Impact of hormonal contraception on prothrombotic activity in vessels.

One of the most common, efficient and convenient methods of contraception is hormonal contraception. Due to its popularity among young women, the safety of this method should be taken into consideration. Alternative ways of hormonal application are used and additional prothrombotic factors are being researched in order to minimize prothrombotic activity. The paper presents current data on the relationship between hormonal contraception and vascular complications based on peer-reviewed medical journals that were published between the years 2001 and 2013.

Altered monocyte calcium-sensing receptor expression in patients with type 2 diabetes mellitus and atherosclerosis.

UNLABELLED: The increased cardiovascular risk in type 2 diabetes mellitus (DM2) is the result of disorders of the immune system, including the enhanced reactivity of monocytes and impaired secretion of inflammatory cytokines. The aim of this study was to analyze the expression of calcium-sensing receptor (CaR) in peripheral blood monocytes of individuals with DM2 and peripheral artery disease (PAD). The study included 88 individuals, among them 37 patients with PAD (group A--atherosclerosis), 27 individuals with DM2 and PAD (group AD--atherosclerosis and diabetes mellitus), and 24 controls (group C--controls). The expression of CaR on isolated peripheral blood monocytes was analyzed at the level of surface protein (CaR(surf)) and mRNA (CaR(mRNA)). Concentrations of pro-inflammatory cytokines were determined by means of ELISA, while the severity of PAD was assessed with Doppler and impedance plethysmography. The expression of CaR(surf) was the highest in the controls (mean 41.27%) and did not differ significantly as compared to individuals from group AD (35.66%); however it was significantly higher than in group A (24.49%). The expression of CaR(surf) was related to the severity of PAD, fasting concentration of glucose, and the concentration of monocyte chemotactic protein (MCP-1). Additionally, significant differences were observed with regards to CaR(mRNA) expression; although, no significant relationships were documented between CaR(mRNA) and laboratory or clinical variables. Different ways of CaR(surf) and CaR(mRNA) expression regulation were associated with the concentration of osteopontin. CONCLUSION: A nearly 1.5-fold higher expression of CaR(surf) on the peripheral blood monocytes of individuals with diabetes and PAD manifests during post-transcription stage and depends on fasting glucose concentration and MCP-1 concentration on one hand, and the severity of PAD on the other.

Chronic lower limb ischemia and advanced renal failure. Do we possess sufficient therapeutic knowledge?

Chronic lower limb ischemia diminishes the quality of life and is associated with a higher risk of limb amputation and cardiovascular mortality. Coexisting chronic renal disease can modulate the response to pharmacotherapy and revascularization, and thus influence prognosis. This paper reviews current literary evidence regarding therapeutic problems observed in patients with obliterative atherosclerosis and renal failure. We reviewed articles from peer-reviewed medical journals which were published between 2000 and 2011. The poorer clinical response in the discussed patients is not only connected with the direct failure of surgical and endovascular procedures, but first of all with the high mortality of the patients. There is still a lack of sufficient evidence on the effectiveness of currently used anti-atherosclerotic agents in patients with end-stage renal failure. A certain priority is the search for an effective therapeutic strategy that would reduce mortality associated with cardiovascular conditions in this particular group of patients. Identifying patients who can benefit most from costly endovascular procedures is another vital issue.

Practical importance and modern methods of the evaluation of skin microcirculation during chronic lower limb ischemia in patients with peripheral arterial occlusive disease and/or diabetes.

Skin ischemia is one of the crucial phenomena during chronic lower limb ischemia in patients with peripheral arterial occlusive disease and/or diabetes. However, risk stratification for development of ischemic ulceration and/or skin necrosis in those patients is not easy, mostly due to the complex structure of the dermal vascular bed and limited possibilities for studying the skin capillaries in everyday practice. All definitions of critical limb ischemia thus far have considered mostly the clinical symptoms and the degree of macrocirculatory impairment. Despite the fact that the reduction of absolute dermal perfusion and improper distribution of perfusion in ischemic feet, primarily diminished perfusion or even a complete loss of blood flow in nutritional capillaries, rather than arterial occlusion per se, is the eventual reason for critical limb ischemia symptoms, the vessels of the microcirculation are not routinely assessed in clinical practice. Monitoring of microcirculatory parameters, as a part of integrated diagnostic approach, may have a considerable value in the evaluation of risk, progression of the disease and the effectiveness of therapeutic intervention in individual patients. Relative simplicity and availability of different non-invasive methods, including video capillaroscopy and laser Doppler fluxmetry, should constitute a premise to their wider application in clinical management of chronic limb ischemia.

