumatology have been discussed. Though there is lack of reliable data enabling statins introduction to standard complementary therapy in rheumatic diseases, the results however of completed studies allow concluding of their utility. The statins that were most frequently evaluated in clinical studies were simvastatin and atorvastatin. Studies on statins have been performed in RA, SLE, osteoporosis and systemic vasculotos.

The vascularization is a very important part of a structure of each tissue both normal, including bone marrow stroma, and pathologically changed. Neoplastic tissues secure supplying in necessary substances for growth and expansion through regulated by its own cells neovasculation. Key role in multipotential cell's differentiation to endothelial cells plays regulatory system consisted of vascular-epithelial growth factor's family (VEGF B, C, D), receptors VEGFR-1, -2, -3, and system Tie2/angiopoetins. Stimulation and importance of angiogenesis for expansion of neoplastic diseases is a current problem in oncology. It is pointed to importance of neovascularization in pathogenesis of acute and chronic leukemias, lymphomas and multiple myeloma. The knowledge of the importance ofvascularization of neoplastic tissues is availing in therapy (researching of substances inhibiting angiogenesis--semaxinib, SU6668, ZD 6474, thalidomid, cetuximab, gefitinib, interferon-alpha, irradiation and others), in diagnostics as a monitoring of a success of the therapy, and in prognosis. Inhibitors ofangiogenesis are antineoplastic drugs with relatively lower toxicity, and lower risk of drug-resistance than conventional chemotherapy what has the importance especially during prolong administration, so they can be an alternative way of therapeutic process. During qualification for antiangiogenic therapy it is necessary to have a consciousness of its limited efficiency.

Unlabelled: In recent studies it was observed antioxidant effects of statin independently on their hypolipemic effects. It is supposed that differences in statins pharmacological properties may cause different antioxidant actions. The aim of the study was to evaluate the effect of simvastatin, atorvastatin and pravastatin on plasma lipids, thio-barbituric acid reactive substances (TBARS) concentrations in the isolated erythrocytes membranes, activities of antioxidants enzymes in erythrocytes: catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) in patients (pts) with dyslipidemia., Material: The study comprised 114 pts, including 94 pts with dyslipidemia without concomitant chronic diseases and 20 healthy volunteers. Pts were qualified to treatment with statins if their LDL-cholesterol concentration (LDL-C) was above 160 mg/dL (4.1 mmol/l), total cholesterol (TC) > 250 mg/dl (6.5 mmol/l) and triglicerydes (TG) < 400 mg/dl (4.5 mmol/L). Pts were randomized to three groups: group I-n = 31 pts treated with atorvastatin (10 mg/d); group II-n = 31-simvastatin (20 mg/d), group III-n = 32 pravastatin (20 mg/d)., Methods: After 4 and 12 weeks of active treatment the following parameters were determined: TC, HDL-C, TG (by enzymatic method using bioMerieux tests); LDL-C was calculated from the Friedewald formula, TBARS concentrations (by method of Stock and Dormandy), CAT (method of Bartosz et al.), GSH-Px (method of Rice-Evansa et al.), SOD (method of Misra) activities., Results: During statin therapy significant decrease of TC, LDL-C, TG was observed, both after 4 and 12 weeks, as compared with the initial values. All statins significantly decreased TBARS concentrations either 4 or 12 week therapy at all. The activities of antioxidants enzymes (CAT, GSH-Px, SOD) significantly increased after 4 weeks therapy in patients treated with atorvastatin and simvastatin. During pravastatin therapy it was noticed only increase of CAT activity after 12 weeks., Conclusion: In patients with dyslipidemia without clinical symptoms of atherosclerosis atorvastatin, simvastatin and pravastatin decreased similar TBARS concentrations in membrane in the isolated erythrocyte membranes. It was observed a significant increase of the antioxidant enzyme activities during atorvastatin and simvastatin treatment. Pravastatin therapy caused increase the CAT activity without any effect on the activities of GSH-Px and SOD.

Background: Hyperlipidaemia is a well-established risk factor of the progression of coronary artery disease (CAD). Statins such as atorvastatin, as lipid-lowering agents, can not only normalise serum lipid levels, but also may improve endothelial function, reduce vascular inflammation and enhance plaque stability., Aim: To evaluate the efficacy of a low-dose atorvastatin regimen (10 mg daily) in patients with CAD., Methods: Seventy-nine patients with stable angina of II or III functional class and angiographically significant stenosis of coronary arteries (>70%) entered a 12-week treatment period with atorvastatin 10 mg/day. Lipid profile, which included total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were assessed at baseline and after treatment at week 12. In addition, flow-mediated vasodilatation (FMD) and nitrate-induced dilation (NID) of the brachial artery were measured before and after treatment., Results: Among 79 patients included in the study, in 54 (68%) the target TC value <5.0 mmol/l, and in 51 (65%) the LDL-C level <3.0 mmol/l were achieved. Atorvastatin decreased TC level by 31% (p<0.01), LDL-C level by 35% (p<0.01), TG level by 23% (p<0.01) and increased HDL-C level by 8% (p<0.01). FMD was increased by 61 % (p<0.01) and normalised in 88% of patients after 3-month therapy of atorvastatin. NID was increased by 16% (p<0.05)., Conclusion: Low-dose treatment with atorvastatin (10 mg daily) is effective in reducing blood lipids and is associated with the improvement of endothelial function in patients with CAD.

The studies results of statin influence on hemostasis are various. The aim of our study was to evaluate the effects of simvastatin and atorvastatin on hemostatic parameters, such as activity of factor X, antithrombin III, fibrinogen concentration and Lp(a). 72 patients (pts) aged 40-65 were involved in the study; 49 of them suffered from hyperlipidemia II (hlp II) with the initial concentration of total cholesterol (TC) >200 mg/dL, cholesterol LDL (LDL-C) >145 mg/dL, triglycerides (TG) <400 mg/dL. The control group consisted of 20 healthy persons. The pts with hlp II who underwent 4 weeks long lipid lowering diet were randomized into two groups: I--27 pts treated with simvastatin (20 mg/d), II--22 pts treated with atorvastatin (10 mg/d). The active statin therapy lasted 8 weeks. The activity of factor X and antithrombin III (AT III) was estimated by amidolytic methods, fibrinogen concentration (Fb) by the Clauss method, Lp(a)-immunoenzymatic method. The mean values of factor X activity and Fb serum concentration were higher in pts with hip II than in the control group, the AT III activity was lower. The Lp(a) concentration didn't differ between groups. Statin treatment was associated with significant reduction of factor X activity. Both simvastatin and atorvastatin markedly increased AT III (87%, 98%) in comparison to the initial values. No changes of Lp(a) concentration were observed during statin therapy. Atorvastatin therapy significantly increased the Fb concentration (12.3%). Simvastatin treatment didn't influence Fb concentration.