Association between Bacterial Infection and Peripheral Vascular Disease: A Review.

There are an increasing number of data showing a clinically important association between bacterial infection and peripheral artery disease (PAD). Bacteria suspected of being involved in PAD pathogenesis are: periodontal bacteria, gut microbiota, Helicobacter pylori, and Chlamydia pneumoniae. Infectious agents may be involved in the pathogenesis of atherosclerosis via activation of a systemic or local host immunological response to contamination of extravascular tissues or the vascular wall, respectively. A systemic immunological reaction may damage vascular walls in the course of autoimmunological cross-reactions between anti-pathogen antibodies and host vascular antigens (immunological mimicry), pathogen burden mechanisms (nonspecific activation of inflammatory processes in the vascular wall), and neuroendocrine-immune cross-talk. Besides activating the inflammatory pathway, bacterial infection may trigger PAD progression or exacerbation by enhancement of platelet reactivity, by a stimulatory effect on von Willebrand factor binding, factor VIII, fibrinogen, P-selectin activation, disturbances in plasma lipids, increase in oxidative stress, and resistance to insulin. Local inflammatory host reaction and induction of atherosclerotic plaque progression and/or instability result mainly from atherosclerotic plaque colonization by microorganisms. Despite these premises, the role of bacterial infection in PAD pathogenesis should still be recognized as controversial, and randomized, controlled trials are required to evaluate the outcome of periodontal or gut bacteria modification (through diet, prebiotics, and probiotics) or eradication (using antibiotics) in hard and surrogate cardiovascular endpoints.

The level of 8-oxo-7,8-dihydro-2'-deoxyguanosine is positively correlated with the size of the labile iron pool in human lymphocytes.

It appears that the labile iron pool (LIP, low molecular weight iron) presence in cells can result in the production of reactive oxygen species (ROS). ROS may be responsible for the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) in cellular DNA. In the present study we report on the relationship between LIP and the endogenous level of 8-oxodGuo in human lymphocytes. Good correlation has been determined between LIP and the oxidatively modified nucleoside. This in turn points out the possibility that under physiological condition there is the availability of LIP for catalyzing Fenton-type reactions in close proximity to cellular DNA. Electronic supplementary material to this paper can be obtained by using the Springer Link server located at http://dx.doi.org/10.1007/s00775-001-0335-x.

Level of antithrombin III, protein C, protein S and other selected parameters of coagulation and fibrinolysis in the blood of the patients with recurrent deep venous thrombosis.

BACKGROUND: Thrombophilia is caused mainly by disturbances of hemostasis involving excessive coagulation system activation, reduction of anticoagulation system (antithrombin III, protein C, protein S, RAPC) or fibrinolytic activity. MATERIAL/METHODS: In 34 young patients (aged <40 years) with recurrent deep venous thrombosis (>2 incidents) the activity of antithrombin III, protein C, S, platelet count, adhesion and aggregation, APTT, stipven-kephalin, prothrombin time and INR were investigated. Fibrinogen, factor XIII, ELT, FDP, Ag t-PA levels, antigen concentration and PAI-1 activity were determined. Patients with idiopathic DVT, after elimination of most important thromboembolism risk factors, were qualified for the study. DVT was confirmed in all patients by phlebography, plethysmography and ultrasonography. Results were compared with a group of 54 healthy controls. RESULTS: In almost 50% of patients with recurrent DVT (15/34) decrease of at least one plasma coagulation inhibitor (AT III, PC, PS) level was observed. In the patient group (with AT III and/or PC and/or PS decrease) statistically significant reduction of kaolin-kephalin time in comparison with controls was observed (a<0. 01). Analysis of fibrinolysis system demonstrated significant factor XIII level decrease (to 58.3%), fibrinogen level increase, ELT prolongation, and fibrinogen and fibrin degradation product increase in comparison with controls. The patients demonstrated 3-fold higher t-PA antigen level (13.1 ng/ml, a<0. 0001) and over 3-fold higher PAI-1 activity (26.7 AU/ml, a<0. 001) than healthy controls. CONCLUSIONS: Reduced antithrombin III, protein C, protein S activity and excessive activation of the coagulation system with secondary fibrinolytic activity increase were found in patients with recurrent DVT.

[Significance of carcinoembryonic antigen levels in peritoneal washings in clinical analysis of patients with colorectal cancer]. / Oznaczanie stezenia antygenu karcynoembrionalnego w popluczynach otrzewnowych u chorych na raka jelita grubego.

The aim of this study was to analyse the level of CEA in peritoneal washings (CEAp) in patients with colorectal cancer (crc) in comparison to the serum CEA level. The study involved 87 patients with crc, the control group included 13 patients operated on due to vascular diseases. At the time of laparotomy, after administration of 200 ml saline, peritoneal washings were collected from the peritoneal cavity. After concentrating, the CEAp level was determined using an immunochemiluminescence assay kit. The cutoff value was set at 100 ng/g protein. The data were analysed using Student t-test, Welch test and Mann-Whitney test. The mean CEA levels in peritoneal washings in patients with colorectal cancer were statistically higher (p < 0.001) than in the control group (except stage A). There was no correlation between CEAp levels and sex, histological type and differentiation, Duke's stage (except D2). The mean CEAp levels were significantly higher in colonic tumour, than in cancer in rectal location (P < 0.03). Positive correlation between CEA level in peritoneal washings and serum was found.