Role of anti-HSP 60/65 antibodies in atherogenesis in patients with type 2 diabetes and lower limb ischemia.

The role of heat shock proteins and anti-HSP 60/65 antibodies in atherogenesis has been widely described in the literature, but the participation of these molecules in the pathogenesis of diabetic macroangiopathy has not been extensively investigated. 30 patients with type 2 diabetes complicated with macroangiopathy of the lower extremities in the intermittent claudication stage. The control group (n=18) consisted of healthy volunteers of corresponding age. Levels of anti-HSP 60/65 antibodies, von Willebrand factor (vWF) and hsCRP in blood serum were measured. We also assessed static effort based on isometric contraction lasting until full fatigue. In patients with lower limb ischemia in diabetic macroangiopathy, a positive correlation between anti-HSP 60/65 antibodies and von Willebrand factor levels in blood serum was found (R=0.543, p<0.05). Concentrations of anti-HSP 60/65 antibodies were higher than in the control group, but not statistically significant (44.77±55.00 vs. 26.09±13.85; NS). The ongoing disease process contributed statistically significantly to the strength of the quadriceps muscle of the thigh (21.47 vs. 27.82 for the right limb, and 20.27 vs. 28.33 for the left limb; p<0.05). Increased concentrations of anti-HSP 60/65 antibodies in blood serum suggests their involvement in the pathogenesis of diabetic macroangiopathy and correlates with the parameters of endothelial cell damage. In patients with type 2 diabetes complicated with atherosclerotic changes, a statistically significant reduction in lower limb muscle strength was found compared with the control group.

Peripheral nerve changes assessed by conduction velocity distribution in patients with primary Raynaud's phenomenon and dysautonomia.

AIM: Different mechanisms (neural and intravascular) are thought to be important in the pathogenesis of Raynaud's phenomenon (RP). In a previous study we confirmed autonomic nervous system impairment in patients with primary RP, but the pathogenic role of peripheral nerves remained unclear. The aim of the current study was an electrophysiological analysis of peripheral nerves using both standard conduction velocity and the conduction velocity distribution (CVD) in patients with primary RP in order to investigate the causes of dysautonomia. METHODS: We examined 34 patients with primary RP and dysautonomia and 31 sex- and age-matched controls. Standard motor and sensory conduction tests in ulnar and peroneal (sural) nerves and a CVD test in the same nerves were performed. RESULTS: Clinically, none of the patients had motor symptoms, while 35.3% of them presented sensory neuropathy. Standard neurographic tests were within the normal limits except for the significant prolongation of mean sensory latency in both examined nerves. CVD revealed significant slowing of motor conduction velocity in all the conduction values, e.g. in the 10th, 50th, and 90th percentiles of velocity. There were no differences in the width of the velocity distribution in the patient group and controls. CONCLUSION: The results of CVD indicated the presence of generalized subclinical peripheral motor nerve impairment (subclinical polyneuropathy) in patients with primary RP and dysautonomia. Based on the present and previous studies, we conclude that the mechanism of autonomic dysfunction in primary RP is mixed, resulting from both central and peripheral neural abnormalities.

Circulating endothelial cells, endothelial apoptosis and soluble markers of endothelial dysfunction in patients with systemic lupus erythematosus-related vasculitis.

AIM: Evidence is accumulating for endothelial cell dysfunction as one of the main factors initiating vessel wall damage in SLE. Enhanced expression of endothelial adhesion molecules is suggested to play a crucial role in the pathogenesis of vasculitis, while the number of circulating endothelial cells (CECs) is believed to be a reliable marker of endothelial damage. It therefore seems relevant to investigate CECs counts and soluble markers of endothelial dysfunction in SLE patients with inflammatory microangiopathy. The aim of this study was to assess the number of CECs, including apoptotic CECs, as well as to determine serum levels of sVCAM-1, sICAM-1 and sE-selectin in patients with SLE-related vasculitis. METHODS: The study included 51 women with SLE, divided into 2 subgroups: I patients with severe disease activity according to SLEDAI score, developing vascular complications, such as central nervous system affection and/or vasculitis and/or glomerulonephritis, II patients with mild or moderate disease activity, without vascular complications. The control group consisted of 16 healthy female volunteers. CECs, including apoptotic CECs, were isolated using anti-CD146-coated immunomagnetic Dynabeads. Serum levels of sVCAM-1, sICAM-1 and sE-selectin levels were determined with ELISA. RESULTS: In patients with SLE, CEC counts were significantly higher than in healthy controls, and strongly correlated with disease activity assessed by SLEDAI score. The number of apoptotic CECs, as compared with healthy subjects, increased considerably only in subgroup I. Serum sVCAM-1 levels were notably increased in subgroup I in relation to subgroup II and in subgroup II in relation to the control group, while serum sICAM-1 and sE-selectin levels in both subgroups were comparable and significantly higher than those of healthy subjects. CONCLUSIONS: The study showed that the number of CECs increases in SLE and strongly correlates with disease activity, reaching maximum values at the stage of inflammatory microangiopathy-related complications. Severe SLE flares are characterized by enhanced endothelial cell apoptosis. Progressive increase in serum sVCAM-1 levels is connected with disease activity aggravation and development of lupus microangiopathy.

Autonomic dysfunction in primary Raynaud's phenomenon.

AIM: The pathogenesis of Raynaud's phenomenon is still unclear. Neural and intravascular mechanisms are thought to be involved in the pathological process. The role of the autonomic nervous system is continually discussed, with particular attention to over-reactivity of the sympathetic part. The aim of this study was the clinical and electrophysiological analysis of autonomic nervous system function in patients with primary Raynaud's phenomenon. METHODS: Thirty four patients with primary Raynaud's phenomenon and 31 sex and age-matched controls were examined. Neurological examination, modified Low's Questionnaire, orthostatic and sustained handgrip tests, conduction velocity study in three nerves, sympathetic skin response (SSR), and heart rate variability (HRV) during deep breathing and at rest with the fast Fourier transform were performed. RESULTS: In the clinical examinations, 35.3% of the primary Raynaud's patients presented sensory neuropathy, but this was not confirmed in the standard conduction velocity tests. The modified Low's Questionnaire revealed dysautonomy in 82% of the patients. Autonomic regulation during the orthostatic and handgrip tests were within the normal limits. HRV at rest and the E/I ratio were significantly lower in the patient group than in the controls, while HRV spectrum analysis revealed the predominance of the low-frequency band in the patients. CONCLUSIONS: These results indicate the presence of sympathetic dysregulation and impairment of parasympathetic modulation of heart function in primary Raynaud's patients. The different cardiovascular and sudomotor functions are not affected to the same degree. These observations might support the theory of a central impairment of autonomic function in primary Raynaud's phenomenon. Peripheral nerve lesion as a coexisting cause of the observed dysautonomy remains uncertain.

Tissue factor, tissue pathway factor inhibitor and risk factors of atherosclerosis in patients with chronic limbs ischemia: preliminary study.

AIM: Thrombus formation plays a critical role in pathogenesis of cardiovascular complications in atherosclerotic peripheral arterial occlusive disease (PAOD). Tissue factor (TF) initiates the clotting cascade and is considered an important regulator of hemostasis and thrombosis. TF activity is regulated by TF pathway inhibitor (TFPI). The aim of our study was to evaluate plasma levels of the TF, TFPI and their relation to coagulation system and various other risk factors of atherosclerosis in patients with chronic limbs ischemia. METHODS: Plasma TF, total TFPI, truncated TFPI, full-length TFPI were assessed by ELISA using commercially available kits (IMUBIND Tissue Factor; Total TFPI; Truncated TFPI ELISA Kit; American Diagnostica Inc. Stamford) in 62 claudicant patients with PAOD and 20 healthy controls. RESULTS: We observed statistically higher levels of TF (94+/-52 pg/mL), total TFPI (43+/-8 ng/mL), and truncated TFPI (22+/-7 ng/mL) in patients with PAOD compared to healthy individuals (TF: 66+/-15 pg/mL; total TFPI: 36+/-4 ng/mL; truncated TFPI: 14+/-5 ng/mL). Full-length TFPI (20+/-4 ng/mL) is lower in patients with PAOD than in controls (23+/-5 ng/mL). The study indicated a positive correlation between TF and truncated TFPI (r=0.34), total TFPI and full TFPI (r=0.5), total TFPI and truncated TFPI (r=0.83) in patients with PAOD, and negative correlation between full TFPI and truncated TFPI (r=-0.65) in the control. CONCLUSION: Elevated levels of TF, disorders of balance between full-length TFPI and truncated TFPI as well as significantly increased truncated TFPI level in patients with PAOD can be independent risk factors of atherosclerotic complications.

Neutrophil surface expression of CD11b and CD62L in diabetic microangiopathy.

The aims of the study are (1) assessment of cell surface expression of adhesion molecules CD11b and CD62L on peripheral blood neutrophils in patients with type 2 diabetes and microangiopathy; (2) analysis of serum levels of soluble adhesion molecules: E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and von Willebrand factor (vWF) and; (3) evaluation of systemic inflammatory markers like interleukin-6 (IL-6), soluble interleukin-6 receptor (IL-6Rs), high sensitivity C-reactive protein (hsCRP) and fibrinogen. Thirty patients with type 2 diabetes and microangiopathy were enrolled in the study. The study group was compared to 22 patients with type 2 diabetes without microangiopathic compliations. The control group included 20 healthy volunteers. Flow cytometry was used to analyse surface expression of adhesion molecules. Both inflammatory markers and soluble adhesion molecules were determined by immunoenzymatic assay. A significant increase in neutrophil surface CD11b expression (P < 0.01) as well as decrease in surface CD62L expression (P < 0.01) were observed in the group with diabetic microangiopathy in comparison with diabetic group without microangiopathic complications and healthy controls. Moreover, significantly higher concentrations of sICAM-1 (P < 0.05), sVCAM-1 (P < 0.05), sE-selectin (P < 0.05), vWF (P < 0.01), hsCRP (P < 0.01), IL-6 (P < 0.01) and fibrinogen (P < 0.001) were also found in patients with microangiopathy in comparison with the control group. IL-6Rs concentrations did not significantly vary between groups. We concluded (1) diabetic microangiopathy is accompanied by increase in CD11b expression and decrease in CD62L expression on peripheral blood neutrophils; (2) in diabetic microangiopathy rise in CD11b expression indicates neutrophil activation and intensified adhesion; (3) the development of diabetic microangiopathy is accompanied by an increase in soluble adhesion molecules and inflammatory markers concentrations in the blood.

The role of endothelin-1 and selected cytokines in the pathogenesis of Raynaud's phenomenon associated with systemic connective tissue diseases.

AIM: In the pathogenesis of Raynaud's phenomenon humoral and immunoinflammatory agents are involved. The aim of this study was the assessment of the level of endothelin-1 (ET-1), tumor necrosis factor (TNF-alpha), interleukin-6 (IL-6), soluble IL-6 receptor (IL-6sR), von Willebrand's factor (vWF) and platelet factor 4 (PF-4) in patients with Raynaud's phenomenon associated with systemic connective tissue diseases. METHODS: The examined group consisted of 32 patients (24 women and 8 men) with Raynaud's phenomenon associated with selected connective tissue diseases, aged 28-50 years. A control group consisted of 13 healthy volunteers. Immediately after a cold provocation test venous blood was taken in order to assess serum concentrations of: TNF-alpha, IL-6, IL-6sR, vWF, PF-4, antinuclear antibodies (ANA), antineutrophil antibodies (c-ANCA). RESULTS: In the group of patients with Raynaud's phenomenon mean serum concentration of ET-1, TNF-alpha, PF-4, and vWF was significantly greater than in the healthy group. In contrast, serum IL-6 and IL-6sR concentrations did not differ significantly between the diseased and healthy groups. In a subgroup of Raynaud's phenomenon patients showing particularly high concentration of serum ET-1 (twice as much as mean control concentration), the increase in IL-6, IL-6sR, vWF and c-ANCA concentration exhibited statistical significance in comparison with patients with lower serum ET-1 concentration. The vWF concentration exhibited positive correlation with time interval between the occurrence of clinical symptoms and serum ANA antibodies concentration. The increase in ET-1 synthesis in Raynaud's phenomenon patients is dependent on the increase in IL-6 level and c-ANCA antibodies level. CONCLUSIONS: The patients with Raynaud's phenomenon show an increase in ET-1 and TNF-alpha concentrations. An enhanced ET-1 synthesis is dependent on the augmentation of serum c-ANCA antibodies and IL-6 concentrations.

The biological role of protease-activated receptors in angiology. The present view.

The mechanism of initiation and growth of a thrombus in atherosclerotic arteries, although investigated extensively, has not been sufficiently elucidated. Understanding the molecular mechanisms that lead to stroke, unstable angina and myocardial infarction is of paramount importance. Protease-activated receptors (PARs) belong to a recently discovered and so far not fully characterized family of transmembrane proteins, which are involved in the initiation growth of thrombi in atherosclerotic arteries. PARs are a G-protein-coupled family of receptors which mediate a cellular function with the aid of enzymes. All of them have identical structural organization and are activated by a very similar mechanism. The enzyme (serine protease) cleaves an extracellular amino-terminal fragment of the receptor in order to unmask a new amino-terminal, 5-6 residues of which serve as the tethering ligand, able to activate its maternal receptor. According to the most recently published reports, in eukaryotic organisms there are 5 different PARs: from PAR 1 to PAR 4 found in human organisms and PAR 5 discovered as a 14-3-3 protein, identified firstly in C. elegans and Drosophila melanogaster. Up to now numerous experiments have been conducted with the aim to understand more precisely the mechanisms of PARs activation and activity. The present paper summarizes the most important and most recently published reports concerning this problem, which seems to be most relevant in angiology.

Platelets' glycoproteins and their ligands in patients with intermittent claudication.

BACKGROUND: Platelet thrombi play critical role in pathogenesis of cardiovascular complications in atherosclerotic peripheral arterial disease (PAOD). The aim of this study was to evaluate the concentration of platelets GP IIb/IIIa, GP I b/IX and plasma levels of their ligands (fibrinogen and vWF) and their relation to other atherosclerotic risk factors in the patients with intermittent claudication secondary to PAOD. METHODS: Consecutive patients of the University Vascular Clinic were studied: 64 claudicants and 38 controls were enrolled. The concentration of platelets GPII b/IIIa and GP Ib/IX was estimated by ELISA method using monoclonal antibody against GPII b/IIIa (CD41a) and GPI b/IX (CD42a Immunotech). Plasma levels of vWF, fibrinogen, and platelets were measured by routine RESULTS: Plasma vWF (145+/-41%), fibrinogen (3.8+/-1 g/l) and platelet concentration of GP Ib/IX (121.1+/-23.39), GPIIb/IIIa (117.9 6 +/-32.7%), as well as plasma lipids and uric acid were statistically higher in claudicants than in controls (vWF: 103+/-42%, fibrinogen: 2.9+/-0.5 g/l, GP Ib/IX: 100+/-16.9%, GP IIb/IIIa: 100+/-29.4%). We have observed statistically higher concentration of GP IIb/IIIa and GP Ib/IX in smoking patients than in non-smoking patients with PAOD and significant correlation between the concentration of GP Ib/IX and GP IIb/IIIa and plasma fibrinogen in patients with PAOD and controls. CONCLUSIONS: Our results demonstrate higher platelet concentration of GP Ib/IX,GP IIb/IIIa and elevated plasma levels of ligands for platelets receptors-fibrinogen and vWF in patients with PAOD. This prothrombotic conditions may explain increased cardiovascular morbidity and mortality in this patient's group.

Coagulation in diabetic and non-diabetic claudicants.

BACKGROUND: In order to compare hemostasis in diabetic and non-diabetic claudicants we evaluated endothelial (von Willebrand factor, vWF), rheologic (fibrinogen, hematocrit), coagulation system (thrombin-antithrombin complex, TAT) and platelet (platelet factor 4, PF4, aggregation on thrombin, collagen and ADP stimulation) parameters in both groups and healthy controls. METHODS: Twenty-five diabetic, 34 non-diabetic patients with claudication and 26 healthy individuals were enrolled into the study. RESULTS: The severity of lower limbs ischemia was similar in two groups of claudicants but coronary heart disease and cerebral ischemia were significantly more common in diabetic than in non-diabetic claudicants. vWF level was significantly higher in diabetic than non-diabetic claudicants and healthy controls (184+/-43%, 147+/-43%, and 103+/-42%, respectively). Fibrinogen was significantly higher in diabetic and non-diabetic claudicants compared to controls (4.2+/-1.7, and 3.9+/-1.1, versus 2.9+/-0.5 g/l) and TAT plasma concentration was much higher in diabetic compare to non-diabetic patients and controls (9.8+/-4.4, 1.7+/-1.1, and 1.3+/-0.6 microg, respectively). PF4 concentration was significantly higher in non-diabetic patients with PAOD (34+/-29 UI/ml) when compare to healthy controls (14+/-9 UI/ml), but diabetic PAOD patients with the disease showed lower PF4 concentration (26+/-30 UI/ml). Platelet aggregation with all used activators was similar in all groups likewise hematocrit values, and platelet count. CONCLUSIONS: Complicated DM is linked with significant endothelial perturbation when compared with healthy, but also with PAOD individuals; rheologic parameters are not different from those found in PAOD patients; coagulation system activation but not platelet hyperactivity is associated with DM complicated by PAOD when compared to both control groups.

[Endothelin-1 in pathogenesis of Raynaud's syndrome]. / Endotelina-1 w patogenezie zespolu Raynauda.

Endothelin is an endogenous vasoconstrictor and plays an important role in pathogenesis of Raynaud's phenomenon. Plasma endothelin-1 (ET-1) and von Willebrand factor (vWF) concentrations following cold exposure in 52 patients with Raynaud's phenomenon were measured. Statistically significant increase of ET-1 and vWF was found in the study group in compare to healthy volunteers. There was positive correlation between ET-1 and vWF in those cases. The dates suggest that ET-changes indicates a vasospastic effect on vascular injury. Treatment with endothelin-receptor antagonist may prevent structural changes in vessel well.

[Chronic peripheral arterial occlusive disease, platelet glycoproteins GPIIb-IIIa and GP Ib-IX, plasma von Willebrand factor and plasma fibrinogen concentrations in patients with type 2 diabetes mellitus]. / Przewlekla obwodowa niewydolnosc tetnicza a stezenie glikoprotein GPIIb-IIIa i GP Ib-IX w krwinkach plytkowych oraz czynnika von Willebranda i fibrynogenu w osoczu u chorych na cukrzyce typu 2.

Diabetes mellitus (DM) type 2 is a very strong risk factor for atherosclerosis. The final event of atherosclerosis is the vessels occlusion by platelet riche thrombus. Platelets adhesion and aggregation is mediated by interaction between platelets glycoproteins: GPIb-IX, GPIIb-IIIa and adhesive proteins: von Willebrand factor or fibrinogen. The expression of platelets GPIb-IX, GPIIb-IIIa, plasma vWF, fibrinogen concentrations were evaluated in 40 patients with diabetes type 2 (22 patients with PAOD stage II and IV according to Fontain, 18 diabetics without paod) and 32 healthy individuals. The expression of platelets glycoproteins GPIIb-IIIa and GPIb-IX was estimated by ELISA using monoclonal antibody against GPIIb-IIIa (CD41a) and GPIb-IX (CD 42a Immunotech). Plasma vWf (189.7 +/- 53.6%), fibrinogen (4.5 +/- +/- 1.3 g/l) level and expression of platelets GPIb-IX (63.2 +/- 19.6% in platelets concentration 125,000/mm3, 104.5 +/- 28.1% in platelets concentrations 250,000/mm3) and GPIIb-IIIa 50.8 +/- 10.1% in platelets concentrations 125,000/mm3, 95.3 +/- 21.3% in platelets concentrations 250,000/mm3 were statistically higher in patients with diabetes type 2 than in controls (vWf: 94.9 +/- 27.1%, fibrinogen: 2.8 +/- 0.4 g/l, GPIb-IX in platelets concentration 125,000/mm3: 43.8 +/- 9.3%, in concentration 250,000/mm3: 83.9 +/- 18.3%, GPIIb-IIIa in platelets concentration 125,000/mm3: 33.7 +/- 10.1%, in platelets concentration 250,000/mm3: 63.2 +/- 15.4%). We found significant correlation between the expression of GPIIb-IIIa, GPIb-IIIa, GPIb-IX and plasma adhesive proteins: vWF, fibrinogen in controls and both subgroups of diabetic patients. The correlation between plasma vWF and fibrinogen level and degree of arterial insufficiency in diabetic patients was also found. We can assume that higher vWf, fibrinogen plasma level in diabetic patients with and without PAOD could account for high expression of platelets GPIIb-IIIa and GPIb-IX.

[Lipoprotein and plasminogen serum levels in patients with diabetes mellitus type 2: risk factors for macroangiopathy? Preliminary study]. / Stezenie lipoproteiny (a) i plazminogenu u chorych na cukrzyce typu 2: czynniki ryzyka rozwoju makroangiopatii? Doniesienie wstepne.

Lipoprotein(a) [Lp(a)] is the specific lipoprotein which physiological role has not been explained. Similarity between apolipoprotein(a) and plasminogen structure suggests, that Lp(a) can be the bridge connecting the lipid metabolism and the coagulation system. The aim of the study was to evaluate if there is any correlation between Lp(a) and plasminogen serum concentrations in patients with diabetes t.2. 20 males and females with diabetes t.2 in the age 19-75 years (mean: 54.9 years). The control group consisted of 15 healthy men and woman in the age of 23 years (medical students). Lp(a) was estimated by ELISA, plasminogen by turbidimetric methods. Lp(a) serum level in the examined group was: 40.06 + 59.45 mg%. In 7 patients it was over 30 mg%. In the control group: Lp(a) concentration was: 13.23 + 10.5 mg%, no one was above 30 mg%. The different was significant. Plasminogen concentration was: in patients: 94.08 + 53.08%, in the control group: 89.08 + 40.7%. There was no significant difference. Correlation index between Lp(a) and plasminogen concentrations was in the patient's group: 0.3, in the control group: 0.2. In patients with diabetes we can find increased Lp(a) commentation in serum and normal plasminogen concentration. Concentration of Lp(a) didn't demonstrate significant correlation with plasminogen serum level.

[Endothelial response for the presence of chosen antinuclear antibodies, anti-Ro (SS-A) and anti-La (SS-B) and anti-Sm in vasculitis against the background of existing lupus erythematosus]. / Odpowiedz sródblonka na obecnosc wybranych przeciwcial przeciwjadrowych: anty-Ro (SS-A), anty-La (SS-B) i anty-Sm w zapaleniu naczyn na podlozu ukladowego tocznia trzewnego.

Systemic lupus erythematodes is a disease commonly associated with peripheric circulation disturbances. The goal of the study was the evaluation of the role of the following nuclear antibodies: anti-Ro (SS-A), anti-La (SS-B) and anti-Sm in the endothelium damage process in the SLE patients with symptoms of microcirculation disturbances. The concentration of plasma thrombomodulin was used as a marker of the endothelium destructive changes intensity. Twenty-four patients with SLE (22 women and 2 man) aged of 18-57 (the average age 40.50 +/- 9.72 years) in which occurred: the Raynauds symptom (16 patients), fingers cyanosis (5 patients) and fingers and/or toes necrosis (3 patients) were investigated. Antinuclear antibodies and thrombomodulin level was estimated with the ELISA method. In all patients, the concentration of anticardiolipin antibodies in serum was determined (ELISA-method, cardiolipin was used as an antigenes, Sigma USA). Higher titers of ANA antibodies in 83%, anti-SM antibodies in 30%, anti-Ro in 42% and anti-La in 42%, examined patients and higher titer of anti-Ro and anti-La antibodies together in 29% of examined patients were stated. Statistical significant correlation between the increased level of thrombomodulin and anti-La antibodies concentrations in serum of patients with the disease lasting over 6 years was found out. The significant statistical correlation of thrombomodulin concentration increasing and anti-La antibodies in serum was proved. The dynamism of limbs circulation disorders depends on the disease duration.

[Syndrome X--open problem of contemporary medicine]. / Zespól X--otwarty problem wspólczesnej medycyny.

Based on the present literature data we have confronted the clinical parameters and some pathogenetic mechanisms of the syndrome X. Especially we stressed the danger of the accelerated development of the atherosclerotic changes in the vessels and the cardiologic complications.